Actual measurements of coronary circulation, myocardial oxygen utilization and myocardial oxygen demand in clinical cases under an anoxaemia test, by coronary and right heart catheterization, and comparison of electrocardiographic changes with these factors revealed the fact that the electrocardiographic quantative analysis in anoxaemia did not correlate with the change of coronary flow itself, but essentially correlated with the change of myocardial oxygen balance of demand and supply, i.e., the myocardial oxygen consumption per heart work, per myocardial tension, or per heart beat.

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Five cases of intermittent right bundle branch block were reported. Four cases were old patients with hypertension and one case was a young man without apparent heart disease. Right bundle branch block were abolished during slowing of heart rate in two old patients and one young man. On the contrary right bundle branch block was induced during slowing of heart rate in the third old patient. In the fourth old patient no definite relationship was found between heart rate and appearance of right bundle branch block. Gradual conversion of right bundle branch block to normal QRS complex was observed following ocular pressure in one of five cases.

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The author attempted to examine the action of theophylline ethylenediamine, so-called coronary dilator, by following the effect of the direct infusion of the drug into the left coronary artery through a coronary artery catheter in anesthetized, closed-chest dogs. Electrocardiographic changes caused by the infusion of the drug were also studied.Method : In addition to the experimental method described in part I, the left coronary artery was also perfused from a donor dog's femoral artery at a constant blood pressure. The experiments were done 6 times on 2 adult dogs. Leads C_ψD and C_ψS, representing right and left ventricular electrocardiogram, respectively, were used in taking serial electrocardiograms.Results : (1) Experiments with coronary artery perfusion from the dog's own femoral artery(a) With 12.5 mg of theophyline ethylenediamine coronary blood flow flincreased, while coronary wedge pressure and femoral arterial pressure showed no change.(b) With 25 mg of theophylline ethylenediamine coronary blood flow decreased, coronary wedge pressure showed no change, and femoral arterial pressure fell.(c) With 125mg of theophylline ethylenediamine coronary blood flow decreased, coronary wedge pressure fell and femoral arterial pressure became markedly reduced.(2) Experiments with coronary artery perfusion from a donor dog's femoral artery under constant blood pressure(a) Infusion of 12.5 mg of theophylline ethylenediamine caused a slight decrease in coronary blood flow, an elevation in coronary wedge pressure and no change in femoral arterial pressure.(b) With 25 mg of theophylline ethylenediamine coronary blood flow increased, while coronary wedge pressure and femoral arterial pressure fell.(c) Infusion of 62.5 mg of theophylline ethylenediamine caused an increase in coronary blood flow, a fall in coronary wedge pressure and a marked fall in femoral arterial pressure.Conclusions : (1) Theophylline ethylenediamine tends to exert a vaso-dilating action on the coronary vessels.(2) Infusion of a large amount of theophylline ethylenediamine caused a dangerous decrease incoronary blood flow followed by a fall in aortic pressure.(3) The electrocardiogram showed a tendency to elevation of the S-T segments with a slight increase in the heart rate.

