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Biomedical subjects

E T MacKenzie

Publications and source records attributed to E T MacKenzie.

At least 127 records · Page 7Linked to original sources
PubMed1977

Effects of intraventricular 6-hydroxydopamine on cerebrovascular CO2 reactivity in anesthetized rats.

Regional cerebral blood flow was measured by the 14C-ethanol technique in anesthetized rats before and after intraventricular injection of 6-hydroxydopamine. This treatment reduced the fluorescence of the central noradrenaline and dopamine nerve terminals, as well as of the perivascular nerve terminals in cerebral vessels. The administration of 6-hydroxydopamine had no significant effect on cerebral blood flow at normocapnia. The cerebrovascular reactivity to hypercapnia was significantly increased in the 6-hydroxydopamine treated animals. The results indicate an involvement of central catecholamine pathways in the cerebrovascular reactivity to hypercapnia.

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PubMed1977

Cerebral circulatory and metabolic effects of 5-hydroxytryptamine in anesthetized baboons.

1. The cerebral circulatory effects of the intracarotid administration of 5-hydroxytryptamine were examined in anaesthetized baboons. Cerebral blood flow was measured by the intracarotid 133Xe technique, cerebral O2 consumption and glucose uptake were measured as indices of brain metabolism and electrocortical activity was continuously monitored. 2. Despite a marked reduction in the calibre of the internal carotid artery (assessed angiographically), the intracarotid infusion of 5-hydroxytryptamine 0-1 microgram/kg. min did not effect any significant changes in cerebral blood flow, O2 consumption or glucose uptake. 3. Following transient osmotic disruption of the blood-brain barrier with the intracarotid infusion of hypertonic urea, the same dose of 5-hydroxytryptamine effected a marked reduction in cerebral blood flow from 51 +/- 2 to 36 +/- 2 ml./100 g. min (mean +/- S.E.; P less than 0-01). Both indices of cerebral metabolism were reduced significantly and the e.e.g. showed a more pronounced suppression-burst pattern. 4. We postulate that the cerebral circulatory responses to 5-hydroxytryptamine are dependent upon the integrity of the blood-brain barrier and the predominant effect of the intravascular administration of 5-hydroxytryptamine is on cortical activity or metabolism, rather than on cerebrovascular smooth muscle.

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PubMed1977

Effects of 5-hydroxytryptamine on pial arteriolar calibre in anaesthetized cats.

1. The responses of individual pial arterioles and small arteries to perivascular injections of 5-hydroxytryptamine were studied in anaesthetized cats.2. Pial arteriolar calibre was measured by a television image-splitting technique.3. At normotension, the average response of pial vessels was dilatatory at injected 5-hydroxytryptamine concentrations between 10(-10) and 10(-4)M.4. These pial vascular changes were, however, dependent upon the resting vessel calibre: those arterioles < 70 mum dilated universally, whereas small arteries >/= 200 mum in resting diameter tended to constrict in response to 5-hydroxytryptamine.5. The 5-hydroxytryptamine-induced dilatation of pial arterioles < 70 mum in resting calibre was directly dependent on mean arterial pressure, although no such relationship was observed with the larger cerebral vessels.6. It is concluded that the specific cerebrovascular actions of 5-hydroxytryptamine are largely tone-dependent. The greater the resting tone of a pial arteriole, then the greater will be the tendency of that vessel to dilate in response to 5-hydroxytryptamine, and vice versa.7. The direct vascular actions of 5-hydroxytryptamine are in contradistinction to the observed changes in cerebral tissue perfusion and it would therefore appear that the effects of this amine on cerebral metabolism and neuronal activity outweigh its cerebrovascular actions under physiological conditions.

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PubMed1977

Response of the cerebral circulation in baboons to changing perfusion pressure after indomethacin.

