Superior Mesenteric Resistance Research Articles

Regional hemodynamic responses to exogenous catecholamines and vasoactive peptides in conscious rats.

The vasoactive hormones vasopressin, angiotensin II, adrenaline, and noradrenaline may all be released after central neural stimulation, but our knowledge of their relative actions on regional vascular resistances is incomplete. A comprehensive account of these patterns will help our understanding of their contributions to centrally generated patterns of blood flow. In the present study, regional blood flows and resistances of five major arteries were measured during sequential intravenous infusions of a range of doses of each substance in conscious rats. Vasopressin strongly increased superior mesenteric, hindquarters, carotid, and renal resistance but did not affect celiac artery resistance until the highest infusion rate. Both angiotensin II and noradrenaline increased resistance, although to different extents, in all vascular beds except the hindquarters, which was unaffected. Adrenaline infused at pressor rates markedly increased superior mesenteric resistance while moderately increasing renal, carotid and celiac arterial resistances. At subpressor rates, however, adrenaline increased celiac resistance but decreased hindquarters vascular resistance without significantly affecting the other beds. It is concluded that each vasoactive substance released into the systemic circulation causes its own characteristic pattern of vascular responses. This information should be useful for understanding the humoral basis of hemodynamic responses to central stimuli.

Vascular areas where clonidine induces vasodilation in hypertensive and normotensive rats.

The aim of this study was to find vascular areas where clonidine decreases the regional vascular resistance when this drug lowers arterial pressure in conscious spontaneously hypertensive rats and normotensive control rats. Arterial pressure was observed with an indwelling catheter at a carotid. Blood flow was measured with an electromagnetic flow probe implanted around the renal artery or the superior mesenteric artery. Regional vascular resistance was calculated as arterial pressure divided by blood flow. Intravenous bolus injection of clonidine at a dose to decrease arterial pressure decreased renal resistance and superior mesenteric resistance. Quantitatively, the combined effect of the decrease in these two resistances was enough to account for the decrease in arterial pressure. Although clonidine is thought to inhibit sympathetic nerve activity centrally, the above vasodilator effect is not ascribable to this inhibitory mechanism: Sympathetic activity to be inhibited does not seem to be present in the superior mesenteric area and clonidine similarly decreased renal vascular resistance even after renal denervation.

Hindquarter sympathetic tone induced by small blood loss in conscious rats.

We have designated the hindquarter (or terminal aortic) vascular resistance (HQR) of the rat as hindquarter compensator (HC) because it increases after such hypotensive interventions as pentobarbital anesthesia and nitrate administration, presumably due to reflex excitation of regional vasoconstrictor fibers. The aim of the present study was to observe whether the HC mechanism is also mobilized in response to hemorrhage. Rats were implanted with a 1.5 or 2 mm diameter electromagnetic flow probe at the terminal aorta for measurement of hindquarter flow (HQF). An indwelling catheter was placed in the right common carotid artery to measure arterial pressure (AP) and withdraw blood. Experiments were performed in conscious rats two or three days after implantation. HQR was calculated by dividing AP by HQF. About 10 min after withdrawing blood (0.3 ml/100 g body weight), ganglionic blockade with hexamethonium bromide significantly decreased HQR, which indicated a mobilization of the HC mechanism, a change not observed with superior mesenteric resistance. A quantitatively similar change was observed in HQR after withdrawing double the amount of blood, i.e., 0.6 ml/100 g body weight, suggesting that the HC mechanism is activated almost fully by the relatively small amount of blood loss of 0.3 ml/100 g body weight.

Hindquarter vascular resistance as compensator for hypotension in conscious rats.

The purpose of this study was to test whether hindquarter (terminal aortic) vascular resistance uniquely increases in order to compensate for interventions which result in a lowering of arterial pressure. Changes in hindquarter resistance were compared to changes in superior mesenteric resistance after the administration of the nitrovasodilator drug, molsidomine. Hindquarter blood flow or superior mesenteric flow was measured in conscious rats using an electromagnetic flow probe implanted around the terminal aorta or the superior mesenteric artery, respectively. Twenty minutes after an intravenous bolus injection of molsidomine (1 mg/kg), ganglionic blockade with hexamethonium bromide (25 mg/kg, i.v.) significantly decreased hindquarter resistance, but not superior mesenteric resistance. In the absence of molsidomine, ganglionic blockade has no effect on resistance in either vascular bed. These findings suggest that excitation of sympathetic vasoconstrictor fibers supplying the hindquarters but not those supplying the superior mesenteric area occurred in response to the hypotensive effect of molsidomine. This is consistent with the hypothesis that augmenting-hindquarter resistance is the first line of defense against hypotensive interventions.

