Abstract
Datura innoxia indigenous shrub in South Asia region belongs to the family Solanaceae which contains medicinal important alkaloids (hyoscine, atropine, hycosamine, etc). Thirty adult rabbits of mixed breed, male and female were pretreated with 0.1 mg/500 mg of crude extract (1% of dimethyl sulfoxide (DMSO) solution) and injected 5 min later with 0.01 mg/500 mg of detomidine (group A, n=15) or Saline (group B, n=15). Mean arterial pressure, measurements and electrocardiography were performed for 65 min. After injecting crude extract of D. innoxia, the heart rate was increased by 45 and 46.34% in groups A and B, respectively. Heart rate remained increased after the injection of detomidine returning to base line values after 15 min. No increase in the mean arterial pressure (MAP) was noted in group B rabbits. Crude extract shortened PR and QT interval in both groups but after detomidine, PR and QT interval were enlarged significantly at the end of the experiment. The second degree atrioventricular was blocked in two rabbits after 40 min only in group B. It was concluded that alkaloid present in D. innoxia prevented detomidine induced Bradycardia and might be useful during combination against the Bradycardia induced by alpha-2 agonist in the rabbits. Key words: Datura innoxia, crude extract, rabbits, detomidine.
Highlights
Detomidine hydrochloride is an alpha-2 agonist drug that produces profound and long acting sedation by reduction of noradrenalin and dopamine release in the central nervous system (CNS) (Jochle and Hamm, 1986)
The purpose of this study was to determine the effects of the extract of D. innoxia on the cardiovascular changes induced by detomidine administration in rabbits
No arrhythmias were noted until 45 min, when atrioventricular heart block was recorded in 2 rabbits
Summary
Detomidine hydrochloride is an alpha-2 agonist drug that produces profound and long acting sedation by reduction of noradrenalin and dopamine release in the central nervous system (CNS) (Jochle and Hamm, 1986). Both alpha-1 and alpha-2 effects are obtained peripherally producing vasoconstriction and increased blood pressure (Clarke and Taylor, 1986; Sarazan et al, 1989; Short et al, 1986; Wagner et al, 1991). 60 minutes after detomidine administration, the blood pressure decreases as a result of bradycardia and persistent effects on alpha-2 receptors in the CNS (Muir, 1992).
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