An earlier study has demonstrated that indomethacin, a prostaglandin synthesis inhibitor, blocks the cerebrovascular response to hypercapnia. This response is believed to be mediated by a lowering of pH in the cerebral interstitial fluid. Should autoregulation of cerebral blood flow (CBF) to changing perfusion pressure also be mediated by a changing interstitial pH (the "metabolic" theory), then indomethacin should impair autoregulation. This hypothesis was tested in anesthetized baboons. CBF was measured by the intracarotid 133Xe clearance technique; the preparation and the indomethacin protocol were identical to those of our previous investigation. Arterial pressure was increased by the intravenous infusion of angiotensin and decreased by controlled hemorrhage. Indomethacin was given by continuous infusion into the internal carotid artery. Although it reduced resting CBF, the cerebrovascular response to changing perfusion pressure was unchanged. Because indomethacin affects the response to changing CO2 but not that to changing perfusion pressure, the mechanisms for these two reactions presumably are different and it is improbable that changing interstitial pH is responsible for autoregulation in the cerebral circulation.

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PubMed1977

Responses of the cerebral circulation to hypercapnia and hypoxia after 7th cranial nerve transection in baboons.

It has been proposed that the responses of the cerebral circulation to hypoxia, hypercapnia and hypotension may be partially mediated by an autonomic reflex with receptors in the carotid body or sinus serving as sensors and the efferent limbs being the 7th cranial nerves. Transection of the 7th cranial nerve has been reported to impair the cerebral circulatory response to isolated chemoreceptor stimulation by hypoxia and hypercapnia. To test this hypothesis we measured cerebral blood flow (CBF) by an intra-arterial 133Xe technique in 10 baboons during periods of induced hypoxia and hypercapnia, both before and after transection of the 7th cranial nerve, We found that the responses of CBF were unaltered by either unilateral or bilateral section of the nerve. Our results showing the preservation of normal CBF responses, following transection, suggest that neurogenic control of the cerebral circulation by an autonomic reflex involving the 7th nerve is unlikely.

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PubMed1977

Choroidal and cerebral blood flow in baboons measured by the external monitoring of radioactive inert gases.

Quantitative measurements of blood flow using xenon-133 to measure cerebral blood flow and krypton-85 to measure choroidal blood flow were made in 12 anesthetized baboons (Papio anubis). Analysis of the clearance curves of krypton from the eye and studies of the diffusion of krypton in the eye show that the inert gas-clearance method measures choroidal blood flow only. The mean choroidal blood flow at normocapnia in this group of baboons is 463 +/- 44 ml./100 mg./min., and the mean cerebral blood flow is 46 +/- 5 ml./100 mg./min. (mean +/- 1 S.D.).

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PubMed1977

The response of the choroidal and cerebral circulations to changing arterial PCO2 and acetazolamide in the baboon.

Having established control values for choroidal and cerebral blood flow in twelve baboons, the response of both circulations to changing arterial PCO2 and intravenous acetazolamide was studied. The blood flow in both circulations varied directly with the PACO2, the magnitude of the response being very similar. There was a 3.6 percent change in both choroidal and cerebral blood flow per millimeter of mercury change in PACO2. Intravenous acetazolamide (25 mg./kg.) produced an increase in flow lasting approximately 50 minutes in both cerebral and choroidal circulations.

Acetazolamide↗
PubMed1976

Cerebral circulation and norepinephrine: relevance of the blood-brain barrier.

The systemic administration of norepinephrine has minimal effects on the cerebral circulation, perhaps due to blood-brain barrier mechanisms. To test hypothesis, the cerebrovascular effects of norepinephrine beyond the blood-brain barrier were studied in anesthetized baboons, Intraventricular norepinephrine (40 mug/kg) resulted in significant increases in cerebral blood flow (40%), cerebral oxygen consumption (21%), and cerebral glucose uptake (153%). Intracarotid hypertonic urea opens the blood-brain barrier by osmotic disruption; Consequent to hypertonic urea, the intracarotid infusion of norepinephrine, 50 ng/kg-min, significantly increase cerebral blood flow (49%), cerebral oxygen consumption (21%), and cerebral glucose uptake (76%), It appears probable that the cerebrovascular responses to norepinephrine are dependent on the integrity of the blood-brain barrier; It is likely that the increase in cerebral blood flow, associated with norepinephrine when it bypasses the barrier, is secondary to an increase in cerebral metabolism.

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PubMed1976

Influence of endogenous norepinephrine on cerebral blood flow and metabolism.

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

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