An Analysis of Active and Passive Effects on the Pulmonary Vascular Bed in Response to Pulmonary Nerve Stimulation

Abstract

In an isolated innervated perfused left lung preparation of the dog the calculated pulmonary vascular resistance overlapped the upper limit of the range reported by others for normal resting animals.The increase in pulmonary vascular resistance in response to stimulation of pulmonary nerves in which pulmonary vasoconstrictor fibres and bronchoconstrictor fibres are intermingled was due to vasoconstriction in the pulmonary vascular bed proper. This response was not appreciably altered or influenced by passive effects due to accompanying bronchoconstriction or changes in the bronchial circulation.PULMONARY vasomotor responses to nerve stimulation in lungs under controlled ventilation and perfusion have been demonstrated in the absence of passive systemic vascular and bronchomotor effects [for literature see Daly, 1958]. Two main criticisms have been levelled against such experiments; the first on the grounds that the techniques necessary to control and measure all variables lead to such small blood flows that the perfused lungs only represent fragments of lung tissue [Hamilton, 1951]. In the experiments reported here improvements in technique and in the nature of the perfusate have reduced the pulmonary vascular resistance (PVR) to within the upper range of the values found by others in normal dogs. The second criticism is that vasomotor responses to nerve stimulation are secondary to change in lung hindrance due to alterations in intrapulmonary pressure caused by stimulation of bronchoconstrictor nerve fibres [Wagner, 1935; Rodbard, 1953]. This problem would be greatly clarified if a quantitative relationship could be established between the PVR responses to nerve stimulation under conditions in which all passive effects were excluded, with those in which bronchial circulation perfusion and/or accompanying bronchomotor responses were a source of potential passive effects on the PVR. This was the main aim of the investigation. It included studies of pulmonary vascular resistance responses to nerve stimulations in ventilated, collapsed and statically inflated lungs in which bronchomotor effects were measured by recording changes in tidal air, in intrapulmonary volume and in intracheal pressure respectively. METHODS Dogs, 160-20-6 kg. weight, premedicated with morphine hydrochloride (1-2 mg./kg. subcutaneously) were exsanguinated and the isolated left lung prepared for perfusion of the bronchial and pulmonary circulations with autologous blood by * Present address: University Laboratory of Physiology, Oxford.