Biomedical subjects

S Sadoshima

Publications and source records attributed to S Sadoshima.

At least 163 records · Page 9Linked to original sources

PubMedDate not supplied

Anticardiolipin antibody-induced sudden profound sensorineural hearing loss.

INTRODUCTION: A link between sensorineural hearing loss (SNHL) and autoimmune disease is postulated. The association of SNHL in a patient with systemic lupus erythematosus is reported. METHODS: An adolescent female with left lateral medullary syndrome and right internuclear ophthalmoplegia was diagnosed with systemic lupus erythematosus. Treatment with prednisolone markedly improved her symptoms. Two years later, profound SNHL developed in the right ear. Extensive serologic testing was undertaken. RESULTS: Serologic tests for syphilis were false-positive. Enzyme-linked immunosorbent assay to the immunoglobulin (Ig)G anticardiolipin antibody was positive. The anticardiolipin antibody is strongly correlated with episodes of recurrent venous or arterial thrombosis. CONCLUSIONS: It appears that the anticardiolipin antibody may be associated with sudden profound sensorineural hearing loss in patients with autoimmune disease.

Adolescent↗

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Blood pressure changes associated with hyperinsulinemia or long-standing diabetes mellitus in spontaneously hypertensive rats.

We studied the long-term change in blood pressures of spontaneously hypertensive rats (SHR) treated neonatally with streptozotocin (STZ). Two-day-old male SHR were injected intraperitoneally with 37.5-75.0 mg/kg STZ or with vehicle as control. STZ-treated SHR were divided into mildly or severely diabetic groups according to the nonfasting plasma glucose level at age 12 weeks (the former less than 300 mg/dl, the latter greater than or equal to 300 mg/dl). In the mildly diabetic group (MD) (n = 5), body weight increased and nonfasting plasma glucose was normalized. At 52 weeks of age, fasting plasma glucose levels were lower than controls owing to hyperinsulinemia, and insulinomas were found in 60% of rats. The systolic blood pressure (SBP) as measured by a tail-cuff method, decreased after 40 weeks, and the mean BP from 44 to 52 weeks (188 +/- 4 mmHg) was significantly lower than that in the control group (209 +/- 3 mmHg, p less than 0.01). In the severely diabetic group (SD) (n = 6), hyperglycemia persisted until 52 weeks, although its severity became less marked. BP in the SD group increased after 36 weeks, and the mean BP from 44 weeks to 52 weeks (224 +/- 5 mmHg) was significantly higher than control (p less than 0.05). The present study demonstrated that hypertension was ameliorated in SHR associated with hyperinsulinemia, and deteriorated with long-standing diabetes mellitus.

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Sympathetic nerves protect against stroke in stroke-prone hypertensive rats. A preliminary report.

Studies were performed to determine whether sympathetic nerves protect against stroke in hypertensive rats. The superior cervical ganglion was removed on one side in 28 stroke-prone spontaneously hypertensive rats (SHRSP) when the rats were 4 weeks old. The rats were fed Japanese rat chow and 1% saline drinking water. When the rats were 19 weeks old, systolic pressure was 206 +/- 4 mm Hg (mean +/- SE). All rats died between 19 and 23 weeks of age. Microscopic and histological examination demonstrated cerebral hemorrhage in seven rats. All the hemorrhages occurred in the denervated hemispheres. Ischemic cerebral infarctions were found in 13 rats; in 10 rats, the infarcts were only in the denervated hemisphere. Pathological changes of cerebral arteries (hyalinosis, fibrinoid changes, and thrombus formation) were observed primarily in denervated hemispheres. Wall-to-lumen ratio was less in arteries of the denervated hemisphere than in arteries of the innervated hemisphere. These preliminary observations suggest that denervation of cerebral vessels increases susceptibility to stroke and inhibits development of cerebral vascular hypertrophy in SHRSP.

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PubMedDate not supplied

Sympathetic nerves protect the blood-brain barrier in stroke-prone spontaneously hypertensive rats.

