Cerebrovascular and Cerebrometabolic Effects of Intracarotid Infused Platelet-Activating Factor in Rats

• Published in: Journal of cerebral blood flow and metabolism 1988-08, Vol.8 (4), p.546-551
• Main Authors: Kochanek, Patrick M., Nemoto, Edwin M., Melick, John A., Evans, Rhobert W., Burke, David F.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Pressure - drug effects; Brain - metabolism; Carotid Arteries; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges; Cerebral Hemorrhage - complications; Cerebrovascular Circulation - drug effects; Fundamental and applied biological sciences. Psychology; Hypotension - etiology; Hypotension - physiopathology; Injections, Intra-Arterial; Male; Oxygen Consumption; Platelet Activating Factor - pharmacology; Rats; Rats, Inbred Strains; Vertebrates: nervous system and sense organs
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1988.95

Platelet-activating factor has been implicated in a variety of disease processes including ischemic brain injury and endotoxic shock, but its effects on cerebral blood flow (CBF) and metabolism in normal brain have not been described. The effects of platelet-activating factor on global CBF (hydrogen clearance) and the global cerebral metabolic rate for oxygen (CMRO2) were studied in halothane-N2O anesthetized Wistar rats. Hexadecyl-platelet-activating factor infused into the right carotid artery (67 pmol/min) for 60 min decreased mean arterial pressure (MAP) from 122 ±4 (x ± SEM) to 77 ± 6 mm Hg and CBF from 159 ± 12 to 116 ± 14 ml/100 g/min (p < 0.002). In contrast, CMRO2 increased from 9.7 ± 0.9 to 11.7 ± 1.1 ml/100 g/min after 15 min (p < 0.05). In controls rendered similarly hypotensive by blood withdrawal and infused with the platelet-activating factor vehicle, CMRO2 was unchanged, whereas CBF transiently decreased then returned to baseline at 60 min. These cerebrovascular and cerebrometabolic effects of PAF are reminiscent of and may be relevant to hypoperfusion and hypermetabolism observed after global brain ischemia and in endotoxic shock.