Chronic antihypertensive treatment in the rat reverses hypertension-induced changes in cerebral blood flow autoregulation

Cerebral blood flow (CBF) autoregulation was studied in renal hypertensive rats receiving chronic antihypertensive treatment. Young Wistar Kyoto rats (WKY) were made hypertensive by the Loomis procedure i.e. partial infarction of one kidney with contralateral nephrectomy. Systolic tail blood pressure was measured at 2-week intervals throughout the study. After two months, by which time the rats had been severely hypertensive for 5-6 weeks, antihypertensive treatment was begun; reserpine, dihydralazine and hydrochlorothiazide were administered in the drinking water. Blood pressure fell rapidly to normotensive levels and remained so. Following two months of antihypertensive treatment, the lower blood pressure limit of CBF autoregulation was studied during controlled bleeding. In age-matched untreated renal hypertensive WKY, the lower limit of autoregulation was in the mean arterial pressure range 90-109 mm Hg, as compared to 50-69 mm Hg in age-matched normotensive WKY. In contradistinction to the untreated rats, the treated rats had a normal lower limit of autoregulation, i.e. 50-69 mm Hg. It was inferred that the reversal of the functional change in CBF autoregulation reflected reversal of hypertension-induced cerebrovascular hypertrophy/hyperplasia.     

Protective effects of angiotensin II type 1 receptor blocker on cerebral circulation independent of blood pressure

Angiotensin II type 1 receptor (AT1R) blocker (ARB) has been reported to modify hypertensive cerebrovascular changes; however, it is not clear whether its protective effects are independent of blood pressure. The aim of this study was to clarify the role of AT1R-mediated signals in cerebral circulation by the chronic treatment with telmisartan, an ARB, at a dose that did not lower the blood pressure. Male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were treated for 4 weeks from 16 weeks of ages with telmisartan (SHR-L: 0.3 mg/kg/day, SHR-H: 3 mg/kg/day, WKY-H: 3 mg/kg/day) or vehicle (SHR-V, WKY-V). Superoxide measured by a chemiluminescent assay or dihydroethidium fluorescence and vascular morphology were examined for the thoracic aorta (Ao), common carotid (CCA), middle cerebral (MCA) and basilar arteries (BA). After 4 weeks of treatment, the blood pressure significantly declined in SHR-H but not in SHR-L in comparison to SHR-V. The lower limit of cerebral blood flow (CBF) autoregulation, evaluated by hemorrhagic hypotension, was significantly lower in SHR-L and SHR-H than SHR-V. In both SHR and WKY, the superoxide levels in the arteries were significantly attenuated by both doses of ARB. ARB also reversed vascular hypertrophy in Ao, CCA and BA and the inward remodeling in MCA. These results suggest that chronic treatment with telmisartan may therefore improve CBF autoregulation with a restoration of the vascular structure and an attenuation of superoxide generation, even at a dose that does not lower the blood pressure.     

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)     

Hypertension impairs leptomeningeal collateral growth after common carotid artery occlusion: restoration by antihypertensive treatment

Chronic mild hypoperfusion has been shown to enlarge pial collateral vessels in normal mouse brains. The purpose of this study was to clarify the effect of hypertension on pial collateral vessel development after chronic hypoperfusion using spontaneously hypertensive rats (SHR). In normotensive rats, unilateral common carotid artery (CCA) occlusion enlarged leptomeningeal collateral vessels. CCA occlusion also preserved residual cerebral blood flow (CBF) and attenuated infarct size after middle cerebral artery (MCA) occlusion 14 days later. In contrast, in SHR, CCA occlusion neither enlarged the leptomeningeal anastomosis nor showed protective effects after MCA occlusion. However, decreasing blood pressure using an angiotensin II AT1 receptor blocker restored the beneficial effect of CCA occlusion on collateral growth as well as on residual CBF and infarct size after MCA occlusion. Adaptive responses in CBF autoregulation curves observed 14 days after CCA occlusion in normotensive rats were impaired in untreated SHR, but were restored after antihypertensive treatment. In conclusion, SHR have impaired leptomeningeal collateral growth after CCA occlusion, but antihypertensive treatment restores the beneficial effect of CCA occlusion on collateral circulation.     

Regional differences in cerebrovascular cholinergic innervation in goats

The presence and distribution of a cerebrovascular cholinergic system were studied in goats. Regional cerebral blood flow was measured in the parietal cerebral cortex, caudate nucleus, and white matter by the hydrogen clearance technique in unanesthetized goats. Intravenous low doses of physostigmine, but not of neostigmine, significantly increased regional blood flow without changing mean arterial blood pressure or behavior. Increases of blood flow were greater in cerebral cortex and caudate nucleus than in white matter although the vasodilation induced by hypercapnia was similar in the three regions. Intracerebral microvessels were isolated from cerebral cortex, caudate nucleus, and white matter to evaluate choline acetyltransferase activity as a marker for perivascular cholinergic nerves. The enzyme level was higher in vessels from cerebral cortex and caudate nucleus than in vessels from white matter, which is in accordance with the functional data. These results suggest the presence of a cholinergic perivascular innervation system in intracerebral microvessels. Such innervation has a nonhomogeneous distribution throughout the brain and might be implicated in the local regulation of cerebral blood flow.     

