Among the recent advances in cancer therapy, the achievements of chemotherapy, especially those of multicombination chemotharapy, are most remarkable. On the other hand, the development of cancer immunology has led to the introduction of immunochemotherapy, i.e. a chemotherapy combined with immunopotentiators which may mitigate the depression of immunological function caused by the cancer itself or by chemotherapeutics. However, it has been found that these immunopotentiators reduce the metabolic activity of the host against drugs, including “masked” chemotherapeutics, which should be activated by metabolization in the body.
Reported here is the result of serial experiments carried out on the metabolic activity of tumor-bearing animals against Cyclophosphamide (CPM), pretreated with Phenobarbital, a drug metabolizing enzyme inducer, and Coenzyme Q₁₀, a physiological activator of the electron transfer system in mitochondrias, in combination with immunopotentiators.
Female Donryu rats (100-120g body weight) impla nted with Yoshida Sarcoma cells (YS)(2.5 × 10⁶ i.p. or 1.0 × 10⁷ s.c. ) were treated with CPM (160mg/ kg × 1 i.p. ),84 hrs after implantation; the levels of the normustard-like substances (active metabolites of CPM) were serially measured. Some of the animals were also treated with PSK (125 mg/kg × 5 i.p. ), a proteinpolysaccharide immunopotentiator obtained from mycelia of the Coriolus vesicolor, or with OK-432 (10 KE/kg × 5 i.m. ), a streptococcal immunopotentiator.
The blood levels of the normustard-like subs tances were lowered, i.e. the CPM actvation was depressed, in the YS-bearing rats; and the depression was markedly intensified by PSK or OK-432 administration. Phenob arbital or Coenzyme Q₁₀ administration could mitigate the depression of the blood levels caused by the immunopotentiators, and the combination of Phenobarbital with Coenzyme Q₁₀ could recover the blood levels up to those of the YS-bearing control rats, or even higher ;the effect was more significant in the I.P. YS-implanted animals than in S. C. ones.
These findings suggest the usefulness of Coenzyme Q₁₀ for the enhancement of can cer immunochemotherapy using masked compounds combined with immunopotentiators; all the more so, because Coenzyme Q₁₀ has also an immuno-stimulating effect, and, morever, it presents almost no side effects in clinical application.

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Plasma ADH levels were estimated by radioimmunoassay before and after hemodialysis in 54patients with chronic renal failure. Mean plasma ADH level was 14.4 ± 0.7 (S. E. ) pg/ml before hemodialysis, which was significantly higher than those of normal controls and patients with essential hypertension. After 6 hours of hemodialysis mean plasma ADH level fell significantly to 10.7 ± 1.0 pg/ml despite volume and blood pressure reduction in most cases.
There was significant correlation between plasma ADH levels and effectiv e plasma osmolalities before and after hemodialysis. The regression line shifted to the left and slope was more gentle before hemodialysis in chronic renal failure than in normal controls. After the hemodialysis it still shifted to the left but ran parallel to the regression line of the normal controls. There were no statistically significant correlations between the change in plasma ADH level and the change in blood pressure or blood volume by hemodialysis.
From these results it may be suggested that there occur resetting and alteration of sensitivity of the osmoreceptor and threshold for ADH secretion will be decreased in chronic renal failure. The sensitivity of the osmoreceptor will be improved by hemodialysis.
Impaired degradation of ADH by the diseased kidney a nd other organs and/or alteration of the sensitivity of baroreceptor by the derrangement of the internal milieu might account in part for the increased plasma ADH level in chronic renal failure. The possibility of removal of ADH by hemodialysis was also discussed.

