Abstract

Efferent activity in the phrenic nerve was recorded during induced hypotension and hypertension in anaesthetized, paralysed, artificially ventilated dogs. Changes in arterial pressure were induced with infusions of sodium nitroprusside, noradrenaline and angiotensin II, after which ventilation was adjusted to return the PaCO2 near to control values. The PaO2 was maintained above chemoreceptor threshold throughout. When a steady state was achieved quantitative measurements of phrenic nerve activity were made. In six dogs an increase in mean arterial pressure from 114 to 167 mm Hg caused a mean reduction of phrenic nerve activity of 28%. In six dogs a decrease in mean arterial pressure from 128 to 82 mm Hg caused an increase in phrenic nerve activity of 22%. This shows that the reduction in arterial pressure induced by vasodilator drugs causes a major sustained stimulus to respiration, while increase in arterial pressure causes marked respiratory depression.

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