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The effects of pneumothorax upon pulmonary function have been studied since long time ago, and many authors have reported their observations with spirometry and blood gas analysis. Some data have been reported upon the effects of pneumothorax on pulmonary circulation by the simple indirect methods; since venous catheterization was introduced in this field, a few authors have reported their studies using this method. But the author can not find a report in which the effects of pneumothorax upon cardiopulmonary function have been generally studied, nor studies on the pulmonary circulation in patients with intrapleural complications caused by pneumothorax. So this paper reports the present author's results upon these points.Methods : The venous catheterization was performed according a modified method of Cournand and Ranges. Pressures were recorded by means of Hamilton's optical manometer or Sanborn strain gauge electromanometer, and the arbitrary zeropoint of all pressures was the midpoint between the second cost-sternal angle and the corresponding point of back. Cardiac output was determined by the direct Fick principle. Alveolar O₂ tension and arterial O₂ and CO₂ tension were determined by O₂-CO₂ Diagram reported by Rahn & Fenn. Alveolar ventilation was calculated by the following formula, provided that arterial CO₂ tension was equal to alveolar CO₂ tension. VA=VCO₂/FAO₂ and the work of right ventricle against pressure was calculated both by Riley's formula and by the present author's following formula.WR (Watanabe)=(mPAP-dRVP)×CO×0.1332 (joules/min) where mPAP=mean pulmonary arterial pressure (mmHg), dRVP=right ventricular enddiastolic pressure (mmHg), CO=cardiac output (1/min). Measurement of lung volume was carried out by means of Gebauer's spirometer, predicted vital capacity was calaulated by the Ebina's vital capacity index. Predicited maximum breathing capacity was calculated by multiplying predicted vital capacity by vital capacity-maximum breathing capacity ratio (VC/MBC) obtained by the present author's measurement of those who are free from cardiopulmonary diseases. The degree of lung collapse caused by pneumothorax was estimated by the dorso-ventral X ray film. When the collapsed area remained within one third of one lung, it was classified as slight ; when it was from one-third to two-thirds of one lung, moderate, and when it became over two-thirds of one lung, high. Patients were classified according to N T A criteria. Muscular exercise was performed with bicycle ergometer.The subjects were 18 patients under pneumothorax (group I) and 5 patients with its intrapleural complications (group II). And group 1 was divided into two groups, the one (group a) consisting of 11 patients under unilateral pneumothorax, and the other (group b) of 7 patients under bilateral pneumothorax (Table II).Results : 1. Group 1 : The decrease in vital capacity was relatively slight, alveolar ventilation ratio (VA/VE), diminished, and the latter decreased remarkably in group b (Table III). Arterial O₂ tension showed negative correlation with A-a O₂ tension gradient (Fig 1). Cardiac index was increased in most cases in group a, showing only slight decrease after air refill, while in group b it was decreased in many cases and decreased markedly again after air refill (Table V). The intrathoracic pressure during cardiac catheterization was almost similar to that during the first pneumothorax in 5 cases whereinformation was available on the first pneumothorax (Table VII).Right auricular pressure was normal in general, and in a few patients it even dropped clearly, while on the other hand it was elevated slightly after the air refill. [the rest omitted]

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Experimental and clinical studies of pulmonary edema have revealed a fact that the early diagnosis of pulmonary edema could be made with reasonable accuracy and within shorter time with the corroborative use of the chest roentgenogram and radiocardiogram.The experimental method used was by inducing a pulmonary edema by the injection of epinephrin in rabbits. Fifty rabbits were examined by means of chest roentgenogram and radiocardiogram at definite intervals as well as roentgenograms of excised lungs were taken following death or sacrifice of the animals.For clinical investigation thirty one selected cardiac cases and four post-operative cases in which occurrence of pulmonary edema was suspected were similarly followed up by the use of radiological and radiocardiographic methods.The following summarized results were obtained : 1. In the experimantal pulmonary edema, the early picture of diagnostic value was characterized by irregular and uneven pulmonary vascular margin and speckled shadow of the vessels.2. The radiocardiogram showed marked prolongation and flatness which prevented a close study of circulation time, hence, a method of estimating the Returning Ratio of Venous Blood Flow (=Returning Ratio) was devised, that is-Returning Ratio of Venous Blood Flow=(Injection to HB time)/(HB to HS time)×100%, and an estimation was made of each case. By this method, it was possible to demonstrate theoretically as well as experimentally that the reduction of the Returning Ratio signified left heart failure, and that its increase signified the right heart failure; and the Ratio necessary for pulmonary edema was found to be less than 8.2 percent.3. The radiocardiographic findings of the average value of fourteen healthy adults were as follows : Returning time to right heart is 3.0 seconds, Mean pulmonary circulation time is 4.6 sec., Executed time by left ventricle is 9.6 sec., Heart phase is 16.4 sec. and Returning Ratio of Venous Blood Flow is 18.3 percent.4. The clinical signs and symptoms and the radiocardiograms, particularly its Returning Ratio were compared of thirty one cases of heart diseases. Seven cases which presented the symptoms of pulmonary congestion showed marked extension of radiocardiogram, having the Returning Ratio somewhere between 3.3 percent to 11.1 percent ; signs of pulmonary congestion was never observable in those cases in which the Returning Ratio was above 13.8 percent.5. Among the seven cases with symptoms of pulmonary congestion, three were clinically suspected of pulmonary edema ; however, none of them gave roentgenological evidence of the pulmonary edema, and these cases were diagnosed as cases of preedematic condition.6. Two cases showed signs of pulmonary edema, and the radiocardiograms were definitely prolonged similar to those of congested lungs, and the Returning Ratio were 10.6 percent and 8.1 percent. There were evidences of specks and irregular vascular margins of the pulmonary vessel shadow in either case.7. The radiocardiographic studies of four post-operative cases, namely, one case of the gastric resection, and three cases of pulmonary lobectomy in which the pulmonary edema was suspected revealed that the Returning Ratio was well over 12.3 percent ; so the occurrence of pulmonary edema was denied.8. The foregoing results seem to demonstrate that the radiocardiogram of prolongation or marked flatness type with Returning Ratio below 11.1 percent signifies a dangerous state, i.e., the onset of pulmonary edema, and then, by closer observation with use of roentgenogram to seek the characteristic pictures of pulmonary vessels, pulmonary edema can be diagnosed in early stage.

