Paul V, Krishnamoorthy M S
Department of Pharmacology and Environmental Toxicology, PGIBMS, University of Madras.
Indian J Physiol Pharmacol. 1989 Jul-Sep;33(3):175-8.
A delay in the onset of isoniazid-induced convulsions was found in rats pretreated with the beta 2-adrenoceptor blocker, butoxamine and the nonspecific beta-blocker, propranolol. In these animals the convulsive responses were inhibited in a dose dependent manner. These compounds were found to be effective even after the induction of convulsions. The beta 1-blocker, acebutolol was able to protect rats only when injected prior to the challenge. The anticonvulsant effect of acebutolol and propranolol but not that of butoxamine was found to be enhanced in animals pretreated with a gamma-aminobutyric acid (GABA) elevating agent, aminooxyacetic acid (AOAA). The findings indicate that the GABA-mediated anticonvulsant action of AOAA seems to be additive with that resulting from beta 1 but not beta 2-blockade.
在用β2-肾上腺素能受体阻滞剂布托沙明和非特异性β阻滞剂普萘洛尔预处理的大鼠中,发现异烟肼诱导惊厥的发作延迟。在这些动物中,惊厥反应呈剂量依赖性抑制。这些化合物即使在惊厥诱导后也被发现是有效的。β1阻滞剂醋丁洛尔仅在攻击前注射时才能保护大鼠。在用γ-氨基丁酸(GABA)增强剂氨氧乙酸(AOAA)预处理的动物中,发现醋丁洛尔和普萘洛尔的抗惊厥作用增强,而布托沙明则没有。研究结果表明,AOAA的GABA介导的抗惊厥作用似乎与β1而非β2阻断产生的作用具有相加性。