As to the pathogenesis of the coronary atherosclerosis, J. B. Duguid proposed the thrombogenic theory in 1946, but there have been some arguments about this.
Infiltration theory is now regarded as important, that is, the infiltration of the plasma constituents into the intima, especially of fibrin (fibrinogen) and β-lipoprotein. But there seems to be some overlap between the thrombogenic and filtration theory concerning the fibrin deposition in the intima.
In this paper, to elucidate the pathogenesis on the initiation and progression of the coronary atherosclerosis, the followings were studied, first, permeability pattern of the rabbit coronary artery, secondly, histochemical and immunohistochemical study on the coronary atherosclerosis, thirdly, pathogenesis of the coronary thrombosis.
1. As a distinct feature of the rabbit coronary artery was there frequent presence of fenestration in the internal elastic lamina and this might contribute to the more enhanced permeability, especially by virture of junctional transport.
2. In the focal and diffuse intimal fibrous thickening, both β-lipoprotein and lipid were often detected in the presence of fibrin. But in the absence of fibrin, both β-lipoprotein and lipid were detected exceptionally. This suggested that the fibrin preceded the β-lipoprotein and lipid deposition. As the pathogenesis of coronary atherosclerosis, the fibrin and β-lipoprotein deposition played the important role and it must be also taken into consideration that the enhanced permeability pattern and pulsative mechanical injury of the coronary artery might contribute to it.
3. As the histological changes of the thrombosed arterial segments, rupture of fibrous cap of atheroma was found in 55.6%, mural hemorrhage in 37.0%, liquefaction of intimal surface lined by foam cells in 1.8% and marked sclerosis in 5.6% of thrombosed segments.

抄録全体を表示

The contents of lipids and GAG of coronary arteries, aorta and cerebral arteries from Japanese autopsy cases were measured.
The percentage of cholesteryl ester. (CE%), which was represented the contents of cholesteryl ester in total cholesterol, of normal intima of cerebral artery under 60 years old was lower than those of coronary artery and aorta. The higher value (40%) of EC% in normal intima of coronary artery even under 20 years old was characteristic feature, which was similar like that of normal intima of aorta, but not like that of normal intima of cerebral artery. This findings suggested that the permeability of endothelial surface of intima of cerebral artery was different from those of coronary artery and aorta.
There were no differences in the percentage of Hyaluronic Acid in total GAG (HA%) between not only each arteries, but also normal intima and atherosclerotic lesions. The percentage of Chondroitin-4/6-Sulfate in total GAG (CS-4/6-S%) of cerebral arteries, however, was showed the lower value both in normal and atherosclerotic intima when compared with those of aorta and coronary artery. Under 60 years old, the CS-4/6-S% of normal intima of coronary artery was lower than that of aorta. This results may suggested that these changes of hyaluronidase resistant GAG would be concerned the permeability from endothelial surface of plasma lipoproteins or the clearances in intima of lipoproteins entered from plasma. The percentage of Dermatan Sulfate in total GAG (DS%) in intima of coronary artery was slightly decreased when compared with those of aorta and cerebral artery and was not changed with aging or atherosclerosis.
The CS-4-S/DS ratio of each arteries with atherosclerosis were examined because the biological role of CS-4-S and DS have been said to have on inhibition of binding and binding capacity with lipoproteins respectivery.
The CS-4-S/DS ratio of coronary arteries and aorta were decreased with atherosclerosis and apparently higher than that of cerebral arteries.
With these results, it may be suggeted that the atherogenesis of coronary arteries would be different in the view point of the differences of GAG contents of intima of coronary arteries when compared with those of aorta and cerebral arteries.
The atherogenesis of coronary arteries was discussed in comparison to those of aorta and cerebral arteries.

