Cyclopropane produces its cardiovascular pressor and tachycardic effects primarily through central supracollicular and subcollicular activation rather than peripheral mechanisms.
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Cautions against extrapolating cyclopropane's central effects to human anesthesia; leaves open mechanistic roles of supracollicular pathways.
1 The anaesthetic cyclopropane was given to intact, decerebrate and pithed unanaesthetized rabbit preparations to determine the relative importance in vivo of its central and peripheral cardiovascular effects. 2 Cyclopropane elevated both the heart rate and the mean arterial pressure in the intact rabbit. 3 In the decerebrate rabbit, cyclopropane elevated the heart rate and efferent cervical preganglionic nerve activity and diminished the magnitude of these components of the aortic baroreceptor reflex, the mean arterial pressure being unaffected. 4 Apart from slight myocardial depression, cyclopropane was largely without effect in the pithed rabbit. 5 It is concluded that cyclopropane produces its cardiovascular effects by supra-collicular activation eliciting an elevation of mean arterial pressure, a central sub-collicular activation producing an increase in heart rate, and that in vivo the peripheral effects of cyclopropane are of minimal importance in comparison to these central effects.
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Hughes et al. (1978) studied this question.
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