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In order to evaluate the filling characteristics of the left ventricule (LV) in the hypertension (H-group) were cpmpared to 16 patients with idiopathic hypertrophic cardiomyopathy (HCMgroup)and 50 normal subjects (N-group) by echocardiography. According to the amount of LV wall thickness (sum of interventricular septum and LV posterior wall thickness), H-group was divided into three groups: H1 group consisted of 20 cases, H2 of 25, H3 of 19; values of wall thickness were 2.5 cm or less,2.6 to 3.1 cm and 3.2 cm or more, respectively. N-group was subdivided into four age groups in order to assess the effect of age on LV geometry and hemodynamics: Ni (29y or less), N2 (30-39y), N3 (40-49y) and N4 (50y or more).
Mitral valve and LV echocardiograms were analyzed by a digitizer-computer sy stem to obtaine isovolumic relaxation time (IRT), diastolic descent rate of mitral valve (DDR), LV dimension, wall thickness, LV posterior wall motion (PWV) and LV volume change. LV diastolic time was divided into three phases; rapid, slow and atrial filling phases (RFP, SFP, AFP respectively). Filling rate (FR) and ratio of the fractional-filling volume to the total LV filling (FF)in each phase were calculated.
LV diameter was slightly smaller in H-groups and remarkably smaller in HCM-group than in N-group. There were no significant differences in the heart rate, P-Q interval and systolic contractile indices among the groups. Mean and maximal PWV in diastole were significantly reduced in H and HCM groups, and maximal rate of LV circumferential fiber lengthening was reduced in H2 and H3 groups as compared to N-group. In H and HCM groups, longer IRT and slower DDR were noted. Filling fractions in RFP and AFP (RFF, AFF) were 64.5and 22.5% in N,54.9 and 28.5% in H2,41,6 and 43,6% in H3,65.7 and 19.8% in HCM group, respectively. In N and H groups, the values of RFF and AFF were signifincantly correlated with LV wall thickness. (r= -0.69, r=0.72, respectively) As for mean filling rates of RFP and AFP (RFR, AFR), RFR were slower and AFR faster in H groups than in N group, while both filling rates were significantly slower in HCM group.
In normal subjects, N4 (2.2 cm) had thicker LV wall than N1 (1.9 cm), while the LV volume and diameter were same in both groups. IRT was more prolonged in N4 than in Ni. As to concerning to filling fraction, N4 group had reduced RFF (60%) and augmented AFF (28%) as compared to N1 group who had 67 and 20%, respectively.
These findings indicate that 1) in the normal heart, LV wall thickens with larger LV volume/mass ratio, and LV filling in the early diastole becomes impeded with aging; 2) in the hypertensive heart, LV early diastolic filling is impeded as LV hypertrophy asvances and the atrial kick mechanism works more forcefully and effectively to compensate the impaired filling; 3) in the hypertrophic cardiomyopathic heart, the atrial filling to the ventricle is not sufficient to compensate the reduced filling in the early diastole, probably because the LV cavity is disproportionately small as compared to the marked hypertrophic wall, and the left ventricular myocardium has a disarray in arrangement of cardiac muscle cells.

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The effect of urea on central nervous system activity was investigated electrophysiologically in the rabbit and the following observed.
1) Intravenous injection of ur ea resulted in the appearance of spindle waves and slow waves in the spontaneous EEG. With injection of a massive dose, evoked muscular discharge of the phasic type became apparent in the hind limb in some cases.
2) With administration of urea, the blood NPN lev el increased and this increase tended to parallel the change in the spontaneous EEG.
3) The threshold of evoked muscular discharge and the arousal reaction due to stimulation of the brain stem reticular formation gradually rose with administration of urea.
4) The frequency of spontaneous unit discharge of the brain stem reti cular formation showed a trend to gradually decrease with adminisration of urea.
5) The threshold of evoked muscular discharge o f the fore and hind limbs due to stimulation of the cerebral cortex rose markedly with administration of urea.
6) The threshold of evoked muscular discharge of the fore and hind limbs due to stimulation of the hippocampus drops with administration of urea.
7) The amplitude of the afferent average evok ed potential appearing in the cerebral cortex, decreases in general with administration of urea and the peak time of the early component becomes extended but N₃ shows a trend to transiently increase with administration of a small amount of urea.
8) The afferent average evoked potential appearing in the hippocampus is somewhat inhibited by the administration of urea.
9) The nociceptive ev oked muscular discharge, H-wave and M-wave are intensified by the administration of a small amount of urea but are then inhibited on increasing the quantity of urea.
10) Intestinal movement is intensified by the administration of a small amount of urea but is gradually inhibited on increasing the amount.
11) The blood flow volume of the common carotid artery showed a trend to slightly decrease with administration of urea.
12) Spontaneous disc harge of the sympathetic nerve is markedly intensified by the administration of urea.
13) MV is inhibited by the administration of a relatively small amount of urea but gradually recovers or even increases on increasing the quantity of urea.
14) Bilateral rigation of the ureters of the rabbit results in a prominent rise in NPN and this rise is accompanied by a pronounced inhibition of MV.