Disruption of the blood-brain barrier may play a major role in the pathogenesis of hypertensive encephalopathy. In this study we determined whether sympathetic nerves to cerebral vessels protect the blood-brain barrier during chronic hypertension. We removed the cervical sympathetic ganglion on one side in 24 stroke-prone hypertensive rats when they were 1 month old. After signs of cerebral dysfunction developed at the mean age of 160 +/- 5 days (SE), we injected 125I-albumin and Evans blue dye intravenously to evaluate the permeability of the 125I-albumin was 3.53 +/- 0.83 (brain albumin x 100/blood albumin) in areas of the cerebrum stained with blue dye and 0.24 +/- 0.02 in unstained areas (p less than 0.05). We conclude that sympathetic nerves protect the blood-brain barrier against disruption during chronic hypertension and thereby may protect against hypertensive encephalopathy.

Albumins↗

PubMedDate not supplied

Evidence that disruption of the blood-brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy.

Alternative hypotheses concerning the pathogenesis of hypertensive encephalopathy are that vasospasm produces cerebral ischemia and cerebral edema, or that passive dilation of cerebral vessels during severe hypertension produces disruption of the blood-brain barrier and cerebral edema. Stroke-prone spontaneously hypertensive rats (SHRSP) were studied when they developed signs of neurological dysfunction. We measured regional cerebral blood flow (rCBF) with 14C-iodoantipyrine, and permeability of the blood-brain barrier with Evans blue dye. Twelve rats had focal disruption of the barrier without histological evidence of ischemic infarction or cerebral hemorrhage: areas with disruption of the barrier had severe focal edema in seven rats and minimal edema in five rats. In areas with disruption of the barrier and marked focal edema, rCBF was decreased to 38 +/- 8 (mean +/- SE) ml/min/100 g vs 102 +/- 13 (p less than 0.05) in other areas of the ipsilateral hemisphere, and 86 +/- 16 in the homologous area of the contralateral hemisphere (p less than 0.05). In contrast, in areas with disruption of the blood-brain barrier with only minimal edema, rCBF was normal or increased: rCBF was 100 +/- 11 ml/min/100 g vs 85 +/- 12 in other areas of the ipsilateral hemisphere (p greater than 0.05) and 64 +/- 8 in the homologous area contralaterally (p less than 0.05). The findings indicate that edema precedes reduction in rCBF in SHRSP and suggest that the initiating event in hypertensive encephalopathy is disruption of the blood-brain barrier, and not vasospasm.

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PubMedDate not supplied

Increased susceptibility to osmotic disruption of the blood-brain barrier in chronic hypertension.

We examined the effects of chronic hypertension and acute reduction of arterial pressure on the susceptibility of the blood-brain barrier (BBB) to disruption. The BBB was disrupted with an intracarotid injection of 1.6 M arabinose in spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP), and normotensive Wistar-Kyoto (WKY) rats. Permeability of the BBB was determined from the ratio of 125I-albumin in brain to 125I-albumin in blood. When the BBB was intact, permeability was less than 0.4%. After hypertonic arabinose, permeability of the BBB was greater (mean +/- SE) in SHRSP (17.6% +/- 1.6%) and in SHR (21.1% +/- 3.1%) than in WKY (10.3% +/- 2.4%) (p less than 0.05). When arterial pressure of SHRSP was reduced acutely with nitroprusside before arabinose, the BBB permeability to albumin was not reduced (21.5% +/- 1.5%). In other rats, we examined survival after osmotic disruption. In SHRSP, 14 of 15 rats died within 1 day after osmotic disruption with marked cerebral edema. In WKY, four of 15 rats died (p less than 0.05 vs SHRSP). When arterial pressure of SHRSP was reduced before arabinose, mortality was reduced to six of 15 (p less than 0.05 vs untreated SHRSP). We conclude that the BBB in SHRSP has enhanced vulnerability that is detrimental to survival. Reduction of arterial pressure improves survival in SHRSP without affecting BBB permeability to albumin.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cerebral artery thrombosis and intramural hemorrhage.

