Angiotensin converting enzyme inhibition and cerebral circulation‐a review.

Waldemar, Gunhild; Paulson, Olaf B.

doi:10.1111/j.1365-2125.1989.tb03593.x

Cited by 30 publications

(12 citation statements)

References 30 publications

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“…318 Consistent with this, studies by Waldemar 20 and Waldemar and Paulson 21 showed that angiotensin-converting enzyme inhibitors increase CBF at lower blood pressure levels. Rajagopalan et al 22 have suggested that captopril may increase CBF in patients with congestive heart failure by decreasing central sympathetic tone.…”

Section: Discussionsupporting

confidence: 65%

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

Werner

Hoffman

Kochs

et al. 1991

Stroke

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We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male SpragueDawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10/igxkg" 1 i.v. bolus, 25 /*gxkg~'xhr~1 i.v. continuous infusion). Animals in group 1 (n=10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n=10) were given 10 mgxkg" 1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score=4) compared with controls (median deficit score=18) (p<0.05). These results suggest that reduced angjotensin II levels or increased tissue kinin concentrations may decrease ischemic brain injury. (Stroke 1991;22:910-914) C ontroversy exists on the influence of the brain renin-angiotensin system 12 in the modulation of cerebral ischemia. Studies in strokeprone spontaneously hypertensive rats and gerbils suggest that the administration of angiotensin-converting enzyme inhibitors reduce stroke-related mortality and neurologic symptoms. 34 In contrast, experiments on unilateral brain ischemia in gerbils demonstrate a reduction of stroke-related mortality in the presence of angiotensin II. 5 The protective effect of angiotensin II could be reversed using angiotensin-converting enzyme inhibitors or angiotensin II antagonists. 6 These results may be due in part to the cardiovascular effects of the drugs. The hypotensive effect of angiotensin-converting enzyme inhibitors may improve outcome from hypertensive stroke while angiotensin II may increase blood pressure and enhance cerebral perfusion during focal ischemia. We investigated the effect of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a model of incomplete cerebral ischemia in rats.

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Section: Discussionsupporting

confidence: 65%

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

Werner

Hoffman

Kochs

et al. 1991

Stroke

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“…However, dur ing a reduction in blood pressure, the greater dila tory capacity of the smaller vessels would shift the lower limit of autoregulation. The experimental re sults were supported by several clinical studies of the effect of acute or chronic ACE inhibition on CBF (reviewed by Waldemar and Paulson, 1989). In all reports, CBF remained constant, or was slightly increased, despite a significant reduction of MABP (Rajagopalan et al, 1984;Frei and Muller-Brand, 1986;Paulson et al, 1986;Minematsu et al, 1987;Waldemar et al, 1989a).…”

Section: Discussionsupporting

confidence: 55%

Acute Sympathetic Denervation Does Not Eliminate the Effect of Angiotensin Converting Enzyme Inhibition on CBF Autoregulation in Spontaneously Hypertensive Rats

Waldemar

1990

J Cereb Blood Flow Metab

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Summary:The effect of angiotensin converting enzyme inhibition with captopril (10 mg/kg i.v.) on CBF autoreg ulation was studied in 16 spontaneously hypertensive rats (8 control and 8 treated with captopril) sUbjected to acute cervical sympathectomy. CBF was measured repetitively by the intra-arterial I33Xe injection method, during the manipulation of MABP by norepinephrine or hemor rhagic hypotension. Prior to the administration of drugs, baseline MABP was 112 ± 10 mm Hg in the control group Although it was speculated that the effect of cap topril was caused by a reduction of the angiotensin II-induced tone in the larger cerebral arteries (Barry et aI., 1984), the mechanism for the observed effect of ACE inhibition on CBF autoregulation remains to be clarified. Since the renin-angiotensin system interacts with the sympathetic nervous system (Zimmerman, 1978), the effect might result from in hibition of cerebrovascular sympathetic tone, rather than direct inhibition of the angiotensin II induced tone in cerebral arteries. In that case, how-