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The technique of a selective continuous coronary perfusion with cold oxygenated blood of low flow rate for protecting the ischemic myocardium under the aortic cross-clamping dur ing open-heart surgery had been applied in our department since November,1973. The effe ct of this technique was searched experimentally and clinically in this study.
Experimentally, the effect of 2-hour period of the selective continuous coronary perfusion with cold blood during the aortic cross-clamping was compared with those of the selective continu ous coronary perfusion with cold Ringer-lactate solution and of the topical cooling with cold physiological saline solution, using normal adult dogs as well as dogs with experimentally produced left ventricular hypertrophy. Twenty adult mongrel dogs, weighing 12 to 15 kilograms, and 10mongrel dogs with left ventricular hypertrophy produced by banding of the ascending aort a were subjected to total body perfusion.
In the group of cold blood coronary perfusion, oxygen amount extracted from myocardium was 0.006 to 0.01ml/min/gm of myocardial weight even at 15°C of myocardial tempe rature and an anaerobic metabolism was not demonstrated during the myocardial hypothermia, which indicated that the metabolic process contnued 15°C of the myocardial temperature. After release of the aortic cross-clamping or after weaning from the cardiopulmonary byass, the myocardial metabolism and the cardiac function were satisfactorily maintained. These findings we re essentially similar to those in the group with left ventricular hypertrophy of cold blood coronary perfusion. Moreover, the findings at 2-hour period of the aortic cross-clamping and at the period after release of it and after weaning from the cardiopulmorary bypass in the group of cold Ringerlactate coronary perfusion without oxygenated blood were almost same as those in the g roup of cold blood coronary perfusion, so far as myocardial temperature was maintained below 15°C.
On the contrary, in the group of topical cooling, an anaerobic metabolism remained during the period after release of the aortic cross-clamping and also after weaning from the cardiopu lmonary bypass. Moreover, in this group, the rate of weaning from the cardiopulmonary bypass was significantly lower than those in both groups of coronary perfusion, although as to the cardiac functions after weaning from the bypass, they differed little. The degree and the duration of anaerobic metabolism in the myocardium after release of the aortic cross-clamping in the group with hypertrophied left ventricle of topical cooling were more severe than those in the group with non-hypertrophied heart of topical cooling. These results showed that topical cooling could not provide a protection for ischemic myocardium in both normal dogs and dogs with left ventricular hypertrophy.
Clinically,25 patien ts with significant myocardial hypertrophy (15 patients with right ventricular hypertrophy and 10, with left or both ventricular hypertrophy) were selected from patientsgroups who underwent the technique of cold blood coronary perfusion from November,1973 to December,1977, in whom the duration of the aortic cross-clamping during open-heart surgery was over 60 minutes (60 to 214 minutes, average 94 minutes). In this series, the myocardial metabolism during and after cold blood coronary perfusion was examined. Furthermore, a serial creatine phosphokinase MB isoenzyme (CPK-MB) activity after weaning from the extracorporeal circulation was measured in other 13 patients who underwent cold blood coronary perfusion and was compared with the data of another group of patients who did not undergo this technique. At 15°C of myocardial temperature,2.5 to 3.0ml/min of oxygen were extracted from the myocardium during hypothermic coronary perfusion. The myocardial metabolism during cold blood coronary perfusion or during rewarming period after release of the aortic cross-clamping were satisfactorily