Effect of antihypertensive therapy on focal stroke in spontaneously hypertensive rats

Spontaneously hypertensive rats subjected to focal cerebral ischemia develop larger infarcts than normotensive rat strains. To determine whether antihypertensive therapy decreases infarct volume in hypertensive rats, 60 13-week-old animals were treated with 20 mg/kg hydralazine added daily to the drinking water for 1.5, 6, 10, or 16 weeks and then subjected to focal cerebral ischemia by tandem right common carotid artery and middle cerebral artery occlusion. Blood pressure in the treated groups was substantially lower than that in untreated groups after 1 week of hydralazine therapy and remained lower for the entire treatment period in all four experiments. Mean infarct volume in spontaneously hypertensive rats treated for 10 (p = 0.02) or 16 (p = 0.005) weeks, but not 1.5 or 6 weeks, was significantly less than that in the untreated controls. The percentage reduction of infarct volume in animals treated for 10 and 16 weeks was similar. This study demonstrates that antihypertensive therapy decreases infarct volume in hypertensive rats subjected to focal cerebral ischemia. This treatment effect appears to be dependent on the duration of therapy, and the magnitude of the treatment effect seems to plateau by 10 weeks of therapy.     

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.     

Influence of long-term antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR--protective effect of nicardipine hydrochloride

We have already reported that the long-term antihypertensive treatment reduced the degree of cerebral ischemia induced by bilateral common carotid artery ligation (BLCL) in stoke-resistant spontaneously hypertensive rats (SHRSR). This antihypertensive treatment was achieved by the combination of captopril and hydroflumethiazide. In this study, nicardipine hydrochloride which is one of the Ca2+ antagonist was similarly administrated to SHRSR for 8-10 weeks (T-SHR). The effect of long-term antihypertensive treatment by this agent on cerebral ischemia induce by BLCL was investigated and compared with untreated SHRSR (U-SHR). The degree of cerebral ischemia 4 hr after BLCL was estimated by the levels of brain energy metabolites (ATP, lactate, c-AMP) and brain water content. The brain metabolites and water content were measured in the forebrain and hindbrain of each hemisphere. And also the histopathological study on brain vessels 3 hr after BLCL was achieved by using scanning electron microscopy (SEM). The blood pressure of T-SHR gradually declined from 185 +/- 10 mmHg (mean +/- S.D.) to 154 +/- 8 mmHg after 8-10 weeks of antihypertensive treatment. However the blood pressure of U-SHR spontaneously changed from 185 +/- 8 mmHg to 206 +/- 12 mmHg after 8-10 weeks. The blood pressure of T-SHR after the treatment was significantly lower than that of U-SHR. The levels of ATP and c-AMP in T-SHR after BLCL were statistically higher than those in U-SHR, and the lactate levels in T-SHR were significantly lower than in U-SHR in the both fore- and hindbrain.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of bilateral sympathetic innervation on cerebral blood flow autoregulation in the thalamus

Effects of bilateral sympathetic innervation on the regulation of cerebral blood flow to the thalamus were examined in spontaneously hypertensive rats (SHR). The superior cervical ganglion was removed on one side or bilaterally, and blood flow in the thalamus was repeatedly measured with a hydrogen clearance technique during a stepwise increase in arterial pressure. Regional blood flow in the thalamus was unchanged following acute ganglionectomy: 55 +/- 6 ml/100 g/min in the intact rats and 56 +/- 4 in the denervated rats. Sympathectomy on one side neither had effects on the pressure-flow relationship nor on the blood pressure levels of upper limits of autoregulation in the ipsilateral thalamus. In contrast, bilateral sympathetic denervation impaired the autoregulatory function in the thalamus and the upper limits were significantly lower than those in intact rats: 206 +/- 8 vs 226 +/- 10 mm Hg, respectively (P less than 0.02). It is concluded that overlapping innervation of sympathetic nerves has an important role in regulation of blood flow to the thalamus during an acute rise in arterial pressure in SHR.     