抄録全体を表示

An extensive histopathological study of 122 patients with acute myocardial infarction who died after having been admitted to our coronary care unit was carried out. These patients had chest pain, clinically diagnosed as acute myocardial infarction by electrocardiogram and other lavoratory data and autopsy revealed coagulation necrosis of the myocardium in every case.
Each main coronary artery and its branches were carefully sectioned transversely at 3mm. intervals along their entire course. Both the occluded segments of the coronary artery and sections taken 3mm. proximally and distally to the occluded segments were embedded in paraffin and sectioned transversely at intervals of 100 microns. In cases where a thrombus was not detected, coronary segments which showed the most severe stonosis were carefully examined by serial section.
Firstly, the relationship between acute myocardial infarction, and coronary thrombosis, and secondly, the pathogenesis of coronary thrombosis is discussed.
The results of this study are as follows:
1. Serial sectioning is needed because the pathology of the lumen is extremely variable within a 2 to 3-mm. segments.
2. A high incidence (84.3%) of thrombus formation, corresponding to the site of the infarction, was observed. These thrombi occluded the lumen and were usually formed at the proximal region of coronary arteries.
3. Fresh occuluding coronary thrombi were formed at the site of the ruptured atheromatous plaque in 84 of the 91 cases (92.3%).
4. Coronary thrombi containing plaque components such as foam cells, cholesterin clefts and the fractured intimal collagen fiber were detected.
5. In two patients who succumbed suddenly after coronary attack, we found the ruptured atheromatous plaque only, but not a thrombus. As these patients showed severe stenosis with recanalisation in 2 of the 3 main coronary arteries, the rupture of the plaque caused significant occlusion of the remaining coronary artery.
6. Increase of intra-plaque pressure resulting from a honeycomb-like accumulation of foam cells, cholesterin clefts, and blood infiltration from lumen to plaque through the injured endothelial cells is the cause of rupture of the atheromatous plaque. This rupture into the lumen might precede, and be responsible for, formation of the thrombus and onset of acute myocardial infarction.

抄録全体を表示

A clinicopathological study of the heart and coronary arteries was performed on 360 residents, autopsied during a study period of ten years, of the community of Hisayama. Mean autopsy rate among the dead aged 20 years or over was approximately 82 per cent during this period. The findings obtained were as follows:
1) There were many myocardial infarct cases where a typical cardiac pain was lacking.
2) There were many cases where myocardial infarct was initially found by autopsy.
3) Reliability of some subitems of the Minnesota code I-1 and I-2 for the diagnosis of myocardial infarct was disappointing.
4) Coronary atherosclerosis had closer correlation with systolic blood pressure than with diastolic blood pressure.
5) Relative frequency of myocardial infarct cases had no correlation with diastolic blood pressure. However, the possibility was suggested that relative frequency of myocardial infarct cases might have some association with elevated systolic blood pressure.

抄録全体を表示

Main branches of the middle cerebral arteries and coronary arteries of normotensive and hypertensive human autopsy cases were investigated electron microscopically.
The cerebral arteries showed intimal thickening consisting of increased smooth muscle cells, basement membrane-like substance, elastin and collagen fibrils with aging. The intimal smooth muscle cells underwent necrotic change, and the internal elastic lamina showed destructive change with aging gradually. Medial muscle cells showed necrotic aging change, such change was severe immediately beneath the internal elastic lamina.
Intimal thickening of the cerebral arteries was marked in hypertensive cases. In hypertensive cases intimal muscle cell injury was slight but medial muscle cell injury was so severe that all of medial cells showed necrotic change and muscle cells near the internal elastic lamina could not be found because of necrosis.
Intimal thickening of the coronary arteries became marked with aging, but intimal and medial muscle cell injuries were extremely rare in both normotensive and hypertensive cases.

