Abstract
Following the intracisternal injection of colloidal kaolin, the rat will develop arterial hypertension associated with increased intracranial pressure. 1 2 For the sake of brevity, we shall refer to such an animal as a kaolin-hypertensive rat. The elevation of blood pressure was interpreted as being the result of hyperactivity of the vasoconstrictor center in consequence of the increased intracranial pressure.
Because ergotamine is known to paralyze peripheral parts of the sympathetic nervous system, it seemed possible that this substance might influence arterial hypertension so produced. Hogler 3 has reported no lowering of the blood pressure by ergotamine tartrate when given in the dose of one mg to dogs made hypertensive by kaolin. However, Hogler's first blood pressure readings were taken one hour after the injection of ergotamine tartrate so that a transitory effect might have been overlooked.
In addition to producing prolonged hypertension associated with increased intracranial pressure, we also elicited an acute type by introducing physiologic saline into the cisterna magna at a measured pressure. This afforded a second type of test animal for investigating the effect of ergotamine.
Normal and kaolin-hypertensive albino rats were used. Light, uniform ether anesthesia was employed for all procedures. Blood pressure determinations were made by an indirect method previously described. 4 Ergotamine tartrate† was given intraperitoneally in the dose of 0.05 mg per 100 gm body weight.
Ten normal rats were injected with ergotamine tartrate, the blood pressure being followed for approximately 10 minutes before and for at least 30 minutes after the injection. No effect on blood pressure was noted.
Thirteen kaolin-hypertensive rats were similarly treated. In every instance there was a marked but transitory fall in the blood pressure (35-160 mm Hg).
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