老年者本態性高血圧症における食塩負荷時の心拍出量及び末梢局所血流分布の解析

Hemodynamic changes with dietary salt loading were assessed by Doppler echocardiography during different sodium intake (7 g/day for 8 weeks, 20 g/day for 1 week) in 29 elderly patients with essential hypertension (81.6 +/- 6.7 years, 4 men, 25 women). With salt loading, 24 patients whose mean blood pressure (MBP) increased by 10% or more were defined as salt sensitive (SS) group, and 5 patients whose MBP did not change, or increased by less than 10% were defined as non-salt sensitive (NSS) group. Based on the mitral flow velocity integral, cardiac output (CO) was calculated, and total peripheral resistance (TPR) was calculated as MBP divided by CO. Nine of the 24 SS patients were termed "SS (COdep)" whose CO increased significantly with salt loading. In the remaining 15 SS patients termed "SS (TPRdep)", TPR increased significantly with sodium repletion. Blood flow in the common carotid, superior mesenteric, or terminal aorta was calculated from each flow velocity integral. The percent change in peripheral resistance calculated by dividing MBP by each blood flow was obtained. There were no significant percent changes in the common carotid resistance in SS (COdep), SS (TPRdep) or NSS groups. The superior mesenteric resistance increased significantly in all three groups. The terminal aortic resistance increased in the SS (TPRdep) group, but decreased in the SS (COdep) or NSS group. These results indicate that salt sensitivity is ascribable to changes in regional vascular resistances.

Superior mesenteric sympathetic tone in conscious renovascular hypertensive rats.

Blood flow in the superior mesenteric artery was observed with a chronically implanted electromagnetic flow probe in two-kidney, one-clip renovascular hypertensive rats (2K1C), one-kidney, one-clip renovascular hypertensive rats (1K1C), and normotensive control rats (NCR) in the conscious state. Arterial pressure was recorded with an indwelling catheter. Superior mesenteric resistance was calculated as arterial pressure divided by superior mesenteric flow. In all three groups of rats, superior mesenteric resistance remained almost unchanged when arterial pressure decreased markedly on ganglionic blockade with hexamethonium bromide. However, subsequent injection of a vasopressin antagonist (Manning compound) decreased superior mesenteric resistance significantly in 2K1C but not in 1K1C and NCR. Injection of vasopressin antagonist alone was without effect on arterial pressure and superior mesenteric flow in the three rat groups. Only 2K1C were judged to have appreciable sympathetic tone in resistance vessels of the superior mesenteric area, which was blocked by hexamethonium but compensated for by secondarily secreted vasopressin.

Age-Dependent Cardiovascular Effects of Verapamil in Newborn Swine

Since there are limited studies concerning the hemodynamic effects of verapamil in pediatric patients, cardiovascular effects of clinical doses (100 or 300 micrograms/kg) of verapamil, given as a 2-min intravenous infusion, were examined in sodium pentobarbital anesthetized swine, aged 1 day (n = 15) and 2 wk (n = 18). Aortic and left ventricular pressures, index of left ventricular contractility, heart rate, and phasic superior mesenteric, renal, and femoral arterial flows were recorded; mean aortic pressure and vascular resistances were calculated. Maximum changes in cardiovascular function (mean % delta +/- SEM) occurred at the end of the infusion. Mean aortic pressure and index of left ventricular contractility decreased in all animals; responses were larger in magnitude with the higher dose. By 30 min after infusion of 300 micrograms/kg verapamil had ended, mean aortic pressure in both 1 day and 2 wk olds and index of left ventricular contractility and femoral flow in 1 day olds were still decreased. During infusion of verapamil, heart rate decreased (-11.6 +/- 2.9) to the high dose in 1 day olds but increased (+6.4 +/- 2.7) to 100 and 300 micrograms/kg verapamil in 2 wk olds. After infusion of 300 micrograms/kg verapamil ended, heart rate decreased and reached the nadir (-10.0 +/- 2.9) by 10 min in 2 wk olds. Decreases in renal resistance (-7.6 +/- 1.7) were not dose dependent while superior mesenteric resistance decreased (-12.9 +/- 2.7) only to low dose verapamil in 2 wk olds. In 1 day olds decreases in renal and superior mesenteric resistance were not sustained throughout the infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

A COMPARATIVE STUDY OF THE EFFECTS OF BRADYKININ, KALLIDIN II AND ELEDOISIN ON SEGMENTAL SUPERIOR MESENTERIC RESISTANCE.

The Journal of PhysiologyVolume 176, Issue 1 p. 1-11 ArticleFree Access A comparative study of the effects of bradykinin, kallidin II and eledoisin on segmental superior mesenteric resistance C. C. Chou, C. C. ChouSearch for more papers by this authorE. D. Frohlich, E. D. FrohlichSearch for more papers by this authorE. C. Texter Jr., E. C. Texter Jr.Search for more papers by this author C. C. Chou, C. C. ChouSearch for more papers by this authorE. D. Frohlich, E. D. FrohlichSearch for more papers by this authorE. C. Texter Jr., E. C. Texter Jr.Search for more papers by this author First published: 01 January 1965 https://doi.org/10.1113/jphysiol.1965.sp007530Citations: 20AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume176, Issue1January 1, 1965Pages 1-11 RelatedInformation