Journal of The Showa Medical Association
Online ISSN : 2185-0976
Print ISSN : 0037-4342
ISSN-L : 0037-4342
EFFECTS OF ISOFLURANE-INDUCED HYPOTENSIVE ANESTHESIA ON CARBOHYDORATE METABOLISM IN RADICAL MASTECTOMY
Tomiaki IKEDAKazuyuki SERADAShouhei TAKEDTeruaki TOMARU
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JOURNAL FREE ACCESS

1995 Volume 55 Issue 4 Pages 399-405

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Abstract
In patients undergoing radical mastectomy, we utilized isoflurane-induced hypotensive anesthesia in 8 patients, and isoflurane-induced normotensive anesthesia in 8 patients. We measured the blood glucose level, plasma insulin concentration, lactic acid, pyruvic acid and nonesterified fatty acid in each group. All patients were premedicated with 0.5mg atropine sulfate, and 50mg hydroxyzine. Anesthesia was induced with thiamylal and the trachea was intubated after vecuronium or succinylcholine administration. Isoflurane was administered until systolic blood pressure decreased to 80-90mmHg in the hypotensive group. In the normotensive group (control group), a concentration of 1-2% isoflurane was administered. Hemodynamic data (blood pressure, heart rate) and blood samples for the measurement of the blood glucose level (BG), plasma insulin concentration, pyruvic acid, lactic acid, and non-esterified fatty acid were collected : 1) before induction (S-1), 2) 30min after (S-2), 3) 60min after (S-3), and 4) 90min after the start of operation (S-4) . Decreases in mean blood pressure below the baseline were significantly greater in the hypotensive group than in the control group. Heart rate did not change in the control group, but in the hypotensive group, it increased significantly. Blood glucose level (S-2, S-3, S-4) in the hypotensive group was significantly greater than in the control group. Insulin concentration did not changed significantly in the hypotensive group, but it (S-3) was significantly below the baseline (S-1) in the control group. Lactic acid (S-2, S-3, S-4) was significanty above the baseline (S-1) in both groups. Lactic acid (S-2, S-3, S-4) in the hypotensive group was significantly greater than in the control group. Pyruvic acid was not changed significantlly in either group. L/P (S-2, S-3, S-4) was significantly greater in the hypotensive group than in the control group. NEFA (S-2, S-3, S-4) was significantly greater in the hyptensive group than in the control group. The result suggests that isoflurane induced hypotension did not markedly affect the carbohydrate metabolism. We speculate that isoflurane causes almost the same effects as other hypotensive agents on carbohydorate metabolism. We conclude that isoflurane can be employed safely and effectively as a hypotensive agent.
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