[Experimental studies on the therapeutic effects of alkalizing agents on acute focal cerebral ischemia].
Metabolic acidosis in cerebral ischemia is considered deleterious to cell function and neurological outcome. Amelioration of systemic and focal cerebral acidosis by an alkalizing agent may reduce ischemic brain damage. The effects of 0.3 mol tris (hydroxymethyl)aminomethane (THAM) and 7% NaHCO3 on focal cerebral ischemia produced by occlusion of the middle cerebral artery (MCA) in cats were examined. In thirty six adult cats, adjustment was made so that PaO2 and PaCO2 would be maintained within the normal range with mechanical ventilation and oxygen inhalation. Focal cerebral ischemia was produced by coagulation of the left MCA using the transorbital approach. The animals were divided into 3 groups as follows. 1) The control group received continuous intravenous administration of physiological saline (2 ml/kg/hour). 2) The THAM group received continuous intravenous administration of 0.3 mol THAM (2 ml/kg/hour). 3) The NaHCO3 group received continuous intravenous administration of 7% NaHCO3 (0.7 ml/kg/hour)+physiological saline (1.3 ml/kg/hour). PaO2, PaCO2 and mean arterial blood pressure were maintained within the normal range in each group. In the THAM and NaHCO3 groups, arterial pH was maintained within the normal range, whereas in the control group, arterial pH gradually decreased from 7.42 +/- 0.04 to 7.30 +/- 0.09 at 6 hours after MCA occlusion. Intracellular pH, measured by magnetic resonance spectroscopy over the ischemic brain, decreased from 7.23 +/- 0.06 to 6.13 +/- 0.61 by MCA occlusion. In the THAM group, intracellular pH increased compared with that in the control and 7% NaHCO3 group. These values, however, were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Fujita
K
K
Department of Neurological Surgery, Kagawa Medical School, Japan.
D000138:Acidosis / Q000188:drug therapy; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D001929:Brain Edema / Q000188:drug therapy / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002415:Cats; D002544:Cerebral Infarction / Q000188:drug therapy; D012964:Sodium / Q000494:pharmacology / Q000627:therapeutic use; D017693:Sodium Bicarbonate; D014325:Tromethamine / Q000494:pharmacology / Q000627:therapeutic use*
D001639:Bicarbonates; D014325:Tromethamine; D017693:Sodium Bicarbonate; D012964:Sodium