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Biomedical subjects

E T MacKenzie

Publications and source records attributed to E T MacKenzie.

At least 145 records · Page 8Linked 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↗
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↗
PubMedDate not supplied

Serotonergic innervation of the cerebral vasculature: relevance to migraine and ischaemia.

Multiple and complex interactions exist between the cerebral circulation and a potent vasoactive (and neurotransmitter) agent, serotonin. The nature and bases of the real and potential relationships are often hotly contested, for example, the serotonergic innervation of brain conducting and resistance vessels. In this review, an attempt is made to reconcile the available literature and to indicate future and possibly fruitful research directions. It appears that, by its very nature, the pattern of the serotonergic innervation is singular to blood vessels of the brain and could provide a neuronal link (or coupling) between functional events within the central nervous system and its perfusion which subserves changes in brain function. Finally, there are sufficient data to suggest an involvement of 5-hydroxytryptamine in different cerebrovascular pathologies.

Animals↗
PubMedDate not supplied

Selective age-related changes in neuronal markers and smooth muscle reactivity in cerebrovascular beds of Fischer 344 rats.

Choline accumulation, choline acetyltransferase (ChAT) and glutamic acid decarboxylase (GAD) activities were measured simultaneously in various cerebrovascular beds and brain areas from Fischer 344 rats aged 4.5 and 22 months. A slight (25%) but not significant decrease in choline accumulation was observed concomitantly with a significant increase (187%, p less than 0.05) in ChAT activity in the major cerebral arteries of the 22-month-old rats. In small cortical pial vessels and selected brain regions, cholinergic and GABAergic biochemical markers remain unaltered in aged rats. The vasomotor reactivity of the basilar artery was investigated in rats of 4.5, 12, 22 and 30 months of age. In the 22-month-old rats, maximal responses to 5-hydroxytryptamine (-25%, no significant) and prostaglandin F2 alpha (-30%, p less than 0.05 by ANOVA) were less intense as compared to other age-groups despite preserved contractile responses to dopamine, uridine triphosphate or a depolarizing concentration of K+. Relaxations induced by histamine, acetylcholine, noradrenaline, adenosine and somatostatin were strictly comparable among the different age-groups. The sensitivity of the basilar artery to all vasoactive agents failed to demonstrate any correlation with age. Our study suggests that cerebrovascular cholinergic and GABAergic markers undergo minor and selective changes with increasing age. Further, basilar artery vasomotor functions appeared relatively spared by the aging process despite age-related selective decreases in contractile responses to 5-hydroxytryptamine and prostaglandin F2 alpha.

Aging↗
PubMedDate not supplied

Central serotonergic nerves project to the pial vessels of the brain.

Serotonin is strongly implicated in the aetiology of several cerebrovascular (circulatory) diseases, including stroke, migraine and vasospasm. Previous studies have suggested the existence of an indoleaminergic system of perivascular nerves in large cerebral arteries of the lamprey. In addition, some authors have observed that cerebral arteries (such as the vertebrobasilar system of the rabbit) and microvessels may take up serotonin and 5-hydroxytryptophan in various species. However, neither large cerebral arteries nor microvessels (primarily capillaries) directly control, or change, cerebral blood flow; as in other vascular beds, it is the arterioles and small arteries that are the major resistance elements. We report here on the presence of a central serotonergic innervation of pial arteries and arterioles in the rat, using immunocytochemical and neurochemical techniques. The fibres seem to have a central neuronal origin, emanating from both median and dorsal raphé nuclei. This perivascular serotonergic innervation may have a role both in the normal regulation of the cerebral circulation and in pathological conditions.

Animals↗
PubMedDate not supplied

Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

The effects of graded hemorrhagic hypotension on electrocortical function was investigated in 12 cats anesthetized with alpha-chloralose. Cerebral function was assessed both in terms of spontaneous activity (EEG) and the somatosensory evoked response. No significant changes in the EEG trace or in the amplitude of the positive/negative waves of the primary evoked response were observed at mean arterial pressures of between 120 mm Hg and 40 mm Hg. At levels of systemic arterial pressure of less than 40 mm Hg cortical rhythms became slower as pressure was decreased and an isoelectric EEG was recorded in the pressure range 10--30 mm Hg. The earliest sign of any change in the amplitude of the primary evoked responses was observed at arterial pressures of approximately 35--40 mm Hg. Below this value the amplitude decreased with decreasing systemic pressure and became zero in the pressure range 15--25 mm Hg.

Animals↗
PubMedDate not supplied

Effects of hemorrhagic hypotension on the cerebral circulation. III. Neuropathology.

A neuropathological examination was made of 15 cats anesthetized with alpha-chloralose, subjected to a stepwise reduction in mean arterial pressure by graded hemorrhagic hypotension. Five animals were sacrificed by perfusion-fixation at a mean arterial pressure of 75 mm Hg, 5 at a mean pressure of 35 mm Hg and 5 at 25 mm Hg. Ischemic brain damage was seen in only 5 animals, one sacrificed at a mean arterial pressure of 35 mm Hg and 4 at a pressure of 25 mm Hg. It was maximal in the selectively vulnerable areas and included the boundary zones between the major arteries of the cerebral hemispheres, the Ammon's horn and the thalamus.

Animals↗
PubMedDate not supplied

Cerebral venous pressure during actively induced hypertension and hypercapnia in cats.

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.

Animals↗