Cerebral vascular response to moderate blood loss: modification by hypertension

• Published in: Stroke (1970) Vol. 14; no. 5; pp. 765 - 768
• Main Authors: HOLLADAY, F. P, BEAN, J. R, YOUNG, B, TODD, E. P, ROY, M. W
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.09.1983
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Blood Flow Velocity; Blood Volume; Cats; Cerebral Hemorrhage - physiopathology; Cerebrovascular Circulation; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Female; Hypertension - chemically induced; Hypotension - etiology; Intensive care medicine; Male; Medical sciences; Phenylephrine; Probability; Regional Blood Flow; Vasodilation; Hypertension; Fissipedia; Carnivora; Vertebrata; Experimental disease; Mammalia; Brain (Vertebrata); Hemodynamics; Hemorrhage
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.14.5.765

To study the effect of non-hypotensive hemorrhage on cerebral blood flow in normo- and hypertensive states, chloralose anesthetized cats were subjected to graded blood loss (5 ml/kg) every 30 min. Cerebral blood flow was measured using radiolabelled microspheres or H2 clearance. Hypertension was produced by infusion of phenylephrine to a diastolic blood pressure of 100 mm Hg. Control animals suffered no net blood loss. PCO2 was between 28 and 32 mm Hg for all groups over the entire experiment. In normotensive cats, cerebral blood flow increased following withdrawal of 10 ml/kg of blood. In hypertensive cats, cerebral blood flow increased after withdrawal of 20 ml/kg of blood. These findings were consistent for all brain regions examined. Animals without blood loss, whether normo- or hypertensive showed no consistent change in cerebral blood flows. Possible explanations for these findings, particularly neurally mediated responses, are discussed.