抄録全体を表示

The present investigations consist of two different experimental studies. Expt. 1; comparison of intimal response for cellular proliferation after endothelial denudation due to the air dried-injury of segmental arteries and veins of dogs, rabbits and rats. Expt. II; comparison of lipid synthesis and of accumulation in abdominal aorta and vena cava, endothelium of which had been denuded by air dried-injury in experimentally produced hyperlipemic rats and rabbits.
Intimal responses for cellular proliferations were obiously high in the arterial walls, particularly in the central portions of the denuded segments which were covered most delayedly by regenerative endothelium compared to the bilateral peripheral portions where endothelium were rapidly regenerated. Venous responses for cellularr proliferation in intima were negligible, except by ovbiou sthrombosis.
Lipid accumulation in denuded arterial intima were tremondous, contrary to undenuded aortae and denuded vena cavae. In addition, ultra-structural microscopy revealed a large number of electron dense lipids in the intercellular spaces of the denuded as well as of the undenuded aortic intima, while the denuded venous walls even seen scattery lipophages had no accumulation of the electron dense lipid in their extracellular matrixes.
On the view of above mentioned findings, arterial smooth muscle cells have different responses for cellular proliferation and for lipid accumulation in intima, compared with venous smooth muscle cells. These cellular differences may cause by different clonal strain of smooth muscle cells, and may play an important role in human atherogenesis.

抄録全体を表示

For the quantitative assessment of atherosclerotic lesions both in experimental animals and humans, a new method has been developed, in which a common xerox machine is the sole equipment. The arterial specimen is opened longitudinally along the anterior margin, laid flat in a transparent polypropylene bag, and then xeroxed. The outlines of the atherosclerotic lesions are traced onto a translucent graph paper sectioned into 1mm squares. The squares within the lesions' outlines are counted and expressed as a percentage of the whole surface.
The xerographic method is rapid and reproducible, and produces a keepable record without changing magnification. It gives comparable or better results than other staining method. Since the arterial specimen is not damaged by fixation or staining, it can be used for subsequent morphological or biochemical studies. Thus, the degree of surface involvement can be corelated with other morphological and biochemical changes in the same arterial samples.

抄録全体を表示

Diet has a powerful effect on not only lipid composition in very low density lipoprotein (VLDL) but also high density lipoprotein (HDL) including apo-HDL.
The present studies were undertaken to investigate whether diet factors were also to produce characteristics of apo-HDL in alimentary hyperlipidemia of rabbits.
Adult rabbits were loaded by 3ml/kg of lanolin or 7g/kg of glucose mixed with 15μCi/kg of ¹⁴C-1-palmitic acid and 30μCi/kg of ³H-2-glycine. Blood was collected at 15 minutes or 30 minutes after ingestion of these and lipoprotein-fraction was separated by ultracentrifugation and lipid-fractions were separated by thin layer chromatogram. Radioactivity of each lipid-fraction and protein were counted by scintilation counter and calculated specific activity of VLDL-triglyceride (VLDL-TG) and VLDL-protein. On the other hand, apo-VLDL (apo-C) and apo-HDL (apo-A) were separated into several subunits by Kane et al. method using polyacrylamide gel electrophoresis.
We obtained as following results and discussed about these results.
1. Incorporation of ¹⁴C-palmitic acid into VLDL-TG was the most increase in hepatic vein at 15 minutes after glucose load. And this increase in the incorporation of ¹⁴C-palmitic acid was accompanied with an increment of apo-AI in apo-HDL against apo-AII. But there was not any significant difference of specific activity of ³H-VLDL.
2. Incorporation of ¹⁴C-palmitic acid into VLDL-TG was the most increase in hepatic vein at 30 minutes after lanolin load. But there was not remarkable change in both apoA-I and apoA-II.
3. There was not any significant observation on apo-C subunits in both periods and in both loads.

