The sausage-string pattern in the pial vessels in acute, angiotensin-induced hypertension--vasospasm or vasodilatation?
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Biomedical subjects
Publications and source records attributed to S Strandgaard.
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Autoregulation of cerebral blood flow (CBF) was studied by the arteriovenous oxygen difference method in 13 patients with untreated or ineffectively treated severe hypertension, nine patients with effectively treated, formerly severe hypertension, and ten normotensive controls. Resting mean blood pressure in these three groups was 145 +/- 17 (1 SD) mm Hg, 116 +/- 18 mm Hg, and 98 +/- 10 mm Hg, respectively. Blood pressure was decreased by trimethaphan infusion combined with head-up tilt. The lower limit of CBF autoregulation in the three groups was 113 +/- 17 mm Hg, 96 +/- 17 mm Hg, and 73 +/- 9 mm Hg, and the lowest tolerated blood pressure where mild symptoms of brain hypoperfusion were encountered was 65 +/- 10 mm Hg, 53 +/- 18 mm Hg, and 43 +/- 8 mm Hg. These pressures were all significantly higher (P less than 0.01) in the group of untreated or ineffectively treated hypertensive patients than in the normotensive group demonstrating a shift of CBF autoregulation in the former. The observations in effectively treated hypertensive patients strongly suggested a readaptation of CBF autoregulation toward normal in some cases. In four hypertensive patients studied twice it was found that 8-12 months of antihypertensive treatment on average did not influence the lower limit of CBF autoregulation.
Acute hypertension was induced in 19 anesthetized cats by the intravenous administration of angiotensin. The caliber of pial arteries was measured by a television image-splitting technique and local cerebral blood flow by the hydrogen clearance technique. As the blood pressure was increased, pail arterioles constricted and cerebral blood flow remained relatively constant, showing that autoregulation of cerebral blood flow was intact. At mean arterial pressures of more than 170 mm Hg arteriolar dilation appeared. In smaller arterioles (initial diameter less than 100 mum) a segmental dilation (the "sausage'string" phenomenon) frequently preceded uniform dilation. This arteriolar dilation was associated with a marked increase in local cerebral blood flow indicating that the upper level of autoregulation had been breached. In no cat was vasospasm or a decrease in blood flow observed during induced hypertension. Hypertension also caused dysfunction of the bloodbrain barrier since, in 17 out of 19 of the cats examined, there was extravasation of protein-bound Evans blue into brain tissue. In only one of the 19 cats subjected to neuropathological analysis was ischemic brain damage identified and this was restricted to minimal ischemic cell change. The results indicate that severe, induced hypertension in cats produces cerebral arteriolar dilation, an increase of cerebral blood flow, and dysfunction of the blood-brain barrier. These observations may be of importance in understanding the pathogenesis of hypertensive encephalopathy.
The effect of chronic renovascular hypertension on the autoregulation of cerebral blood flow was studied in anesthetized baboons. Cerebral blood flow was measured by the intracarotid 133Xe clearance method. Six baboons with renal hypertension of 8-12 weeks' duration were compared with six normotensive controls. The lower limit of autoregulation was determined following controlled hemorrhage. In the initially normotensive baboons, cerebral blood flow remained constant until mean arterial pressure had decreased to the range of 45-59 mm Hg. Thereafter, cerebral blood flow decreased with each further decrease in mean arterial pressure. In the chronically hypertensive baboons cerebral blood flow autoregulated until the mean arterial pressure had decreased to the range of 75-89 mm Hg. Therefore, the lower limit of autoregulation of cerebral blood flow was shifted to higher absolute levels of mean arterial pressure in baboons with chronic renovascular hypertension presumably due to adaptive changes in the cerebral circulation.
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Uretero-cystostomy was used as reconstructive procedure in 298 cadaver kidney transplantations. Necrosis of the graft ureter occured in 10 cases (3.4%). 2 of these graft ureters had malformations and 1 was denuded at donor nephrectomy. The occurrence of ureteral necrosis was not related to histocompatibility or number of rejection crises nor to the duration of the warm ischemia. A higher incidence of ureteral necrosis after long cold ischemia is demonstrated, but the material is too small to permit conclusive evidence on this point.
The effect of arterial hypertension on cerebral blood flow was studied by the intracarotid 133Xe clearance method in baboons. The arterial blood pressure was raised in gradual steps with angiotensin. Baboons with renal hypertension of 8-12 weeks duration were studied along with normotensive baboons. In initially normotensive baboons, cerebral blood flow remained constant until the mean arterial blood pressure had risen to the range of 140 to 154 mm Hg; thereafter cerebral blood flow increased with each rise in mean arterial blood pressure. In the chronically hypertensive baboons, cerebral blood flow remained constant until the mean arterial blood pressure had been elevated to the range of 155 to 169 mm Hg. Thus, in chronic hypertension it appears that there are adaptive changes in the cerebral circulation which may help to protect the brain from further increases in arterial blood pressure.
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Explore the source record for details and available documents.
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The upper limit autoregulation of cerebral blood flow was investigated in eight young baboons with the intracarotid 133xenon clearance method. Blood pressure was increased by intravenous angiotensin infusion. Autoregulation was effective during blood pressure increase from normotensive levels to a mean pressure of 130 to 139 mm Hg. At this pressure, cerebrovascular resistance reached a maximum. With further blood pressure increase, autoregulation was broken, and the vascular resistance dropped significantly. This flow increase was restricted to the fast component of the 133xenon clearance curve, leaving slow component unchanged.
Cerebrovascular reactivity to CO2 inhalation and voluntary hyperventilation was studied in seven normotensive subjects and nine hypertensive patients without clinical or angiographical signs of arteriosclerosis. Cerebral blood flow (CBF) was measured by the intracarotid 133Xe clearance method and calculated as the initial slope index. Three to five CBF measurements were made in each patient in the PaCO2 range of 20 to 55 mm Hg. No difference was observed in reactivity between hypertensive and normotensive patients, either during CO2 inhalation or during hyperventilation. The shape of the CBF:PaCO2 curve suggested a decrease in reactivity below a PaCO2 of 30 to 35 mm Hg in both groups. Above a PaCO2 of 35 mm Hg, exponential regression analysis yielded a mean reactivity of 6 +/- 2%, whereas below a PaCO2 of 30 mm Hg it was about 2%. The rise in CBF during CO2 inhalation was not influenced by the intravenous infusion of a small dose of trimethaphan which blocked the concomitant rise in blood pressure.