Halothane was administered in oxygen to a young man in status asthmaticus whose bronchospasm did not respond to usual treatments. Plasma catecholamine concentrations were measured during and after bronchospasm. Fifteen minute inhalation of halothane produced marked bronchodilatation as reflected in decreased peak airway pressure, decreased wheezing and fall in PaCo2 from 110 mmHg to 45 mmHg. Treatment with halothane was discontinued after 120 min inhalation. Arterial blood samples were obtained to determine free and total catecholamine (CA) on the following four occasions: 1. during status asthmaticus, 2. fifteen minutes after inhalation of halothane, 3. one day after bronchospasm and 4. two days after bronchospasm. During attack, free norepinephrine and epinephrine concentrations were markedly elevated. These values decreased remarkably after administration of halothane. Total norepinephrine and epinephrine were also elevated during bronchoconstriction, and these high concentrations persisted after bronchodilatation. The changes in CA els suggest that sympathoadrenal hyperactivity elicited by acute asthma can be suppressed by halothane as evidenced by the decreased concentration in free catecholamines, which are physiologically active. The levels in total catecholamine did not correlate with the patient's condition. Therefore, judgement based only on the levels in total CA might lead to misinterpretation in estimating sympathoadrenal activity.
|Japanese Journal of Anesthesiology
|Published - 1991
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