抄録全体を表示

In this in vivo study, uptake of serum LDL into the arterial wall obtained from normocholesterolemic rabbits has been investigated under the condition of 6 hours continuous infusion of various humoral factors such as norepinephrine, epinephrine, hog renin, angiotensin II and insulin. Concentration of the humoral factors were as follows: 1.0μg/kg/min. for norepinephrine, 0.1μg/kg/min. for epinephrine, 0.05 Goldblatt units/kg/min. for hog renin, 0.003μg/kg/min. for angiotensin II and 1.0U/kg/hr. for insulin. Blood pressures during the infusions were less than 150 mmHg. Blood sugar was maintenined between 70-90mg% during the insulin infusion. Uptake of the LDL into the arterial wall was observed by immunofluorescent technique.
RESULTS: No immunofluorescent of LDL was observed by the infusions of norepinephrine, epinephrine, and hog renin. On the other hand, uptake of LDL was observed when angiotensin II and insulin were given.
DISSCUSSION and CONCLUSION: Previously, we had report that LDL u0take of arterial wall increased in the renovascular hypertensive rabbit. It should be obvious that blood pressure plays important role to the increase of the LDL uptake. However, it seems that effect of the humoral factors can not be disregard. It is of interest that only the angiotensin II among the various substances which affect the blood pressure increase the permeability of arterial wall to the LDL. Mechanism which angiotensin II increase the endotherial permeability to the LDL may be considered that this substance cause the organic change of endotherial cell but not constriction of the cell since the both catebholamines and angiotensin II constrict the arterial wall.
In this. experiment, insulin increased the LDL uptake into the arterial wall but precise mechanism is still unknown.

抄録全体を表示

¹²⁵I-VLDL was incubated with the triglyceride lipase rich plasma at 28 degree of centigrade for one hour, NaCl concentrations of the incubation media were 0.15 and 1.0 mol in order to know the effects of the hepatic and extrahepatic triglyceride lipases on VLDL conversion to LDL respectively. And, LDL was fractionated into the two fractions, LDL₁ (1.019<d<1.045) and LDL₂ (1.045<d< 1.063) to compare the influx rates of VLDL B-protein to LDL₁ and LDL₂, B-protein specific activities of IDL, LDL₁ and LDL₂ were also measured.
Radioactivities increased mainly in LDL₁ and small in IDL and LDL₂ after one hour ¹²⁵I-VLDL incubation with the triglyceride lipase rich plasma at 0.15M. NaCl concentration, when B-protein specific activities increased significantly big in LDL₁ and small in LDL₂. However, these changes disappeared when ¹²⁵I-VLDL was incubated at 1.0M. NaCl concentration.
So, we concluded that VLDL was converted to LDL with the extra-hepatic triglyceride lipase, when the influx of VLDL B-protein was seen mainly in LDL₁ and small in LDL₂. We could not get any information that the hepatic triglyceride lipase acted on VLDL.

抄録全体を表示

To study the role of carnitine in the pathogenesis of atherosclerosis, urinary excretion of carnitine and serum concentrations of carnitine and lipids were determined in normal subjects and in patients with abnormal lipid metabolism. Urinary excretion and serum concentration of carnitine were highly increased in Graves′ disease when compared with those in the normal controls. In contrast, carnitine levels were consistently low in hypothyroidism, in which atherosclerosis and hyperlipaemia were common. In atherosclerotic patients carnitine levels were subnormal or within normal range.
Carnitine levels were also investigated in the same normal and atherosclerotic subjects under several dynamic conditions. The carnitine levels were greatly increased up to 6-fold in the normal subjects in the states with increased lipolysis induced by ACTH injection. This response, however, was suppressed and delayed in the atherosclerotic patients and was similar to that in hypothyroid patients. When the patients were treated with triiodothyronine, the response curve to ACTH injection was shifted to the normal profile. Serum triglyceride concentrations changed inversely, making a mirror image to the change of the carnitine levels.
The results suggest that carnitine exerts a homeostatic regulation on the serum lipids concentrations through “lipid-carnitine system”, and that the impaired or delayed response of this system to the lipolysis-stimulation induces atherosclerosis. Thyroid hormone plays an important role in the regulation of the lipid-carnitine system.

