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.

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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.

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PubMedDate not supplied

Cerebral blood flow in rats during physiological and humoral stimuli.

The technique for estimating cerebral blood flow (CBF) in anesthetized rats by injecting 133Xe into the internal carotid artery represents a potentially useful and inexpensive model for screening cerebral vascular responses to pathophysiological and pharmacological stimuli. We have examined associated neuropathology, the validity and the reproducibility of the method, and made comparisons of initial slope estimates of CBF with those obtained by stochastic analysis. Initial slope estimates (CBF = 1.62 +/- 0.04 ml min-1g-1, X +/- SE, N = 38) were linearly related to stochastic measurements (CBF = 1.42 +/- 0.09 ml min-1g-1, N = 6), and overestimated mean CBF by about 15%. A reactivity to CO2 of 0.05 ml min-1g-1 per mm Hg, and an auto-regulation range of 70 to 180 mm Hg were found. CBF responses to the intra-arterial infusion of aminergic drugs were determined before and after opening of the blood-brain barrier with hypertonic urea. Serotonin reduced CBF after, but not before, the administration of urea. Acetylcholine increased CBF when the barrier was intact, the effect being augmented when the barrier was disrupted; these responses were reduced by atropine. Histamine increased CBF only after barrier opening, and this response was attenuated by the H2-receptor antagonist, metiamide. These studies indicate that initial slope estimates of CBF derived in rats from intracarotid 133Xe injection, which represents an inexpensive and simplified approach for screening cerebral circulatory adjustments, may facilitate the characterization of stimuli affecting CBF.

Acetylcholine↗

PubMedDate not supplied

Studies on the cerebral circulation of the baboon in acutely induced hypertension.

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.

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