Studies on the Venous Return in Experimental Hypertension. : Japanese Circulation Journal 24 : 1529-1538, 1960.

Abstract

The purpose of this experiment was to study whether the unusual findings on venous return and its regional distribution in essential hypertension previously reported by Ninomiya, could be produced in experimental hypertension, and if it could be realized, how would it be possible. Further, the author wishes to discuss the pathogenesis of essential hypertension. To make experimental hypertension, three methods, that is, continuous drip infusion of noradrenalin, ablation of both carotid sinus nerves and obliteration of unilateral renal artery, were adopted. In each experiment, venous return and its regional distribution were measured and the comparison was made with that of essential hypertension. Experimental animals and method Normal adult dogs were used for the experiment under morphine and urethane anesthesia. Venous return was measured by already published Electric Conductivity Method which is based on Stewart-Hamilton's principle and the return flows of the superior and inferior caval, hepatic and renal vein, and of the upper and lower extremities, were measured respectively. Taking the total venous return as 100, ratio of respective regional venous return to it, i.e., return ratio, was calculated. Peripheral blood pressure and E.C.G. were also recorded simultaneously. Moreover, regional vascular resistances were calculated from the above obtained data, and renal function was studied by renal clearance method. The following three procedures were adopted to produce the experimental hypertension.A. Hypertension due to noradrenalin drip infusion.The noradrenalin saline solution was infused during 20 to 30 minutes at the rate of 0.5, 2.0 and 6.0 μ g/min/kg (small, middle and large doses). Before and during this procedure circulatory hemodynamic changes were measured.B. Hypertension following the denervation of both carotid sinus nerves. The bifurcated region of the internal and external carotid artery in the common carotid artery was destroyed by concentrated carbolic solution and then change in blood pressure and pulse rate were observed during the period of 30 to 90 days.C. Hypertension caused by an unilateral obliteration of the renal artery. An unilateral renal artery was ligated in such a way that it narrowed down to 1 mm in diameter. Blood pressure and pulse rate were measured for a period of 30 to 75 days following the arterial occlusion.Results A. The noradrenalin hypertension : Elevation of both systolic and diastolic blood pressures was observed after the infusion of noradrenalin ; the more graded noradrenalin was infused, the more marked elevation of blood pressure was seen. The cardiac rate was unchanged with the small dose, but the brady-cardia appeared with increasing dose of infused noradrenalin. The cardiac output and the total venous return were unchanged with the small dose, but decreased with the moderate or the larger dose. Speaking of the venous return and its distribution, the cranial venous flow (C.V.F.) decreased with the small dose infusion, in spite of the fact that the hepatic venous flow (H.V.F.) and the renal venous flow (R.V.F.) increased. With the a larger dose of noradrenalin the C.V.F. and the R.V.F. markedly decreased, but the H.V.F. decreased slightly. The peripheral vascular resistance showed marked increase in the cranial and the renal region and slight increase in the abdominal visceral region. With respect to the renal function, RBF, RPF and GFR showed a little increase with the noradrenalin infusion of small dose but the notably decreased as the noradrenalin dose was increased. The increase of the renal vascular resistance was observed in afferent vessels rather than in efferent ones.B. The neurogenic hypertension due to the carotid sinus denervation. : An immediate rise of the blood pressure after the carotid sinus denervation was followed by the prolonged fluctuation, resulting in a sustained elevation. [the rest omitted]