The effects of poststroke captopril and losartan treatment on cerebral blood flow autoregulation in SHRsp with hemorrhagic stroke

The ability of captopril and losartan treatment to restore cerebral blood flow (CBF) autoregulation after intracerebral hemorrhagic stroke (HS) was assessed in Kyoto–Wistar stroke-prone hypertensive rats (SHRsp). Laser Doppler techniques assessed CBF autoregulation in the middle cerebral artery (MCA) perfusion domain and a pressure myograph was used to measure pressure-dependent constriction (PDC) in isolated MCAs before and after stroke and after 13, 33, and 63 days of poststroke captopril or losartan treatment. The treatments did not lower blood pressure (BP) and equally suppressed plasma aldosterone after HS. The HS development was associated with the loss of CBF autoregulation, high CBF, increased CBF conductance to elevations in BP, and the loss of PDC in the MCAs. Both treatments restored these functions to prestroke levels within 13 days. The PDC and CBF autoregulation subsequently deteriorated after 63 days of captopril treatment while being maintained at prestroke levels over all durations of losartan treatment. The SHRsp subjected to 35 days of poststroke losartan treatment exhibited less blood–brain barrier (BBB) disruption and brain herniation than captopril-treated SHRsp. The superior ability of losartan to restore CBF autoregulation and myogenic function may have contributed to the more effective attenuation of cerebral damage after HS.     

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike

There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 +/- 6 ml/100g/min, in the left 38 +/- 6 (p less than 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p less than 0.01 and p less than 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right (p less than 0.001 and p less than 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism.     

Effect of long-term prior antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR

The susceptibility to cerebral ischemia was studied in stroke-resistant spontaneously hypertensive rats (SHRSR) treated by a long-term antihypertensive treatment, and compared with untreated SHRSR and Wistar rats (WR). Male SHRSR, aged 8 weeks, were divided into two groups and a long-term antihypertensive treatment for 4-6 weeks was started on one group (treated SHRSR: T-SHR) while the other group was left untreated as control (untreated SHRSR: U-SHR). The changes of blood pressure were checked on these rats. The prior treatment of hypertension was achieved by administration of hydroflumethiazide (120 mg/kg/day) and captopril (15-30 mg/kg/day) orally for 4-6 weeks by mixing in drinking water. All the experiments were performed at the age of 12-16 weeks and WR of similar age served as normotensive untreated control. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and blood pressure was always checked before BLCL. The survival ratio was observed from 1 hour to 24 hours after BLCL. The regional cerebral blood flow (rCBF) were measured before and 4 hours after BLCL periodically. The brain energy metabolites were measured 4 hours after BLCL. rCBF were measured at the thalamus by the hydrogen clearance method. ATP concentrations were determined by luciferine-luciferase method, c-AMP was measured by RIA and lactate by enzymatic method. The brain water content was measured by freeze-dry method.(ABSTRACT TRUNCATED AT 250 WORDS)     

Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

临界关闭压在脑血流动力学评价中的应用

目的探讨检测脑血流动力学的快捷、实用的新方法,为临床检测奠定基础。方法利用经颅多普勒(TCD)检测大鼠大脑中动脉(MCA)的血流速度,同步记录有创血压,按照临界关闭压(CCP)的理论计算出脑血流自动调节的下限和微动脉阻力,与改变血压测定的结果进行比较。结果CCP法检测到的脑血流自动调节下限为70.88±24.05mmHg,与常用血压改变测定的结果数值接近,可以相互替代。肾血管性高血压大鼠(RHR)的脑血流自动调节下限和微动脉阻力的升高,与动脉血压的升高,特别是脉压差的增大密切相关。结论按照CCP理论测定脑血流自动调节下限和微动脉的阻力,可以准确、快捷地反映脑血流动力学的生理状态和病理改变。     

Leuko-araiosis--regional cerebral hemodynamics

To investigate the cerebral hemodynamics of leuko-araisosis (L-A), we made SPECT measurement of regional cerebral blood flow (rCBF) in 31 patients with L-A. Cerebral vascular reactivity to carbon dioxide and blood pressure was studied. Changes in rCBF during sleep were also studied. SPECT measurements of rCBF were made using radioactive tracer I-123-iodoamphetamine and Tc-99m-HMPAO. Regional CBF was reduced in patients with L-A in the white matter and in the frontal and the parietal cortex. Cerebrovascular CO2 reactivity was impaired in the white matter but was preserved in the frontal and parietal cortex. Cerebral blood flow autoregulation was impaired in the frontal cortex and in the parietal cortex. During sleep (stage 2-3) rCBF was reduced most markedly in the frontal and in the parietal cortex. Blood pressure was also reduced during sleep suggesting that the reduction of rCBF in L-A was partly due to dys-autoregulation.     

