Renal vascular responses to ganglionic stimulants and to renal nerve stimulation were studied in the dog anesthetized with pentobarbital sodium. 1) Ganglionic stimulants, nicotine, DMPP and acetylcholine in the presence of atropine, when given into the renal artery elicited a biphasic elevation in renal perfusion pressure. The first rise in perfusion pressure was completely blocked by phenoxybenzamine and by C₆, but not by adrenalectomy. The second rise and a concomitant elevation in the systemic blood pressure were abolished by these two agents as well as by adrenalectomy. 2) Reserpinization of the dog resulted in a marked reduction in the biphasic response thus developed, especially in the first response. Tyramine no longer had a renal vasoconstrictor action, but responses to catecholamines were potentiated. 3) On the seventh to fourteenth day after renal nerve section both tyramine and DMPP lost their immediate vasoconstrictor action. 4) Electrical stimulation of the renal nerve or the splanchnic nerve produced a monophasic or a biphasic elevation in renal perfusion pressure. Such elevations were fully blocked by phenoxybenzamine or C₆ as was the case with ganglionic stimulants. However, the blocking site of C₆ for splanchnic nerve stimulation was found to be in the extrarenal synapse when a cross-circulation preparation was employed. 5) Perfusion of the kidney with the anoxic blood resulted in a marked reduction in responses to ganglionic stimulants, but no or slight reduction in responses to nerve stimuli. The present data indicate that the biphasic response to ganglionic stimulants is mediated through catecholamines, released from the kidney accounts for the development of the initial response and released from the adrenal gland is attributable to the second response. The catecholamine releasing mechanism of ganglionic stimulants differs from that of tyramine. It is postulated that certain elements, with ganglionic function, even in the absence of anatomical evidence exists in the dog's renal vessels and that the elements have no synaptic function.

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The purpose of this paper is to clarify relationship between venous thrombosis and microthrombi on the intact endothelium. ADP-infusion caused a remarkable adhesion of platelets to the apparently unbroken endothelium of dog femoral vein and enhanced the development of microthrombi under partial stasis, and by these procedures, occlusive venous thrombus occurred very frequently under the serum-induced hypercoagulability without endothelial injury. It is concluded that ADP acts on platelets not only to aggregate to each other but to adhere to the intact endothelium and increased microthrombi play an im-portant role to promote formation of venous thrombus without endothelial injury.

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The reconstruction of the vasa vasorum in the autogenous venous graft and homogenous venous graft was investigated microangiographically and histologically. The vasa vasorum began to be reconstructed within 1 week and were accomplished 2 to 3 months after the operation. The reconstructed vasa vasorum formed rich networks in the media and adventitia, similarly to those of the normal vein. The thickening of graft walls was not found to be progressive with time after 2 months. In autografts enclosed in the Tetoron sheet, leakage at the suture line, perforation and degeneration etc. were found. In homografts, late thrombosis was recognized frequently, and its etiology was discussed.

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Plasma ADH levels in patients with chronic congestive heart failure were determined. In about half cases with moderate to severe right heart failure, ADH increased and it normalized after the cardiac function had improved. There were some cases where ADH increased in response to decreased circulating blood volume. In chronic congestive heart failure, ADH seems to play a role in edema formation together with aldosterone or change in the renal circulatlon.

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The determination of urine and tissue catecholamine levels were undertaken in rabbit with or without cardiac failure produced by aortic obstruction. The tissue catecholamine have tended to be lowered in cardiac failure, especially in the heart, while urinary catecholamine levels showed elevation. Uptake of the exogenous noradrenaline by the heart was lowered in cardiac failure than that of the normal subject. It was found that with nialamide, propranolol, or bethanidine, catecholamine concentration of heart could have increased in normal health, but in cardiac failure, such increase could be suppressed. It has been known that a condition of catecholamine depletion of the tissues by reserpine appears to be associated with aggravation of cardiac failure. The failing heart seems to yield acceleration of the sympathoadrenal activity, which results in depletion of tissue catecholamine perhaps due to the increased release of stored catecholamine and deficient retention by enhanced turnover rate, or lowered uptake in the tissues. It is concluded that the tissue catecholamine plays a compensatory role in cardiac failure.

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A case of primary pulmonary hypertension of a 30-year-old female was reported. The onset of symptoms was noticed 2 months after the second delivery. The patient died one year later thereafter. Autopsy findings did not reveal any definite gross anatomical evidence to cause pulmonary hypertension. Histological examination demonstrated concentric and eccentric thickening of the intima of pulmonary arteries and arterioles, stenosis and obliterative lesions in smaller arteries and arterioles, and hematoxylin-stained bodies in these vessels. The etiology of primary pulmonary hypertension was discussed, especially in regard to the role of the reproducing period of female.