Thirty-nine thrombosed arterial segments of the branches of the circle of Willis were studied by a complete serial section technique. Twenty-two patients had been hypertensive and 8 had hypercholesterolemia before the onset of cerebral artery thrombosis. The histological characteristics of the thrombosed arterial segments were intramural hemorrhage in 28 segments, superficial edema of the fibrous cap of the atheroma of fibrous plaque in 4, rupture of the atheromatous plaque in 1, superficial accumulation of foam cells in the atheroma in 1 and an atheroma or fibrous plaque without any other changes in 5. They were many intramural small blood vessels in the atheroma or fibrous plaques of 22 segments with intramural hemorrhage. Fibrinoid degeneration of these small blood vessels was noted in 5. These findings suggested that intramural hemorrhage from the intramural small blood vessels was the major cause of cerebral artery thrombosis and that persistent hypertension not only promoted cerebral atherosclerosis but also induced hemorrhage from the intramural small blood vessels.

Adult↗

PubMedDate not supplied

Regional cerebral blood flow during hypotension in normotensive and stroke-prone spontaneously hypertensive rats: effect of sympathetic denervation.

This study was performed to determine whether, in hypertensive and normotensive rats, chronic sympathetic denervation impairs cerebral vasodilator responses during hypotension, and to determine whether there are regional differences in the autoregulatory response of brain vessels during hypotension. The superior cervical ganglion was removed on one side in stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive (WKY) rats. Cerebral blood flow (CBF) was measured with microspheres when the rats were 5-6 months old. Chronic sympathetic denervation had little or no effect on cerebral vasodilator responses during acute hypotension in SHRSP and WKY. We suggest that the increase in incidence of ischemic infarction that we have observed previously after chronic sympathetic denervation in SHRSP probably is not the result of ischemia during episodes of hypotension. We also observed major regional differences in the response of cerebral vessels during acute hypotension in SHRSP: blood flow to brainstem was preserved better than flow to cerebrum and cerebellum. Thus the "lower limit" of the autoregulatory plateau differs in various regions of the brain in SHRSP.

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PubMedDate not supplied

Disruption of blood-brain barrier following bilateral carotid artery occlusion in spontaneously hypertensive rats. A quantitative study.

The present study was designed to clarify the relationship of cerebral blood flow (CBF) to blood-brain barrier (BBB) in the ischemic brains with or without recirculation, which were produced by clipping of both common carotid arteries in spontaneously hypertensive rats. CBF was measured by the hydrogen clearance method and BBB function was evaluated by the permeability of 131I-albumin and Evans blue dye. Cortical CBF was reduced from 48.8 +/- 9.5 to 4.0 +/- 1.2 ml/100 gm/min during 1 hr ischemia and further to 2.6 +/- 0.3 ml/100 gm/min during 3 hrs ischemia, while thalamic CBF was reduced much less from 50.0 +/- 3.6 to 17.9 +/- 6.5 ml/100 gm/min and to 17.5 +/- 11.0 ml/100 gm/min, respectively. There was no increase in permeability to protein tracers observed in such 1 hr or 3 hrs ischemic brain. Both cortical and thalamic CBF were markedly increased 2.5 to 6 fold of resting values at 5 min after recirculation in the 1 hr ischemic brain. In the 3 hrs ischemic brain, however, both CBF were only slightly increased but never restored to the resting level even at 30 min after recirculation. In such reperfused brains, exudation to Evans blue dye was observed in none of 16 animals with 1 hr ischemia, but in 18 of 23 with 3 hrs ischemia. Disruption of BBB was twice more frequent in the cortex (77.8%) than in either thalamus (33.3%) or hippocampus (33.3%). Permeability index of 131I-albumin (brain albumin/blood albumin) was significantly higher in the ischemic areas stained with blue dye (2.07 +/- 0.45%) than in non-ischemic control brain (0.10 +/- 0.01%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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Cerebrovascular diseases and their underlying vascular lesions in Hisayama, Japan--a pathological study of autopsy cases.

