Renal denervation inhibits hypothalamo-sympathetic nerve system in normotensive and hypertensive rats.

The role of the renal nerve in influencing the hypothalamo-sympathetic nerve system to regulate the cardiovascular system was studied in normotensive Wistar and spontaneously hypertensive rats (SHR). Renal denervation attenuated pressor and sympathetic nerve responses to electrical stimulation of the hypothalamus without lowering the basal blood pressure at 48 hours after denervated operation. These findings suggest that renal denervation could inhibit the hypothalamo-sympathetic nerve system in normotensive rats. The development of hypertension in SHR was completely inhibited by renal denervation during 2 weeks of observation (from 7 to 9 weeks of age) without increasing water intake and urine volume. Pressor responses to intravenous injection of norepinephrine were not affected by renal denervation. The results show that the antihypertensive effect of renal denervation was not due to the changing of vascular reactivity. Pressor and sympathetic nerve responses to hypothalamic stimulation were strongly diminished in renal denervated rats. These results suggest that renal denervation strongly inhibited they hypothalamo-sympathetic nerve system. It is also suggested that the renal afferent nerve may facilitate the hypothalamo-sympathetic nerve system in regulating blood pressure and that this facilitation may contribute to the development of hypertension in SHR.

[Exercise echocardiography to evaluate left ventricular function in mitral and aortic regurgitation].

To assess differences in left ventricular (LV) performance between mitral regurgitation (MR) and aortic regurgitation (AR), exercise echocardiography was performed for 12 patients with MR and 18 patients with AR, and the results were compared with those of 11 normal subjects. These patients with LV volume overloads were all in the NYHA class I or II. There were no differences in age or sex distributions between the two groups. Symptom-limited submaximal exercise was performed on an ergometer in the supine position. The results obtained were as follows: LV dimensions at end-diastole (EDD) and end-systole (ESD) were greater in the diseased groups than in the normal group. Resting EDD and ESD showed no differences between the MR and the AR groups. There were no differences in exercise-induced increases in heart rates or elevations of systolic blood pressures among the three groups. During exercise, EDD increased and ESD decreased in the normal group, and similar results were obtained for the MR group. However, in the AR group, EDD and ESD remained unchanged. Ten of the 18 patients with AR had decreased ESD, and eight had unchanged or increased ESD during exercise. Resting shortening fractions were equally distributed among the three groups. During exercise, the shortening fractions were significantly increased in the normal and the MR groups. In the AR group, shortening fractions remained at resting values, with variable responses in individual cases. Systolic wall thickening of the interventricular septum and the LV posterior wall showed similar responses of shortening fractions. The relation between the peak systolic wall stress index (PSSI) and ESD, or PSSI and the shortening fraction revealed that exercise induced an afterload mismatch of LV performance in some patients with AR. Thus, though resting LV performances did not differ from each other, an afterload mismatch is more easily induced with exercise in patients with AR than in patients with MR. This may be one of the cause of the different clinical courses in these two groups with LV volume overloads.

[Analysis of coronary hemodynamics in exercise by T1-201 scintigraphy: examination of rates of change of cardiac output, myocardial blood flow distribution, coronary blood flow and coronary vascular resistance].

From our observation that initial distribution of 201T1 in tissue is mainly dependent on blood flow distribution, we designed the method to obtain the rates of change of coronary blood flow and coronary vascular resistance and applied it to the analysis of coronary hemodynamics in patients with ischemic heart disease during submaximal exercise. We measured the rates of change of cardiac output (delta CO) and myocardial blood flow distribution (delta Fract ) in two occasions by the sequential two injections of T1, and obtained the rate of change of coronary blood flow (delta Flow) from delta CO and delta Fract . Using the rate of change of mean blood pressure, we calculated also the rate of change of coronary vascular resistance (delta CVR). The initial components of histograms of the right ventricle by the first and second injections of T1 were fitted into gamma function curve. S1 and S2 were the areas bounded by the curve and baseline of the first and second injections, and then the cardiac output ratio was estimated by R X S1/S2, where R was the dose ratio measured by another camera system. The five min count rates on the myocardium by the first (H1) and second (H2) injections of T1 were calculated five min after the injection. H2 was approximately H1 X R in the same condition of T1 injection but H2 was not equal to H1 X R, when the T1 injection was done in the different loading condition. Therefore the rate of change of myocardial blood flow distribution was calculated as delta Fract = (H1 X R-H2)/H2.(ABSTRACT TRUNCATED AT 250 WORDS)