抄録
The usual cause of death in tetanus is thought to be exhaustion following repeated convulsions and paralysis of respiratory centre (1-4). However, cardiac arrest, pulmonary oedema, hypertension or hypotension have also been observed and attributed to central or medullary intoxication (1, 5-7). Histopathological and elect rocardiographic evidences indicate involvement of the myocardium (8-10). Further, fluctuations in blood pressure and tachycardia often complicate the clinical picture.
Previous investigations carried out in our laboratory had revealed that intravenous injection of tetanus toxin in dogs and rats produces a triphasic response on systemic blood pressure. An initial slight pressor effect is followed by a sharp depressor response which is next followed by a sustained pressor phase. The depressor phase was absent in dogs pretreated with the antihistamine drug, mepyramine and in rats pretreated with cyproheptadine which is both antihistamine and antiserotonin. The delayed pressor phase was absent after treatment with phenoxyhenzamine, a drug with α-adrenergic blocking properties. The toxin was also shown to produce a stimulation of the isolated rabbit heart and reduce the coronary flow in the same preparation. It also reduced the flow through isolated perfused rat hind limbs. The toxin mimicked the action of adrenaline on guinea pig vas deferens and this was blocked by phenoxybenzamine. Thus there was a resemblance between the actions of the tetanus toxin and those of adrenaline. Studies were undertaken to assess this relationship further and are now being reported.