Frequency of cerebrovascular diseases (CVD) and their underlying vascular lesions were analyzed in 724 autopsy cases, aged 40 years and over, in the community of Hisayama, Japan during the period 1961 to 1981. Cerebral infarction (CI) was more frequently found at autopsy than cerebral hemorrhage (CH) with a ratio of infarction and hemorrhage of 4.4. Small CI occupied 75.7% of the cases with CI. The cases with any type of CVD showed more severe atherosclerosis of the major cerebral arteries than did those without CI or CH. Cerebral atherosclerosis of those with large and medium CI was the greatest, and with decreasing severity in those with small CI and with CH sequentially. Fibrinoid necrosis of the intracerebral small arteries was frequently found in cases with hypertension and particularly associated with CH. The decline in frequency of CH was confirmed; however, changes in frequency of CI were not evident. Fibrinoid necrosis was also reduced, although the severity of cerebral atherosclerosis showed no definite change. The decline of CH seemed to be ascribed to the reduction of fibrinoid necrosis of the intracerebral small arteries.

Adult↗

PubMedDate not supplied

Upper limit of cerebral autoregulation during development of hypertension in spontaneously hypertensive rats--effect of sympathetic denervation.

The upper limit of cerebral autoregulation was studied in pre- or early established hypertension in spontaneously hypertensive rats (SHR). Cerebral blood flow (CBF) was measured with the hydrogen clearance method, and wall/lumen ratio of cerebral arteries was morphometrically measured with the freeze-substitution technique. To test autoregulation, phenylephrine was intravenously infused to cause stepwise increments of blood pressure. Unilateral superior cervical ganglionectomy was carried out to examine the effects of sympathetic denervation on CBF autoregulation and thickness of vascular wall. Resting blood pressure at 4 weeks, 3 months and 6 months of age were 89 +/- 3 mm Hg (mean +/- SEM), 140 +/- 6 and 165 +/- 6, respectively. Baseline CBF was slightly diminished with age; 50.6 +/- 9.2 ml/100 g/min at 4 weeks, 49.8 +/- 8.1 at 3 months and 44.1 +/- 5.6 at 6 months. The upper limit of autoregulation was markedly raised with age; 118 +/- 5 mm Hg at 4 weeks, 180 +/- 7 at 3 months and 208 +/- 10 at 6 months. Acute sympathetic denervation lowered the upper limits to 105 +/- 2, 162 +/- 4 and 185 +/- 7 mm Hg, respectively. On the other hand, in chronic denervation which was made at 4 weeks of age, the upper limit of autoregulation in the denervated hemisphere was slightly lower than that in innervated hemisphere at 2 months (165 +/- 5 and 178 +/- 6 mm Hg), and at 5 months (202 +/- 8 and 215 +/- 8 mm Hg) after ganglionectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

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Effects of hematocrit on brain metabolism in experimentally induced cerebral ischemia in spontaneously hypertensive rats (SHR).

Brain tissue lactate, pyruvate, and adenosine triphosphate (ATP) were measured 60 min after bilateral carotid ligation in spontaneously hypertensive rats, of which hematocrit (HCT) was varied by exchanging with isovolemic homologous red cells, plasma or whole blood. Supratentorial lactate of the ischemic brain was increased more in high HCT (greater than or equal to 50%) and less in low HCT (30-39%) compared with normal HCT (40-49%). In very low HCT (less than 30%), however, lactate was increased to further extent compared with any other group of HCT (ANOVA p less than 0.0001). Lactate/pyruvate (L/P) ratio of the ischemic brain showed similar changes, namely U-shaped correlation to HCT. In contrast, supratentorial ATP was decreased more markedly in very low HCT, followed by high and normal HCT, and minimally decreased in low HCT, demonstrating an inverse U-shaped relationship to HCT. Mean arterial pressure and arterial acid-base parameters in ischemic animals did not differ among HCT groups. There were no HCT-related changes of brain metabolites in non-ischemic control rats. These findings indicate that cerebral ischemia following carotid ligation is more severe in high HCT but less in low HCT, probably due to hemodynamic effects of HCT changes. When HCT is reduced to below 30%, however, insufficient oxygen supply to the brain or anemic hypoxia may superimpose on ischemia, resulting in more markedly impairment of brain metabolism. The role of HCT as a cause of cerebral ischemia and its severity is discussed.

