Effects of lung inflation on abdominal vascular resistance in anaesthetized dogs.

In chloralose-anaesthetized dogs, the airways to each lung were separated by cuffed endobronchial cannulae and one vagus nerve was cut. We determined the effects of inflation of the innervated lung on abdominal vascular resistance, assessed in the unopened abdomen from changes in perfusion pressure at constant flow. Both static and phasic lung inflation resulted in variable responses of heart rate and abdominal vascular resistance. However, there was a significant correlation between the responses and when heart rate increased there was a significant vasoconstriction. When vasodilatation occurred this was unaffected by vascular isolation of the abdomen indicating that it could not have resulted directly from a blood-borne agent. The bradycardia and vasodilatation were prevented by administration of antagonists to histamine and prostaglandin synthesis. These experiments indicate that, when lung inflation results in tachycardia, abdominal vascular resistance increases. The responses of bradycardia and vasodilatation appear to involve the action of histamine and/or prostaglandins.