Treatment Of Brain Ischemia Research Articles

Effect of nimodipine on cerebral blood flow and metabolism in rats during hyperventilation.

Nimodipine shws promise in the prevention and treatment of brain ischemia. We examined the interaction of nimodipine pretreatment in a dose sufficient to prevent postischemic hypoperfusion and hyperventilation. We studied four groups of rats: normocarbia plus vehicle (Group 1, n = 5), hypocarbia plus vehicle (Group 2, n = 4), normocarbia plus nimodipine (Group 3, n = 7), and hypocarbia plus nimodipine (Group 4, n = 6). Groups 3 and 4 received 1 mg/kg i.p. nimodipine, and Groups 1 and 2 received an equivalent amount of vehicle. Ventilation was left unaltered in Groups 1 and 3 or increased to lower PaCO2 to 21-24 mm Hg in Groups 2 and 4. Determination of regional cerebral glucose utilization (rCGU) was carried out using the [3H]2-deoxyglucose method, and regional cerebral blood flow (rCBF) was determined by the indicator fractionation method using [14C]iodoantipyrine. The brain regions studied were the cerebral hemispheres, the diencephalon, the cerebellum, and the brainstem. Hyperventilation in Groups 2 and 4 from approximately 38 to 22 mm Hg reduced rCBF to 60% of normocarbic levels (p less than 0.05). The slope and intercept of this response were similar in vehicle- and nimodipine-pretreated rats. Nimodipine modestly decreased mean arterial blood pressure by 20% and increased plasma glucose concentration by 60% (p less than 0.05). Although nimodipine tended to increase rCBF and decrease regional cerebrovascular resistance (rCVR), this was significant only for hemispheric rCVR (p less than 0.05). There was a borderline effect for nimodipine to increase rCGU, especially during hypocarbia.(ABSTRACT TRUNCATED AT 250 WORDS)

Advances in neurology, Vol 30: Diagnosis and treatment of brain ischemia. Edited by Andrew L. Carney and Evelyn M. Anderson New York, Raven Press, 1981 424 pp, illustrated, $49.50

Annals of NeurologyVolume 13, Issue 4 p. 468-468 Book Advances in neurology, Vol 30: Diagnosis and treatment of brain ischemia. Edited by Andrew L. Carney and Evelyn M. Anderson New York, Raven Press, 1981 424 pp, illustrated, $49.50 Cesare Fieschi MD, Cesare Fieschi MD Università di RomaSearch for more papers by this author Cesare Fieschi MD, Cesare Fieschi MD Università di RomaSearch for more papers by this author First published: April 1983 https://doi.org/10.1002/ana.410130423AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume13, Issue4April 1983Pages 468-468 RelatedInformation

Intravenous Digital Subtraction Angiography in Brain Ischemia

Recent advances in computer and radiological technology have permitted a reassessment of intravenous (IV) angiography in the evaluation of extracranial and intracranial vessels. This report reviews our initial experience with IV digital subtraction angiography in the diagnosis and treatment of brain ischemia. Two hundred seventy-three IV digital subtraction angiograms (146 extracranial, 127 intracranial) were performed on a total of 178 patients with suspected cerebral ischemia (159 patients), brainstem/cerebellar ischemia (13 patients), or asymptomatic bruit (six patients). Extracranial studies clearly demonstrated ulceration, stenosis, and occlusion of the carotid arteries. Intracranial studies usually detected major artery occlusive disease and provided insight into the collateral flow patterns. Intravenous digital subtraction angiography allowed the accurate assessment of arteries after carotid endarterectomy and brain bypass surgery. Although conventional angiography was usually recommend in patients treated surgically, IV digital subtraction angiography obviated the need for conventional studies in the initial evaluation of many patients.

The treatment of brain ischemia following arteriography.

Focal brain ischemia developed in 10 normotensive patients during arteriography without systemic hypotension or cardiac ischemia, arrhythmias, or failure. Eight patients improved when blood pressures were increased with vasopressor drugs. Low-molecular-weight dextran, hyperosmotic agents, or corticosteroid drugs did not lower the blood pressure level needed for preservation of brain function in these patients and were not beneficial in the treatment of 4 others. Vasopressor drugs were useful in the treatment of 5 patients with brain ischemia secondary to systemic arterial hypotension who did not have cardiac ischemia, arrhythmias, or failure. Contraindications for vasopressor drug treatment include vascular dissections, myocardial and renal ischemia, left ventricular failure, and subaortic muscular stenosis.

Treatment of Brain Ischemia after Cardiac Angiography.

Excerpt Five normotensive patients developed severe brain dysfunction during cardiac angiography. Four had angiography because of recurrent, severe angina pectoris, and one patient had valvular aor...

The treatment of brain ischemia with vasopressor drugs.

Vasopressor drugs were administered to 13 patients soon after the development of focal brain ischemia even though there was no significant decrease in their blood pressure. The neurological function of five patients improved following an increase of their blood pressure to levels of 150 to 170/85 to 100 mm Hg. Focal brain dysfunction recurred whenever the blood pressure was allowed to fall to the initial level during the immediate postinsult period. Significant recovery was maintained in three of these five patients; neurological function in these three did not deteriorate when the blood pressure was allowed to fall to levels of 90/60, 100/70 and 120/80, respectively, after the immediate postischemic period. The critical blood pressure level required for improvement of brain function during the ischemic episode was not lowered by simultaneous treatment with low-molecular-weight dextran, hyperosmotic agents, dexamethasone and aminophylline in case 1 or by treatment with papaverine in case 3.