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Biomedical subjects

A M Harper

Publications and source records attributed to A M Harper.

At least 109 records · Page 6Linked to original sources
PubMed1976

Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier.

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.

Animals↗
PubMed1976

Lower limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon.

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.

Animals↗
PubMed1976

Liver blood flow measurement the interpretation of xenon133 clearance curves.

Liver tissue perfusion can be measured by analysis of the clearance of the radioactive inert gases Xenon133 and Krypton85 from the liver. The technique commonly gives rise to multiexponential clearance curves which have previously been quoted as evidence of complex intrahepatic blood flow patterns. The clearance of 133Xe from the canine liver was studied in 17 dogs and by screening out extrahepatic radioactivity it was found that the true intrahepatic clearance is monoexponential. The slower components seen in the multiexponential curve recorded without screening represent 133Xe in tissue other than the liver and much of this activity was shown to originate from 133Xe which accumulates in the stomach and intestines. These findings simplify the interpretation of inert gas clearance curves in the measurement of liver blood flow and therefore encourage further application of the technique in both experimental and clinical situations.

Animals↗
PubMed1975

Upper limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon.

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.

Angiotensin II↗
PubMed1975

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system.

The influence of the sympathetic nervous system on the cerebral circulatory response to graded reductions in mean arterial blood pressure was studied in anesthetized baboons. Cerebral blood flow was measured by the 133Xe clearance method, and arterial blood pressure was decreased by controlled hemorrhage. In normal baboons, the constancy of cerebral blood flow was maintained until mean arterial blood pressure was approximately 65% of the base-line value; thereafter, cerebral blood flow decreased when arterial blood pressure was reduced. Superior cervical sympathectomy of 2-3 weeks duration did not affect the normal response. In contrast, both acute surgical sympathectomy (cervical trunk division) and alpha-receptor blockade (1.5 mg/kg of phenoxybenzamine) enhanced the maintenance of cerebral blood flow in the face of hemorrhagic hypotension in that cerebral blood flow did not decrease until mean arterial blood pressure was approximately 35% of the base-line value. The results indicate that the sympathetic nervous system is not involved in the maintenance of cerebral blood flow in the face of a fall in arterial blood pressure. Indeed, the implication is that the sympathicoadrenal discharge accompanying hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

Adrenergic alpha-Antagonists↗
PubMed1973

Raised intracranial pressure and cerebral blood flow. 2. Supratentorial and infratentorial mass lesions in primates.

Changes in cerebral blood flow with increasing intracranial pressure were studied in anaesthetized baboons during expansion of a subdural balloon in one of two different sites. With an infratentorial balloon, cerebral blood flow bore no clear relation to intracranial pressure, but was linearly related to cerebral perfusion pressure. Apart from an initial change in some animals, cerebrovascular resistance remained constant with increasing intracranial pressure, and autoregulation appeared to be lost from the outset. With a supratentorial balloon, cerebral blood flow remained constant as intracranial pressure was increased to levels around 60 mm Hg, corresponding to a cerebral perfusion pressure range of approximately 100 to 40 mmHg. Cerebrovascular resistance fell progressively, and autoregulation appeared to be effective during this phase. At higher intracranial pressure levels (lower cerebral perfusion pressure levels), autoregulation was lost and cerebral blood flow became directly dependent on cerebral perfusion pressure. The importance of the cause of the increase in intracranial pressure on the response of the cerebral circulation and the relevance of these findings to the clinical situation are discussed.

Animals↗
PubMed1972

Raised intracranial pressure and cerebral blood flow. I. Cisterna magna infusion in primates.

Changes in cerebral blood flow during incremental increases of intracranial pressure produced by infusion of fluid into the cisterna magna were studied in anaesthetized baboons. Cerebral blood flow remained constant at intracranial pressure levels up to approximately 50 mm Hg. At intracranial pressure levels between 50-96 mm Hg a marked increase in cerebral blood flow occurred, associated with the development of systemic hypertension and changes in cerebrovascular resistance. Further increases of intracranial pressure led to a progressive fall in cerebral blood flow. Prior section of the cervical cord prevented both the increase in cerebral blood flow and the systemic hypertension. Alteration of cerebral perfusion pressure by bleeding during the hyperaemia in a further group of animals suggested that autoregulation was at least partially preserved during this phase. After maximum hyperaemia had occurred, however, autoregulation appeared to be lost. The clinical implications of these findings are discussed.

Animals↗