Acid-Base Equilibrium↗

PubMedDate not supplied

Cerebral blood flow and tissue metabolism in experimental cerebral ischemia of spontaneously hypertensive rats with hyper-, normo-, and hypoglycemia.

The present study was designed to clarify the effect of blood glucose level on cerebral blood flow and metabolism during and after acute cerebral ischemia induced by bilateral carotid ligation (BCL) in spontaneously hypertensive rats (SHR). Blood glucose levels were varied by intraperitoneal infusion of 50% of glucose (hyperglycemia), insulin with hypertonic saline (hypoglycemia) or hypertonic saline (normoglycemia). Cerebral blood flow (CBF) in the parietal cortex and thalamus was measured by hydrogen clearance technique, and the supratentorial metabolites of the brain frozen in situ were determined by the enzymatic method. In non-ischemic animals, blood glucose levels had no influence on the supratentorial lactate, pyruvate or adenosine triphosphate (ATP) concentrations. In ischemic animals, however, cortical CBF was reduced to less than 1% of the resting value at 3 hours after BCL. However, there were no substantial differences of CBF during and after ischemia among 3 glycemic groups. Cerebral lactate in the ischemic brain greatly increased in hyperglycemia (34.97 +/- 1.29 mmol/kg), moderately in normoglycemia (23.43 +/- 3.13 mmol/kg) and less in hypoglycemia (7.20 +/- 1.54 mmol/kg). In contrast, cerebral ATP decreased in hyperglycemia (0.93 +/- 0.19 mmol/kg) as much as it did in normoglycemia (1.04 +/- 0.25 mmol/kg), while ATP reduction was much greater in hypoglycemia (0.45 +/- 0.05 mmol/kg). At 1-hour recirculation after 3-hour ischemia, ATP tended to increase in all groups of animals, indicating the recovery of energy metabolism. Such metabolic recovery after recirculation was good in hypo- and normoglycemia, and was also evident in hyperglycemia. Our results suggest that hyperglycemia is not necessarily an unfavorable condition in acute incomplete cerebral ischemia.

Adenosine Triphosphate↗

PubMedDate not supplied

The effect of long-term antihypertensive treatment on medial hypertrophy of cerebral arteries in spontaneously hypertensive rats.

The effects of antihypertensive treatment on the structural changes of middle cerebral arteries (MCA) were studied quantitatively and morphometrically in young spontaneously hypertensive rats (SHR). Fifteen male SHR, 10 weeks of age, were divided into control and experimental groups. In the experimental group, the animals were administered hydralazine and guanethidine for the following 10 weeks. At the age of 20 weeks, mean arterial blood pressure of experimental animals was 177 +/- 9 mm Hg (mean +/- SD), being significantly lower than that of 195 +/- 12 mm Hg in control ones. Media thickness of large (external diameter greater than or equal to 200 micron) and medium sized MCA (150-200 micron) in treated SHR was 12.3 +/- 2.8 and 6.3 +/- 1.1 micron, respectively, being significantly smaller than that of 14.0 +/- 2.2 and 8.5 +/- 2.6 micron, respectively, in control SHR. The media cross-sectional area and the ratio of media thickness to external diameter were also significantly reduced by antihypertensive treatment. In the smaller vessels (75-150 micron), however, vascular morphometry revealed no difference between the two groups. Long-term antihypertensive treatment during the early phase of hypertension attenuates the development of medial hypertrophy in large cerebral arteries.

Animals↗

PubMedDate not supplied

Regional cerebral blood flow autoregulation in normotensive and spontaneously hypertensive rats--effects of sympathetic denervation.