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It has not been established yet how to estimate intracranial pressure (ICP) by a simple, practical and non-surgical method at the early stage of intracranial hypertension in case of head injury and cerebral vascular accident. The author payed attention to the ocular findings under the condition of intracranial hypertension, and designed an experimental study for understanding the correlation between the ocular circulation and intracranial pressure.
Intracranial hypertension was made by means of inflation of epidural balloon (0.05 ml/min)placed on the right frontal region. Epidural pressure was measured on the left frontal region and EEG was recorded on both frontal areas. Ocular circulation was recorded by fluorescein angiography on the left eye.0.15 ml of 0.05% fluorescein sodium was injected through the catheter canulated into the lingual artery under the condition of external carotid artery ligation. Vital signs were checked and fluorescein angiography was done at the following stages in each dog; Control: before inflation of the balloon, Stage A: no increase in ICP, (spacial compensation), Stage B: EEG change, Stage C: midriasis on the right eye, Stage D: Cushing phenomenon.
The experiment was carried out under two different conditions; Group 1: und er controlled respiration, Group 2: under spontaneous respiration. The results obtained are as follows:
A: Group 1
1) The order of the appearance of the retinal arteries is not affected by the increase in ICP.
2) Refilling phenomenon, that is, reincrease of fluorescence in the retinal arteries once after the decrease in its intensity, was observed in 10 dogs out of 14. This phenomenon bec a me remarkable as ICP increases up to Stage C. At Stage D, it became more prominent in 4dogs and obscure in 6 dogs.
3) Retinal circulation time was not prolonged at Stage A. Nine dogs at stage B and all dogs at Stage C showed prolonged circulation time which became prominent in proportion to the increase of ICP. At Stage D, circulation time was prolonged in.4 dogs and shortened in 8 dogs.
4) Retinal circulation time had relationship with cerebral perfusion pressure in linear fashion.
5) Washout curves of fluorescence in the eye ground and optic disc were comparatively resembling. At Stage A, no difference from the control was observed. At Stage B in som e dogs and at Stage C and D, fluorescence was observed till late in all dogs and two-peak pat t e rn and prolonged washout curve were observed in accordance with the degree of the r e filling phenomenon.
6) Neither hemorrhage nor leakage of fluorescence was found in any dogs.
B: Group 2
No critical difference from the results of Group 1 was obtained in the retinal circulation time and appearance curve of fluorescence, respectively. Hemorrhage and leakage of fluorescence were not remarked at all.

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Circulatory dynamics at rest and after the oral administration of 80 mg furosemide were evaluated in 46 patients with normal-renin hypertension,34 patients with low-renin hypertension and 28 normal subjects. The normal-renin hypertensives were comprised of 29 men and 17women, and the low-renin hypertensives of 13 men and 21 women. Cases with severe staged hypertension were excluded from this study.
Hemodynamic parameters were determined by Impedance Cardiography at rest and three hours after administration of furosemide in supine position.
At rest, the normal and the low-renin hypertensives showed smaller stroke index than the normal subjects, but cardiac index did not differ significantly among three groups. In the lowrenin hypertensives, mean and diastolic blood pressure and total peripheral resistance were higher than the normal-renin hypertensives.Hematocrit was significantly lower in the low-renin group than the other two groups.
Urine volume following three hours of furosemide administration was smaller in the hypertensive group than the normals, but no difference was found between the normal-renin and the low-renin groups. Hematocrit increased indentically in all three groups.
The normal subjects responded to the provocation of furosem ide by significant reduction of cardiac output and elevation of total peripheral resistance without any significant changes in heart rate and mean blood pressure. These observations indicate that the blood pressure was maintained by the elevation of total peripheral resistance in response to the reduction of circulatory blood volume and cardiac output induced by the diuretic effect of furosemide. The normal-renin hypertensives responded to furosemide by significant reduction of blood pressure and stroke index with significant increase in heart rate and total peripheral resistance. This group showed greater reduction of stroke index and increase of heart rate compared to lowrenin group. These findings suggest that in addition to the effect of angiotensin II, the increased sympathetic activity was one of the major compensatory mechanism following the provocation of furosemide. On the other hand, low-renin hypertensives responded to furosemide by significant reduction of cardiac output and marked reduction of blood pressure. There were no significant changes in heart rate and total peripheral resistance in low-renin hypertensives. In low-renin hypertension, it is assumed that hypervolemia is one of the most important factor to maintain the high blood pressure. Therefore, it is suggested that the reductin of blood pressure and cardiac output following furosemide were observed without compensatory sympathetic activity.