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“…33,36,37 Experiments using captopril and other angiotensin-converting enzyme inhibitors suggest that this feature also occurs with the activation of the renin-angiotensin system. 33,38,39 Nitric oxide also plays a major role in maintaining the cerebral vasculature in a dilated state. 40 Presently, evidence indicates that the maintenance of renal perfusion in cirrhosis with ascites is critically dependent on the intrarenal synthesis of prostaglandins 41 and nitric oxide 42 and on the circulating plasma levels of natriuretic peptides, 43 which are powerful renal vasodilators.…”

Section: Discussionmentioning

confidence: 99%

Increased cerebrovascular resistance in cirrhotic patients with ascites

et al. 1998

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Studies assessing regional hemodynamics in patients with cirrhosis and ascites have shown vasodilation in the splanchnic circulation and vasoconstriction in the renal circulation and in the brachial and femoral artery vascular territories. The aim of this study was to assess the cerebral vascular resistance in cirrhotic patients with ascites. The resistive index in the middle cerebral artery (an index of the cerebral vascular resistance) and in a renal interlobar artery were measured by Doppler ultrasonography in 7 healthy subjects: 13 patients with compensated cirrhosis and 24 patients with ascites (13 with renal failure). The arterial blood pressure and the activity of the renin-angiotensin and sympathetic nervous systems, as estimated by plasma renin activity and plasma norepinephrine concentration, respectively, were also measured. The resistive index in the middle cerebral artery was significantly increased in patients with ascites (0.68 ؎ 0.05, mean ؎ SD) as compared with patients without ascites (0.60 ؎ 0.01, P F .05) and with healthy patients (0.52 ؎ 0.01, P F .01). Renal resistive index was also increased in patients with ascites (0.77 ؎ 0.01) compared with the other two groups (0.68 ؎ 0.02 and 0.62 ؎ 0.00, respectively; P F .001). The resistive index in the middle cerebral artery showed a direct correlation with renal resistive index (r ‫؍‬ .73, P F .01), plasma renin activity (r ‫؍‬ .61, P F .01), and norepinephrine (r ‫؍‬ .53, P F .01). The resistive index in the middle cerebral artery showed an inverse correlation with mean arterial pressure (r ‫,54.؊؍‬ P F .01). These results indicate that in patients with cirrhosis and ascites there is a cerebral vasoconstriction which is probably related with the arterial hypotension and the overactivity of vasoconstrictor systems. (HEPATOL-OGY 1998;28:39-44.)Portal hypertension in cirrhosis is associated with a hyperdynamic circulation, which is characterized by hypervolemia, high cardiac output, arterial hypotension, and low peripheral vascular resistance. 1 These circulatory abnormalities are thought to be secondary to a splanchnic arteriolar vasodilation related to the increase in portal pressure. Portal hypertension in experimental animals is associated with a generalized splanchnic arteriolar vasodilation. 2,3 There is indirect evidence that this also occurs in human cirrhosis, as hepatic blood flow is usually normal or increased in these patients, even though 60% to 80% of portal flow is shunted through the collateral circulation. 4 In addition, the mean transit time in the splanchnic vascular bed is substantially reduced in alcoholic cirrhotic patients, which indicates a hyperkinetic splanchnic circulation in these patients. 5 Finally, studies using echo-Doppler have documented increased splenic and mesenteric blood flow in patients with cirrhosis. 6,7 Investigations assessing regional circulations in human cirrhosis are also consistent with that concept. Renal blood flow is reduced and renal vascular resistance is increased in most patients with cirrhosi...

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Angiotensin converting enzyme inhibition and cerebral circulation‐a review.

Cited by 30 publications

References 30 publications

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

Captopril improves neurologic outcome from incomplete cerebral ischemia in rats.

Acute Sympathetic Denervation Does Not Eliminate the Effect of Angiotensin Converting Enzyme Inhibition on CBF Autoregulation in Spontaneously Hypertensive Rats

Increased cerebrovascular resistance in cirrhotic patients with ascites

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