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Large doses of adrenaline result in death accompanied by an acute pulmonary edema in rabbit. Luisada claimed that adrenaline pulmonary edema was mediated via the central nervous system controlling the permeability of the pulmonary capillaries. But there is no evidence of the nervous control of capillary permeability. To investigate the role of central nervous system on adrenaline pulmonary edema in rabbit, an experiment was performed with blockage at various part of central nervous system. Material and Method : Male as well as female rabbits weighing about 2 kg were used. Anesthesia was induced by the intraperitoneal injection of 1 gm of urethan per kilogram of body weight. In all cases artificial respiration was maintained through a tracheal cannula, and arterial pressure was measured from the left femoral artery by a mercury manometer. In some cases venous pressure was measured from the jugular vein and electrocardiogram was recorded. 1.0 mg/kg of adrenaline was injected through the right auricular vein.The thorax was opened immediatly after death, then lung and heart were dissected off. The lung and heart were weighed and lung body ratio and lung heart ratio were calculated as follows, Lung Body Ratio (L/B)=(Lung Weight)/(Body Weight)×100 Lung Heart Ratio (L/H)=(Lung Weight)/(Heart Weight) The grade of pulmonary edema in macroscopic finding was evaluated according to Jordan's classification and histological examination was made. To investigate the influence of the central and autonomic nervous system blockage on adrenaline pulmonary edema several procedures were carried out prior to adrenaline injection as follows : I Control II Decerebration or Labonal anesthesia III Incision of diencephalon IV Cervical spinal transection or high spinal anesthesia VI Hexamethonium (C₆) administration VII Vagotomy or atropine administration VIII Dextran transfusion after cervical spinal transection IX Dextran transfusion after C₆ administration Result : In control group massive pulmonary edema was induced by 1.0mg/kg of adrenaline in all cases. No pulmonary edema occurred after neither transection of diencephalon, high spinal transection and anesthesia nor C₆ administration. Decerebration, low spinal transection and anesthesia had no influence on adrenaline pulmonary edema. Vagotomy or atropine administration seems to tend to accelerate the development of adrenaline pulmonary edema. By the transfusion of dextran solution after high spinal transection or C₆ administration, pulmonary edema developed with adrenaline injection. Blood pressure decreased remarkably after high spinal blocking or C₆ administration and very instable after transection of diencephalon, but no remarkable change after other procedures. In case of development of pulmonary edema, lung body ratio was 0.96±0.75, peak, level of elevated blood pressure 182±20 mmHg, change of venous pressure +46±9.4 mmH₂0 ; in case of no pulmonary edema, lung body ratio was 0.41±0.03, lung heart ratio 1.60±9.16, peak level of elevated blood pressure 111±26 mmHg and change of venous pressure +21±10 mmH₂O.Discussion : The intravenous injection of adrenaline provoked marked hypertension without exception. The evidence suggests that the left ventricle may be greatly burdened from the hypertension induced by adrenaline. Under these conditions, adequate performance of the right ventricle leads to a pulmonary engorgement and edema. Adrenaline pulmonary edema was prevented by transection of diencephalon or high spinal blocking. It is obvious that central nervous system does not control the permeability of the pulmonary capillaries, because pulmonary edema occured when dextran solution was transfused after the high spinal transection. [the rest omitted]

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