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Hemodynamic parameters including systolic time intervals were evaluated non-invasively at recumbent rest and during uninterrupted multi-graded exercise with a sitting bicycle ergometer in thirty-three men with essential hypertension and thirty-five healthy men by Minnesota impedance cardiography.
Subjects were subdivided with age: group NI, comprised 24 normotensives under 40: group NII,11 normotensives from 40 to 60: group HI,13 untreated hypertensives under 40: group HII,20 untreated hypertensives from 40 to 60.
Exercise was started at 25 watts for three minutes and increased by 25 watts every three minutes.
1) At recumbent rest: Group NII showed higher diastolic blood pressure, lower SI/ET (left ventricular mean ejection rate) and (SI/ET) /PEP ratio than group NI. There were no significant differences in other hemodynamic parameters between the normotensive groups. Both hypertensive groups showed lower stroke index, cardiac index, higher total peripheral resistance and longer PEP than the age-matched normotensives. Group HI showed higher heart rate, shorter LVET and Q-IIA interval than group NI. These findings indicate that the hypertensives have increaed resistance to left ventricular ejection and that in group HI, the increased sympathetic stimulation may play a part in maintaining the elevated blood pressure.
2) During exercise: The increment of stroke ind ex, cardiac index, SI/ET and the decrement of total peripheral resistance were greater in the middle-age groups than in the young-age groups. These findings indicate that the middle-age groups have inproper blood distribution during exercise. The (SI/ET) /PEP ratio, which is thought to demonstrate the reactivity of left ventricle, increased identically in all groups. The changes of systolic time intervals were not significantly different among each group. These findings indicate that although the resistance to left ventricular ejection had increased in the hypertensive groups, the cardiac function itself was maintained in the normal range.

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In order to asses the cardiac function of ischemic heart disease, 31 patients (6 stable angina and 25 old myocardial infarction) without overt heart failure were studied. Pulmonary artery diastolic pressure (PADP), mean right atrial pressure (mRAP) and cardiac index (CI) were measured by SWAN GANZ catheter prior to infusion (control) and at every 100 ml infusion of 6 % hydroxyethyl starch (infusion rate was 20 ml/min. ). Slope of cardiac function curve was calculated from maximum change of CI divided by PADP. We terminated the infusion when the PADP rearched 18 mmHg or the total infusion volume of 400 ml. The patients in this study were subdivided into 5 groups according to the ECG findings and clinical features in acute phase.
Group I consists of 6 patients with stable angina. Control PADP was 6.5 ± 2.1 mmHg mean ± 1SD), mRAP was 1.8 ± 1.0 mmHg and CI was 3.58 ± 0.54 L/min/m². Group II consists of 9 patients with /inferior myocardial infarction. Control PADP was 6.5 ± 2.1, mRAP was 1.3 ± 0.9 and CI was 3.15 ± 0.46. Group 3 consists of 5 patients with anteroseptal myocardial infarction. Control PADP was 9.6 ± 2.1, mRAP was 2.8 ± 1.9 and CI was 3.25+ 0.55. Group IV consists of 6 patients of myocardial infarction with previous history of myocardial infarc tion. Control PADP was 10.2 ± 4.3, mRAP was 1.2 ± 1.6 and CI was 2.97 ± 0.87. Group V consists of 5 patients with right ventricular infarction. Control PADP was 8.0 ± 4.1, mRAP was 3.8 ± 1.6 and Cl was 2.96 ± 0.87. Control PADP and CI were normal in all groups there were no significant differences between earch groups. Group V showed significantly higher mRAP than other groups. Although the patients in group I showed significant increase in PADP (2.7± 1.0 ), mRAP (0.8 ± 0.4) and CI (0.22 ± 0.13) from control, these changes were smaller than other groups. Group 11 showed significant increase in PADP (7.8 ± 2.0), mRAP (1.9 ± 1.2)and Cl (0.95 ± 0.37) from control. Group II showed significant increase in PADP (8.4 ± 2.7), mRAP (1.6 ± 1.5) and Cl (0.47 ± 0.33) from control. Group IV showed significant increase in PADP (10.0 ± 3.8), mRAP (3.0+1.3) and CI (0.45+0.34) from control. One patient in group III and four patients in group N, the PADP increased over 18 mmHg and CI decreased at this higher pressure. The slope of cardiac function curve of group III (0.06+0.04) and group IV (0.07 ± 0.07) were significantly smaller than group II (0.13+0.06). Group V showed significant increase in PADP (5.2± 1.6) and mRAP (3.6± 1.7), but there was no significant increase in CI (0.28+0.36). The change of mRAP from control in this group was significantly larger than other groups.
Hemodynamics being identical among the 5 groups (mRAP in group V was higher than other groups but was in normal range), the cardiac function and reserve could not be assesed prior to volume expansion. Our findings by volume expansion suggests: 1) In group I cardiac reserve was maintained by the neuro-humoral regulatory mechanisms.2) Regulatory mechanism to preload augumentation is fairly well reserved in group II, but compromised in group III and was severly compromised in group IV.4)In group V right ventricular failure which was suggested in control became overt after volume expansion.
Volume loading test is a interesting test to understand the natural history and pathologic phisiology of ischemic heart disease.

