Localization of regions mediating the Cushing response in CNS of cat.
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Biomedical subjects
Publications and source records attributed to J T Hoff.
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We studied the mechanism of barbiturate protection from focal cerebral infarction in cats by examining in detail edema formation 72 hours after acute, permanent occlusion of the left middle cerebral artery (LMCA). Neurological function, gas exchange, vital signs, and intracranial pressure (ICP) were observed during the post-occlusion period, and infarct size and cerebral edema were measured after sacrifice. Infarct size was reduced only when pentobarbital was given before occlusion and continued for 24 hours. Edema formation was not suppressed even though the extent of infarction was. Clinical evidence of stroke developed and ICP rose in most cats after occlusion despite the presence of pentobarbital sufficient to reduce infarct size. Elevated ICP accounted for most premature deaths despite intensive cardiopulmonary support. Water and electrolyte changes in the ischemic hemisphere continued to develop throughout the 72 hour post-occlusion period in pentobarbital-treated cats, suggesting that resolution of edema was delayed by the drug. We conclude that pentobarbital reduces infarct size and attenuates the expected time course of ischemic edema in cats, but that the drug has little effect on the severity of edema that develops after arterial occlusion.
Eicosapentaenoic acid prevents platelet aggregation and inhibits arachidonate conversion into thromboxane A2 and prostaglandins. Consequently eicosapentaenoic acid might protect the brain from the ischemia that follows cerebral arterial occlusion. We studied the effect of eicosapentaenoic acid on cerebral ischemia in anesthetized gerbils. Ischemia was produced by bilateral carotid occlusion for 10 min, followed by reperfusion for 60 min, in gerbils fed either a standard diet (control) or a diet supplemented with menhaden fish oil for 2 months. The menhaden fish oil contained 17 mole % eicosapentaenoic acid. Regional cerebral blood flow was measured by the hydrogen clearance method and brain water by the specific gravity technique. In control animals cerebral blood flow was decreased 30 and 60 min after reperfusion (p less than .001) and brain water was increased (p less than .001). In the experimental group cerebral blood flow did not fall during reperfusion and edema did not appear. Brain prostaglandins and thromboxane were measured by radioimmunoassay. PGF2 alpha, PGE2, 6-keto PGF1 alpha and TXB2 increased after severe ischemia and reperfusion. The synthesis of brain diene prostaglandins was not altered by eicosapentaenoic acid. Our study indicates that eicosapentaenoic acid prevented post-ischemic cerebral edema and hypoperfusion, without affecting the levels of brain diene prostaglandin and thromboxane.
Brain water and sodium increase during ischemia, suggesting that the blood-brain barrier permeability to sodium is increased. To test this hypothesis we measured the permeability-surface area products of 22Na and [3H]sucrose in gerbils following 3 hours of unilateral ischemia. In animals with neurologic symptoms, unilateral carotid occlusion reduced the cerebral blood flow in the ipsilateral cerebral hemisphere to 13 +/- 4 ml/100 g/min (n = 6). The water content of the ischemic hemisphere increased from 79.0 +/- 0.6 to 80.8 +/- 0.2% (n = 7, p less than 0.001) and tissue sodium content increased from 231 +/- 17 to 359 +/- 23 mEq/kg (p less than 0.0001). However, there was a 40% reduction in the sodium permeability-surface area product of the ischemic hemisphere compared with the control side (1.65 +/- 0.44 vs 2.79 +/- 0.29 microliter/g/min, n = 6, p less than 0.001). The sucrose permeability-surface area product, a measure of blood-brain barrier integrity, was unchanged. Although ischemia was less severe in the diencephalon, the tissue water and sodium contents increased significantly on the ischemic side. In contrast to the cerebral hemisphere, however, the permeability-surface area products for both sodium and sucrose were unchanged in the ischemic diencephalon. These results suggest that the increase in tissue sodium seen in ischemic edema is not due to enhanced sodium uptake; we speculate that it results, in part, from a reduction in sodium and water clearance from the tissue.
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Cervical myelography was performed by lateral C1-C2 puncture in 60 patients. Thirty patients received iohexol (an investigational aqueous contrast agent) and 30 received metrizamide in order to provide a prospective, randomized, double-blind trial comparing these contrast media. The two media produced radiographs of equal quality. Contrast-related morbidity was suffered by four patients (13%) in the iohexol group and by 11 patients (37%) in the metrizamide group. These features indicate that iohexol is superior to metrizamide as a contrast agent for cervical myelography.