Cerebral Vascular Resistance in Experimental Renal and DCA Hypertension

Flohr, H.; Dahners, H. W.; Conradi, Henk Jan; Redel, D. A.; Breull, W.; Kikis, D; Stoepel, K.

doi:10.1159/000114463

Cited by 3 publications

(1 citation statement)

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“…These studies indicate that the cardiac output is normal and that the hypertension is attributable to an increase in peripheral vascular resistance, fairly uniformly distributed in the various regional vascular beds (15). Blood flow to the limbs (10), the heart (16), the brain (17), and the nonstenotic kidney (18,19) is reported to be normal.…”

Section: Discussionmentioning

confidence: 95%

Mesenteric hemodynamics in early experimental renal hypertension in dogs.

Simon¹,

Pamnani²,

Dunkel³

et al. 1975

Circulation Research

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To investigate mesenteric hemodynamics in early perinephritic hypertension, we measured blood flows and intravascular pressures in innvervated, collateral-free, naturally perfused loops of ileum in 50 male mongrel dogs anesthetized with sodium pentobarbital. In addition, we studied venous pressure-volume relationships in temporarily occluded segments of mesenteric veins in vivo and in excised segments of mesenteric veins in vitro. In 10 dogs (group H-1), one kidney was wrapped in silk 11 days before study; in 15 other dogs (group H-2), one kidney was wrapped 4 weeks before study and the other was removed 2 weeks before study. Twenty-five additional dogs were prepared as normotensive controls: in 10 one kidney was sham-wrapped (group C-1), and in 15 one kidney was sham-wrapped and the other was removed (group C-2). A significant rise in mean arterial blood pressure occurred in groups H-1 and H-2. Compared to controls, (1) ileal blood flow in the hypertensive dogs (H-1 plus H-2) was increased by 17% (P smaller than 0.05), (2) calculated ileal vascular resistances (total and segmental) were unchanged (P smaller than 0.05), and (3) in vivo and in vitro mesenteric vein pressure-volume curves of H-2 (but not of H-1) hypertensive dogs were shifted in the direction of the pressure axis (P smaller than 0.05). These data suggest that in the early stages of perinephritic hypertension in dogs (1) ileal blood flow is increased. (2) ileal vascular resistance is not elevated, and (3) mesenteric venous compliance is reduced. Analysis of the venous pressure-volume curves suggests that the decreased venous compliance is attributable to factors other than smooth muscle contraction.

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Section: Discussionmentioning

confidence: 95%

Mesenteric hemodynamics in early experimental renal hypertension in dogs.

Simon¹,

Pamnani²,

Dunkel³

et al. 1975

Circulation Research

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Regional distribution of vascular resistance in two models of experimental renovascular hypertension

et al. 1976

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The regional distribution of the peripheral vascular resistance was studied in normotensive and hypertensive Wistar rats. Two models of experimental hypertension were investigated: (I) in 32 animals the right renal artery was constricted by a silver clip (two-kidney Goldblatt hypertension); (II) in 46 animals the left kidney was removed and the right renal artery was clipped as in the first group (one-kidney Goldblatt hypertension). The normotensive control group comprised 61 untreated animals of the same strain and age. The distribution of cardiac output to 14 tissues was determined by means of the particle distribution technique. The resistance was increased in all regions investigated, a decreased or unchanged resistance was not observed. For most of the investigated tissues the regional resistance was increased exactly in proportion to the total peripheral resistance (TPR). Exceptions to this were found in 2 regions where the change of local resistance deviated from that of TPR: the splanchnic area and the skeletal muscle. In both cases the 2 models differed from each other. In the two-kidney model the increase of resistance in the splanchnic circulation was more intense than in other organs. In contrast, in the one-kidney model the local change of resistance was less than that of TPR. The change of skeletal muscle resistance was not significantly different from the change of TPR in the two-kidney model, while in the one-kidney model the increase of local resistance was significantly higher than that of TPR. It is concluded that the etiology of the abnormal resistance is different in the 2 models investigated and that known extrinsinc pressor factors may play a role in the two-kidney, but not in the one-kidney Goldblatt hypertension.

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Brain Metabolism and Arterial Acid-Base Balance Following Bilateral Carotid Occlusion in Normotensive and Experimental Hypertensive Rats

Fujishima

Morotomi

Tamaki

et al. 1978

Can. j. neurol. sci.

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SUMMARY:The effects of bilateral common carotid artery occlusion en brain metabolism and arterial acid-base balance were studied in normotensive and experimental renovascular hypertensive rats.One hour after carotid occlusion in hypertensive rats, supratentorial lactate increased to 383% and lactate-pyruvate ratio to 280% of the controls, while adenosine triphosphate (ATP) decreased to 69%. These metabolic changes were thought to be due to cerebral ischemia. Arterial pC02 was lowered and the pH was raised in the hypertensive animals due to cerebral ischemia induced hyperventilation. In the normotensive rats, carotid occlusion had minimal effects on cerebral metabolism and arterial acid-base balance.These results suggest that hypertensive rats are more susceptible to cerebral ischemia caused by carotid occlusion than normotensive rats. Increased cerebrovascular resistance in hypertension is discussed as a casual factor in cerebral ischemia.

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Cerebral Vascular Resistance in Experimental Renal and DCA Hypertension

Cited by 3 publications

References 0 publications

Mesenteric hemodynamics in early experimental renal hypertension in dogs.

Mesenteric hemodynamics in early experimental renal hypertension in dogs.

Regional distribution of vascular resistance in two models of experimental renovascular hypertension

Brain Metabolism and Arterial Acid-Base Balance Following Bilateral Carotid Occlusion in Normotensive and Experimental Hypertensive Rats

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