Brain metabolism and arterial acid-base balance following bilateral carotid occlusion in normotensive and experimental hypertensive rats.
The effects of bilateral common carotid artery occlusion on brain metabolism and arterial acid-base balance were studied in normotensive and experimental renovascular hypertensive rats. One hour after carotid occlusion in hypertensive rats, supratentorial lactate increased to 383% and lactate-pyruvate ratio to 280% of the controls, while adenosine triphosphate (ATP) decreased to 69%. These metabolic changes were thought to be due to cerebral ischemia. Arterial pCO2 was lowered and the pH was raised in the hypertensive animals due to cerebral ischemia induced hyperventilation. In the normotensive rats, carotid occlusion had minimal effects on cerebral metabolism and arterial acid-base balance. These results suggest that hypertensive rats are more susceptible to cerebral ischemia caused by carotid occlusion than normotensive rats. Increased cerebrovascular resistance in hypertension is discussed as a causal factor in cerebral ischemia.
D000136:Acid-Base Equilibrium; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002339:Carotid Arteries / Q000502:physiology; D002340:Carotid Artery Diseases / Q000150:complications / Q000378:metabolism*; D003250:Constriction; D006863:Hydrogen-Ion Concentration; D006977:Hypertension, Renal / Q000097:blood / Q000150:complications / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000097:blood; D011773:Pyruvates / Q000378:metabolism; D051381:Rats
D007773:Lactates; D011773:Pyruvates; D002245:Carbon Dioxide; D000255:Adenosine Triphosphate; D010100:Oxygen