抄録全体を表示

Plasma Malondialdehyde (MDA) value was measured by simple fluorometric assay for lipoperoxide in blood plasma (Yagi's method).
The conclusion are as follows: Yagi's method is simple and suitable for clinical purposes. The measurement must be completed as quickly as possible, since prolonged measurement, using old specimens or employing needless manipulations thereby increasing the time span during measurement, gives falsely higher plasma MDA value.
Although the reason is obscure, the frequency of subjects having distinctly elevated plasma MDA value is significantly higher in the pregnant women than in identically aged unpregnant females.
For determination of normal MDA value in plasma, futher examination is necessary.

抄録全体を表示

ThromboxaneA₂-Mixture solution (TXA₂-Mix.) was prepared by mixing washed rabbit platelets (1.6×10⁹-3.6×10⁹) with thrombin (3-30 U), in a similar manner as (Hamberg, et al) described. TXA₂-Mix. was perfused into coronary artery by means of a Swan-Gantz catheter through the right common carotid artery. Significant serial changes of ST-T on ECG was observed in 9 of 10 rabbits, and Q wave appeared in 3 rabbits with in one or two days after the injection. Out of 17 rabbits pretreated with phthalazinol (EG-626) intravenously in doses of 0.1-1.0mg/kg, 4 rabbits showed transient changes of ST-T on ECG, but no change in the remaining 13 rabbits.
Histological studies of the heart showed focal myocardial necrosis or fibrosis in all rabbits, but phthalazinol pretreated rabbits showed necrosis of small size and slight fibrosis in 4 of 17 rabbits. TXA₂ converted from PGH₂ (0.1-1.0μg) by platelet microsome induced dose-dependent changes of ST-T. The inactivated TXA₂-Mix, prior the injection induced transient changes of ST-T in 2 of 6 rabbits.
The intracarotid injection of TXA₂-Mix. induced a slight to severe stroke-like response including forced movement, convlusion, collapse in all 11 rabbits, and often cerebral death (4 rabbits) due to respiratory paralysis. Pretreatment with phthalazinol prevented stroke-like response in 5 rabbits but slight forced movement appeared in 3 rabbits.
Histological studies of the cerebral showed infarction of small size, arterioles accompanied by platelet thrombi, swollen nerve cell and piknosis of nucleous. Eight rabbits pretreated with phthalazinol did not show cerebral infarction, except slight platelet thrombi or swollen nucleous. TXA₂ is presumably capable of inducing acute myocardial ischemia, necrosis and cerebral transient ischemic attack, infarction. Pretreatment with phthalazinol prevented significantly the effects of TXA₂.

抄録全体を表示

A total of 70 femal albino rabbits weighing around 2kg each were used. To clarify the influence of the serum lipids to the fibrinolytic system and to clarify the pathophysiological significance of the fibrinolytic system in atherosclerosis, the present paper is an attempt to determine the behavior of the systemic and local fibrinolysis in association with the process of the generation and development of atherosclerosis in experimental rabbits in which atherosclerosis had been induced with a lanolin diet for 12 weeks.
1) Atherosclerosis of the aortic arch was estimated from the severity of the intimal lipids deposition and the intimal thickening. These findings were remarkably pronounced after eighth week.
2) Total cholesterol increased significantly at 2 and 6 weeks. Triglyceride was significantly increased at 4 and 10 weeks. Free Fatty Acid was significantly increased at 8 weeks.
3) Plasma fibrinogen content was higher in the experimental group than in the control group throughout the twelve weeks period, the difference being significantly higher was observed at 2 and 8 weeks.
4) The change in the plasma fibrinolytic activity, expressed by plasminogen activator, plasminogen, plasmin and anti-plasmin, was periodic in experimental group. The fibrinolytic activity decreased at 2 weeks, after which it increased at 4 and 6 weeks. After the eighth week, it decreased again. The significant positive corelation observed between the serum cholesterol and ELT, as well as the serum cholesterol and antiplasmin values at 2 weeks. The coefficient of correlation between the serum cholesterol and ELT was 0.47, and that between the serum cholesterol and anti-plasmin values 0.57.
5) The plasma fibrinolytic activity decreased at 2 and 8 weeks, but EDP significantly increased.
This discrepancy was suggested that the systemic fibrinolytic activity including the vessel wall might occur hyperfibrinolysis in local and this phenomena reflected the elevation of EDP.
6) only slight fibrinolytic activity on the arterial wall recognized up to the sixth week. From the eighth week on, however, it could be recognized in none of the experimental group.
The results lead us to believe that the decreased systemic and local fibrinolysis may be an important modyfing factor and one of the pathogenic factors in the generation and development of atherosclerosis.