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The plasma levels of β2-microglobulin (2-MG) were measured by radioimmunoassay in 25healthy subjects of various ages and 54 patients on regular dialysis treatment (RDT) 3 times during a 4.5-5 hours hemodialysis.
In healthy subjectsit revealed fairly stable individual values, an increase with age and no sex difference. In patients on RDT its levels were very high (45.75 ± 18.12mg/l, mean ± S. D. ), increased slowly during a hemodialysis and in some of the cases within the first one year after beginning hemodialysis treatment, revealed more often higher values.
Hence, it was the aim of this study to investigate if hemodi alysis treatment exerted influences on the plasma, β2-MG.
1. Considerin g that plasma β2-MG levels raise in some inflammatory disorders with immunopathological features, these patients were divided into CRP positive and negative groups. Although it was expected that in the CRP positive group plasma β2-MG levels increased highly during a hemodialysis, there was not a statistically significant difference.
2. After a hemodialysis the plasma levels of β2-MG decreas ed slowly, and the pre-dialysis levels of this time returned to the pre-dialysis levels of last time. β2-MG was not measurable in dialysate. Hence, β2-MG was shown to be a non-dialysable substance.
3. Although the plasma levels of β2-MG revealed a good cor relation with duration of hemodialysis, in the hemodialysis two times and three times per week the correlation was not observed. There was a fairly good correlation between its levels of β2-MG and urine volume per day. Consequently the plasma β2-MG in hemodialysis patients was found to be one index of residual renal function.

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In order to assess the hemodynamic effects of OP-1206, oral prostaglandin E1 derivative,7healthy controls and 48 patients (20 with essential hypertension,11 with old myocardial infarction,7 with acute myocardial infarction and 10 with atrial fibrillation) were studied at rest and 60 minutes after oral administration of the drug (30, μg).
Hemodynamic studies were made by means of impedance cardiography, echocardiography and Swan-Ganz right heart catheterization technique. Brachial arterial pressure was measured by the air-cuff method. Left ventricular function curves were constructed for in patients with atrial fibrillation: preceding R-R intervals and stroke volumes computed from impedance cardiogram were plotted on x and y axes, respectively.
The healthy control group sho wed significant decrease in mean systemic arterial blood pressure by 7% without any significant changes in heart rate, cardiac index and total peripheral resistance index. In the hypertensive group, the mean arterial pressure decreased by 14%, cardiac index increased by 13% and the resistance decreased by 23%. In the patients with old and acute myocardial infarction, mean arterial pressure decreased by 8-13%, cardiac index increased by 14-19% and the resistance decreased by 17-28%. However, no significant change in heart ra te was observed in these groups. No significant changes in left ventricular end-diastolic and endsystolic volumes were demonstrated in the hypertensive group. In the patients group with acute myocardial infarction, pulmonary diastolic pressure showed significant decrease by 21%; this reduction of left ventricular filling pressure was considered to be secondary to afterload reduction to the left ventricle by vasodilating effect of OP-1206. The maximum hemodynamic effects of the drug were observed within an hour and the effects continued four hours or more from op-1206 (30μg) administration.
The circulatory changes observed in this study indicate that prostaglandin E1 derivative, OP-1206, has a vasodilating and/or antihypertensive effect. The drug is considered to be effective and benefical against hemodynamic state with excessive afterload to the left ventricle.