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The application of the resistance-wire strain gauge arch by BONIFACE et al. to the beating heart in situ has recently conducted to allow the direct measurements of the mechanical function of the heart, and several models of apparatus for this purpose have been devised. The use of a semiconductor as the transducing element makes the strain gauge arch smaller and more efficient in transduce than the use of the wire strain gauge. The present report describes the structures and the performances of some models of the new instruments which have been designed using semiconductor strain gauge elements. This report also provides the discussion on the propriety of this method manifesting the accurate myocardial contractility of the left ventricle through the detailed analysis of myocardial tension curves recorded with the new strain gauge arch. Methods 1) Mechanical properties of the strain gauge arch. The strain gauge arches, which were used in this investigation, were transducers capable of translating the forces acting on their attachments into proportional changes in the bridge output voltage. The body of the transducer was made of a kind of spring-steel in the form like an arch as a whole, consisting of a beem between two legs with two attachments. The distance between two legs was 15 mm (in Model L-3) or 10mm (in Model L-6), and the whole weight was less than 1g. The modified arch (Model VL-5), which could be adjusted the distance between two legs by means of a micro-screw, was also developed. As strain gauge elements, four pieces of n type Ge [111] were cemented on both sides of the upper parts of the legs. A "four active full-bridged circuit" which was constituted by the semiconductor elements was supplied with 3V in DC. There was a linear relation between the force necessary to displace the attachments and the increase of the distance between the attachments, and even a force of 250g wt. could move the attachments less than 5 per cent of length of the beem. There was also linear relation between the force acting attachments and the bridge output voltage and 210mV of output voltage was obtained by 250g wt of force in Model L-3. The frequency response of the strain gauge arch was found to be uniform through 350cps.

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Only a few experiments have been done investigating the hemodynamics of idiopathic orthostatic hypotension (I.O.H), but no report has yet been known made on the hemodynamics of the brain, heart and kidney in I.O.H. especially. In this report, the influences of autonomic dysfunction on hemodynamics of I.O.H. are examined in 122 patients and in experimental animals. Methods The function of the autonomic nervous system was observed by the pharmacodynamic methods (mecholyl, noradrenaline, atropine, adrenaline and pilocarpine test), intracuti-reaction of acetylcholine/adrenaline and Ashner's phenomenon. The circulating blood and the plasma volume were measured by the Evans Blue method, and the time for circulation from arm to tongue or from vena dorsalis pedis to tongue was measured by the Decholin method. The circulating and the output quotient were calculated as follows. Circulating quotient = (circulating blood volume (1))/total circulation time × 60 Output quotient = circulating quotient / pulse rate The concentration of carbonic acid in the serum was measured by CONWAY'S method and the blood pressure of arteria centralis retinae by an ophthalmodynamometer (SCHlOTZ). The character test was performed by C.M.I. and Y. G., and renal function was measured by the renal plasma flow (RPF) and glomerular filtration rate (GFR). In animal experiments rabbits weighing 2.5-3kg were used. For the blocking of the sympathetic nerve, bilateral cervical sympathectomy was done or a ganglion blocking agent (tetraethylammonium bromide) was injected intravenously. The output volume of the heart was measured before and after hypothalamic lesion. In order to produce lesion experimentally, a stainless steel bipolar electrode was inserted stereotaxically in the sympathetic area of the hypothalamus and 0.5 mA D.C. was electrified for 60-120sec. with the object of coagulating brain structures.

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The heart consumes and stores a large amount of fats as its energy source in addition to carbohydrate. It is supposed that other lipases than lipoprotein lipase, which has been investigated so far, are concerned in the hydrolysis of the triglyceride fatty acid reserved in the myocardium. However, few investigations about them have been done. A lipase activity, sensitive to epinephrine, was detected from the rat heart homogenate. Its properties were studied about the optimal pH, the presence of fractions, the effect of fasting, the degree of activity increased by activators, the effect of lipase inhibitors and the effect of β-blocking agent. Methods : Wister strain male albino rats weighed about 2OOg were killed by decapitation. The hearts were removed quickly and rinsed in the ice-cold Krebs-Ringer phosphate buffer. The homogenate was prepared by homogenizing the tissue in 6ml of 0.25 M sucrose solution per gram of tissue in a glass homogenizer. The homogenate was centrifuged at 12, 000 × g for ten minutes at 4°C. The supernatant fluid was taken for the assay of lipolytic activity. The reaction mixture consists of the following ; 0.4 ml of enzyme solution, 0.1 ml of 50 per cent Fatgen (20 per cent sesam oil emulsion), 0.5 ml of 20 per cent extracted albumin (pH 7.0), 0.2 ml of 0.06 M phosphate buffer (pH 6.8) and 0.8 ml of distilled water: Free fatty acid was assayed before and after the one hour incubation at 37°C. Free fatty acid was extracted according to the method of DOLE and determined photometrically by that of MOSINGER.

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It was reported recently that some types of the derivatives of benzoylcarbinol have a function to restore the altered vascular permeability and also anti-inflammatory activities, probably acting as a mediator through the adrenal cortex. In the view of this point the present experiment was undertaken to know whether the drug inhibits in any degree the occurrence of the damages to the medium-sized and/or small arteries in many organs of rats suffering from renal hypertension. The later was produced by the conventional method of the renal mass reduction. Renal hypertensive rats, given daily 50 mg and 25 mg of Benzoylcarbinol trimethylacetate respectively per kg for either 12, 22 or 40 days, revealed a moderate to significant reduction of both extent and degree of the arterial lesions in the abdominal organs examined histologically, when compared with those of control rats. Such a reduction was not found in the hypertensive rats with daily administration of 100mg/kg/day throughout the experiments. The drug, when administered to the renal hypertensive rats, was observed to have no function to decrease elevated blood pressure, measured by the plethysmography method, even in rats of a high dose group.

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