抄録全体を表示

We studied on the lipid and lipoprotein fractions in sera of myocardial infarction (MI), angina pectoris (AP) and control groups, using routine chemical methods, agarose gel (AGE) and polyacrylamide gel (PGE) electrophoresis and ultracentrifugation. While serum total cholesterol were almost equal among these three groups, the concentration of free cholesterol, triglycerides, total phospholipids, total lipids and free fatty acids were higher, though statistically not significant, in the AP and MI groups than in control one. The percent concentration of β, and the ratios of β/α, pre-β+β/α increased significantly in the AP and MI groups. So-called extra pre-β lipoprotein (ELp) were seen in 18% cases of atherosclerotic diseases (AS) by the method of AGE, while 52% in AS, 38% in hypertension and 25% in controls by the method of PGE. ELp appeared and disappeared in the same individuals, but was more consistently found in persons with AS. Lipid moiety in relation to protein moiety of VLDL and the ratio of total cholesterol in VLDL to serum triglycerides tended to be higher in ELp positive sera than ELp negative ones. ELp was found mainly in the density between 1.050 and 1.070g/ml and showed abnormally faster immunoelectrophoretic mobility than usual β-lipoprotein. The SDS disc gel electrophoretic pattern of the apoprotein of the subfraction (1.050<d<1.070) of ELp (+) serum was different from that of ELp (-) serum. Close association that we found between the high frequency of the ELp appearance and coronary heart disease does not prove any causal relationship, but suggests that even slight changes in serum lipid and lipoprotein patterns might be related to atherogenicity.

抄録全体を表示

Plasma renin activity (PRA) in 64 patients hospitalized for rehabilitation between March, 9 and November, 11, 1977 after the acute attack of cerebrovascular accident (CVA) was determined to investigate the relationship between PRA level and CVA PRA was measured by radioimmunoassay using RENIN-RIAKIT. The minimum detectable level of PRA is 0.3ng/ml/h. Blood samples were collected from a cubital vein in 64 patients with CVA (42 to 74 years old) at 6 a. m. and its value was taken as PRA at rest. The patients were maintained on normal dietary sodium intake (13 to 15g per day) for one week before the examination. As the control, PRA levels were determine with the healthy persons in the same age range under the same conditions.
Since there was no tendency that PRA decreases in parallel with age, the control and the CVA patients were investigated as the whole without considering individual age. The CVA patients with PRA levels above 1.64ng/ml/h (mean-2 S. D. of the control) are considered to be high renin group. While those CVA patients whose PRA levels at rest were below 0.5ng/ml/h and less than 1.0ng/ml/h after the stimuli of upright posture and of sodium restriction (2-3g per day for 3 days) are considered to be low renin group. Normal renin patients are those with PRA between 0.5 and 1.64ng/ml/h. The mean value of PRA levels in CVA patients was 1.62±0.16ng/ml/h (mean±S.E.), which was significantly higher than that of control (0.86±0.10ng/ml/h). Only 40.6% of C. V. A. patients belonged to high renin group. 10.9% of CVA patients were low renin group and the rest (48.4%) were normal renin group. 61.9% of 21 patients with intracranial hemorrhage showed high PRA levels, while only 25% of cerebral thrombosis were high renin group. 66.7% of cerebral thrombosis had normal PRA levels. No correlation was found between PRA values and the times until its measurement after the attack of CVA.
The blood pressure at the time of addmission did not show any remarkable difference in relation to high, normal, and low renin group. About a half of the cases had no history of hypertension. In low renin group, however, almost all the patients had history of hypertension and its duration was twice longer than that of high or normal renin group. The atherosclerotic changes of eye fundus appeared rather high frequency in CVA patients independently their PRA levels.
Although Brunner et al. have reported that the patients of essential hypertension with low PRA levels have a lower incidence of myocardial infarction and stroke than those with normal or high PRA, our present observations revealed that many patients with low PRA were found with CVA patients having long history of hypertension. Moreover, in patients with low PRA levels, hypertensive changes in eye fundus and cadiovascular abnormalities were observed in the same frequency as in those with high renin group.
Since the rise in PRA level after stroke is thought to be caused as the result of mechanical disturbance in cerebral vessels which induce the decrease of blood flow, the facts that high level of PRA is found in many cases even after the acute state suggests not only the existence of vascular disturbance but also the continuance of decrease in blood flow. If the purpose of the treatment of CVA is to maintain the normal cerebral blood flow, the PRA which fluctuate in parallel with cerebral blood flow will serve as the indicator of cerebral circulation without giving any untoward invasion to the patients in clinical examination, and it must be essential to keep it normal.