The present study was designed to investigate the effect of acute sympathetic denervation on the regional cerebral blood flow (CBF) autoregulation during acute elevation of blood pressure in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). CBF to the parietal cortex and thalamus was measured by the hydrogen clearance method and, to test autoregulation, systemic arterial blood pressure was elevated by intravenous infusion of phenylephrine. Superior cervical ganglia were removed on both sides to interrupt sympathetic innervation in the deeper structures of the brain. Acute bilateral sympathetic denervation did not alter the resting blood pressure or CBF in either SHR or WKY. In innervated SHR, resting mean arterial pressure (MAP) was 165 +/- 5 mm Hg (mean +/- SEM) and the upper limit of autoregulation in the cortex was 210 +/- 3 mm Hg, which was significantly lower than that in the thalamus (229 +/- 3 mm Hg, p less than 0.02). In bilaterally denervated SHR, the upper limits were lowered to 193 +/- 4 mm Hg in the cortex (p less than 0.02 vs. innervated SHR) and to 207 +/- 5 mm Hg in the thalamus (p less than 0.02 vs. innervated). In WKY, resting MAP was approximately 55 mm Hg lower than that in SHR. Acute denervation reduced the upper limits from 142 +/- 3 mm Hg to 130 +/- 4 in the cortex (p less than 0.05) and from 158 +/- 4 to 145 +/- 4 in the thalamus (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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Effects of long-term antihypertensive treatment on cerebral, thalamic and cerebellar blood flow in spontaneously hypertensive rats (SHR).

Cerebral blood flows (CBF) were measured in the parietal cortex, the thalamus and the cerebellum by the hydrogen clearance technique in anesthetized spontaneously hypertensive rats, of which hypertension was treated for 16 weeks (long-term) or 8 weeks (short-term) with antihypertensive agents of hydralazine and guanethidine. As compared to non-treated control animals, CBF in the three regions were significantly increased while the calculated cerebrovascular resistances (CVR) were decreased in hypertension-treated animals. Such CBF and CVR changes were greater in SHR with long-term than short-term therapy. Both an increase in CBF and a decrease in CVR were closely related to a fall in the blood pressure. From the present results, it was concluded that earlier and longer treatment of hypertension could lessen or even prevent the increased CVR due to the hypertensive vascular changes, and increase CBF as a result.

Animals↗

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Cerebral and cerebellar blood flow autoregulations in acutely induced cerebral ischemia in spontaneously hypertensive rats--transtentorial remote effect.

Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 +/- 6.2 and 58.9 +/- 4.6 ml/100 g/min (mean +/- SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 +/- 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74% and further to 58% of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 +/- 4.9 and CeBF to 53.9 +/- 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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Renal blood flow in acute cerebral ischemia in spontaneously hypertensive rats: effects of alpha- and beta-adrenergic blockade.

The influences of acute cerebral ischemia on renal hemodynamics were examined in spontaneously hypertensive rats in which cerebral ischemia was induced by bilateral carotid artery occlusion. Renal and cerebral blood flow were measured with a hydrogen clearance technique. Either phenoxybenzamine (0.5 mg/kg body wt) or propranolol (2 mg/kg) was given i.v. immediately after ischemia was induced to examine the drugs' effects on cerebral and renal hemodynamics. One hour after ischemia, cerebral blood flow was markedly reduced to 5, 3, and almost 0% of the preischemic value in the untreated, phenoxybenzamine-treated, and propranolol-treated rats, respectively. In contrast, renal blood flow at that time was decreased to 65, 88, and 67%, respectively. The calculated renal vascular resistance was similarly increased to 151% in the untreated and 136% in the propranolol-treated rats, but decreased to 82% in the phenoxybenzamine-treated rats. The present results indicate that in acute cerebral ischemia renal blood flow was considerably decreased with concomitant increased renal vascular resistance, and that such reduction in renal blood flow was minimized by alpha-adrenergic blockade but not by beta-blockade. It is concluded that activation of the alpha-adrenergic system in acute cerebral ischemia causes renal vasoconstriction.

Acid-Base Equilibrium↗