Impaired cerebral autoregulation 24 h after induction of transient unilateral focal ischaemia in the rat

Cerebral blood flow (CBF) and cerebral autoregulation have been investigated 24 h after transient focal ischaemia in the rat. Cerebral blood flow was measured autoradiographically before and during a moderate hypotensive challenge, to test autoregulatory responses, using two CBF tracers, (99m)Tc-d,l-hexamethylproyleneamine oxide and 14C-iodoantipyrine. Prior to induced hypotension, CBF was significantly reduced within areas of infarction; cortex (28 +/- 20 compared with 109 +/- 23 mL/100 g/min contralateral to ischaemic focus, P = 0.001) and caudate (57 +/- 31 compared with 141 +/- 32 mL/100 g/min contralaterally, P = 0.005). The hypotensive challenge (mean arterial pressure reduced to 60 mmHg by increasing halothane concentration) did not compromise grey matter autoregulation in the contralateral hemisphere; CBF data were not significantly different at normotension and during hypotension. However, in the ipsilateral hemisphere, a significant volume of cortex adjacent to the infarct, which exhibited normal flow at normotension, became oligaemic during the hypotensive challenge (e.g. frontal parietal cortex 109 +/- 15% to 65 +/- 15% of cerebellar flow, P < 0.01). This resulted in a 2.5-fold increase in the volume of cortex which fell below 50% cerebellar flow (39 +/- 34 to 97 +/- 46 mm3, P = 0.003). Moderate hypotension induced a significant reduction in CBF in both ipsilateral and contralateral subcortical white matter (P < 0.01). In peri-infarct caudate tissue, CBF was not significantly affected by hypotension. In conclusion, a significant volume of histologically normal cortex within the middle cerebral artery territory was found to have essentially normal levels of CBF but impaired autoregulatory function at 24 h post-ischaemia.     

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)     

Amlodipine lowers blood pressure without significant effect on cerebral blood flow in hypertensive patients with a history of stroke: a quantitative single photon emission computed tomography study

Appropriate antihypertensive therapy is important to prevent cerebrovascular disease. The purpose of the present study was to investigate the effect of such therapy on cerebral blood flow in stroke patients. Twenty hypertensive patients with a history of ischemic stroke received amlodipine 2.5 or 5 mg daily for 12 weeks. Blood pressure and cerebral blood flow as measured by ¹³³Xe single photon emission computed tomography at baseline and were compared at 12 weeks. There were statistically significant reductions in both systolic (167.0 to 140.9 mm Hg) and diastolic (97.8 to 81.8 mm Hg) blood pressures after 12 weeks of amlodipine treatment. No statistically significant effect was observed on cerebral blood flow (46.7 to 46.9 ml/100g brain/min). A weak but statistically significant change was observed in cerebellar blood flow (44.1 to 46.9 ml/100g brain/min). We concluded that amlodipine reduces blood pressure without affecting cerebral blood flow in hypertensive patients with a history of ischemic stroke. Investigation about its effect on cerebellar blood flow is mandatory.     

Regional cerebral hemodynamics among hypertensive patients with lacunar infarctions during blood pressure control in subacute and chronic phases.

In hypertensive acute stroke patients, the use of antihypertensive treatment is often delayed because autoregulation of cerebral blood flow (CBF) is often impaired during the first 4 weeks after large brain infarctions. However, little is known as to whether such delay is necessary in cases of small to moderate size brain infarction. We compared changes of regional CBF during antihypertensive treatment in subacute and chronic phases of lacunar infarction. Blood pressure was controlled with an angiotensin-converting enzyme inhibitor (n=6) or dihydropyridine calcium antagonist (n=8), administered orally for 2 weeks during the subacute (n=7) and chronic phases after (n=7) lacunar infarction. CBF was measured by the stable xenon-computed tomography (CT) method. Blood pressure decreased significantly from 132+/-20 mm Hg (mean+/-standard deviation) to 118+/-14 mm Hg (P<.05, paired t-test) in subacute patients and from 135+/-17 mm Hg to 113+/-12 mm Hg (P<.001, paired t-test) in chronic patients. There was no significant reduction either in mean hemispheric blood flow or in deep white matter blood flow during each phase. We condlude that mild control of blood pressure among hypertensive patients with lacunar infarctions does not produce clinically significant decreases in regional CBF during subacute phases of infarction.     

Regional variation in cerebral perfusion during acute hypertension

Regional cerebral blood flow (rCBF) was measured in rats to define the autoregulatory response at different levels of hypertension. Mean arterial blood pressure (MABP) was raised with IV metaraminol. rCBF was measured using 14C-iodoantipyrine. Autoregulation was intact in normotensive animals and those with MABP of 152 to 158 mm Hg. At higher pressures, autoregulation was abnormal and heterogeneous. Hyperperfusion was most prominent in cerebellum, parietal gray matter, thalamus, striatum, and pons. These anatomic sites are recognized sites of hypertensive hemorrhage in humans.