抄録全体を表示

The determination of cholesterol concentration in corb shell (shijimi), bloody clam (akagai), shortneck clam (asari), clam (hamaguri) and oyster (kaki) has been described.
Colorimetric, Enzymatic, Thin-layer chromatography, gas-liquid-mass-spectrometry method are employed for the determination.
Concentration of cholesterol was 125mg/100g for shijimi, 78mg/100 g for akagai, 76mg/100g for asari, 69mg/100g for hamaguri, 76mg/100g for kaki.
A number of sterols other than cholesterol in shellfish was studied using Gas-liquid-massspectrometry method
Sterols in shellfish were identified to be 22-trans-24-norcholesta-5, 22-dien-3β-ol, 22-dehydrocholesterol, Brassicasterol, Campesterol, 24- methylenocholesterol, β-sitosterol.

抄録全体を表示

Cyclic nucleotides play a definite role in pathophysiological states. For further elucidation, changes in serum cyclic AMP lelesl and cAMP phosphodiesterase (cAMPPDE) activities were determined in 26 Japanese patients with cerebral hemorrhage (5), subarachnoidial hemorrhage (9) and cerebral thrombosis (12). Blood smaples were withdrawn dialy after the attack for 1 week, then once weekly for 4 weeks. In 15 cases, samples were taken every 4 hours on the first day of admission.
In the cerebral hemorrhage patients, cAMP showed statistically high levels on day 2, as compared to the patients in the other two groups. These high levels decreased with improvement in the clinical picture. cAMPPDE activities were also high on the first day, gradually decreased and showed a positive correlation with cAMP levels (γ=0.8, p<0.01).
In the critical patients, levels of both CAMP and cAMPPDE remained elevated right up to the time the patient expired. In two patients, recurrence of the attack was associated with an abrupt increase in the levels of these nucleotides. No characteristic changes were seen in patients with subarachnoid bleeding or thrombosis. There was no correlation between cyclic nucleotides and cerebral lesions.
The levels of these nucleotides in patients with cerebral vascular disease, in the chronic stage (over 6 months) were compai ed with those in 46 normal controls. The low levels of these nucleotide swere statistically significant (p<0.01) in the afflicted patients. These data indicate that determination of cyclic nucleotide activities should provide pertinent information concerning diagnosis prognosis and clinical conditions in cases of cerebrovascular diseases.

抄録全体を表示