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In order to evaluate the acute antihypertensive and hemodynamic effects of nifedipine,53patients in sinus rhythm were subdivided into 5 groups according to diastolic blood pressure (DBP) and cardiac index (CI). Hemodynamic variables were obtained by impedance cardiography before and 30 minutes after 10 mg of oral nifedipine. Group N (healthy subjects) showed 10%reduction in total peripheral resistance index (TPR I),16% increase in CI and 15% increase in heart rate (HR) after nifedipine. Group HT-1 (hypertensive patients with normal cardiac output) showed 30% decrease in BSP and DBP,58% reduction in TPRI,16% increase in CI and 14% increase in HR. Group HT-2 (hypertensive patients with low cardiac output) showed 21% decrease in SBP,19% decrease in DBP,45% reduction in TPRI,17% increase in CI and 11% increase in HR. Group OMI-1 (old myocardial infarction patients with normal card iac output) showed 16% decrease in SBP,11% decrease in DBP,30% reduction in TPRI,11% increase in CI and 15% increase in HR. Group OMI-2 (old myocardial infarction with low cardiac output) showed 22% decrease in SBP, no change in DBP,30% reduction in TPRI,9%increase in CI and no change in HR. Cardiac function curves were obtained from the patients in lone atrial fibrillation and these curves shifted to the left and upward after administration of nifedipine.
It is concluded that oral nifedipine is not only a effective drug to hypertensive patients but also a drug of choice afterload reduction in patients with congestive heart failure.

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The early introduction of impedance reducing therapy in acute coronary care is considered to prevent the development of overt heart failure.
Hemodynamic effect of oral nifedipine 10mg was evaluated under monitoring with Swan-Ganz catheter in 16 cases after acute myocardial infarction: 8 cases (AMI-1 group) with pulmonary arterial diastolic pressure (PADP) of 17mmHg or less and 8 cases (AMI-2 group) with PADP of 18mmHg or more. All the cases had cardiac index (CI) of 2.2L/min/sqM or more and with inappropriately augumented total peripheral resistance (TPR) in the baseline states. Th irty minutes after nifedipine administration, the hemodynamic changes were manifested by significant decrease in TPR and mean arterial pressure and modest increase in CI, without any significant change in mean right atrial pressure. These changes were accompanied by significant decrease in PADP in AMI-2 group, but not so in AMI-1 group.
These findings indicate that the left ventricular output workload is significantly reduced by oral nifedipine and that it has a vasodilating effect on systemic as well as coronary arteries, but not on venous vessels. It is concluded that oral nifedipine may be one of the drugs of choice for afterload reduction therapy for acute myocardial infarction patients care.

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A 62 year old male was hospitalized on Dec.13,1979. He was complaining of back pain and his previous doctor had pointed out an abnormal shadow on his chest X-ray film.
Although cytological examinations of the patient's sputum revealed Pap. Class I V-V, a keratinized squamous cell carcinoma of the lung, his plain chest X-ray examination, tomography and computerized tomography suggested the presence of a possible extrapulmonary tumor on the right lung and adenocarcinoma in the lower lobe of the left lung. Lab. data: liver and renal functions normal
CRP 1+
CEA 33.3
PPD skin test positive
PHA skin test positive
blood gas analysis within normal limit
He was treated with Pepleomycin and Mitomycin-C regimen (PM regimen). After the 5th course of PM regimen, his genral condition deteriorated. The patient died of respiratory failure on April 15,1980 and the autopsy revealed that he had suffered from bilateral, primary double lung cancer. A epidermoid carcinoma, which originated from the S6 region of the right lung, had invaded right pleural cavity, the diaphragm, the percardium, the right IXth rib and the IXth thoracic vertebrae. On the other hand, a well differentiated adenocarcinoma was located mainly in the lower lobe of the left lung. Microscopic examination revealed no evidence, in either lung, of metastatic sites from the cancer of the opposite lung. In addition, the hilar lymphnodes were determined to be free of any metastatic sites from either lung.
Primary double lung cancer is of very rare incidence. In Japa n, in 1976 and in 1977, it was found in autopsy reports in approximately 0.6% of all lung cancer cases. The percentage of occurence drops even lower to 0.16% for primary double lung carcinomas, in which each lung has independently developed histologically different cancers.

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