Pulmonary Artery Pulse Pressure Research Articles

PULMONARY CAPILLARY FLOW PULSE AND THE SITE OF PULMONARY VASOCONSTRICITON IN THE DOG.

A nitrous oxide-plethysmographic method was used to measure simultaneously the instantaneous pulmonary capillary blood flow and the pressure gradient across the pulmonary vascular bed. The method entailed the use of lightly anesthetized, curarized dogs for the moment-to-moment measurement of nitrous oxide uptake and the corresponding pulmonary arterial and wedge pressures. After establishing the usual patterns of pulmonary capillary blood flow, the flow patterns were modified by atropine, norepinephrine, and acute hypoxia. Before the exhibition of these agents, pulmonary capillary flow was pulsatile, with peak rates of flow of approximately twice the mean. After atropine, the amplitude of the flow pulse decreased passively as stroke volume and the pulmonary arterial pulse pressure decreased. In contrast to atropine, acute hypoxia elicited precapillary vasoconstriction as manifested by an increase in pulmonary arterial pressure and an unchanged pulmonary arterial wedge pressure in conjunction with an unchanged, or diminished and blunted, pulmonary capillary flow pulse. The predominant effect of norepinephrine appeared to be exerted distal to the pulmonary capillary bed since pulmonary arterial and wedge pressures increased in parallel while the capillary flow pulse changed passively according to changes in stroke volume.

Transmural Ventricular Pressures and Pulsus Paradoxus in Experimental Cardiac Tamponade

Transmural pressures were measured from both cardiac ventricles before, during and after experimental cardiac tamponade in open chest dogs. During the control and recovery periods, the transmural pressures were positive in both ventricles. During tamponade, the transmural diastolic pressures became negative in both ventricles. In a series of closed chest dogs, subatmospheric transmural pressures were measured during cardiac tamponade from both atria and both ventricles. With severe tamponade, the intrapericardial pressure exceeded the right ventricular systolic pressure, and with very severe tamponade, even the left ventricular transmural systolic pressure was negative. In the control and recovery tracings, inspiration was accompanied by an increase in the pulmonary arterial pulse pressure and a simultaneous decrease in the aortic pressure pulse. This phenomenon was exaggerated during cardiac tamponade. The implications of this finding regarding the genesis of pulsus paradoxus were discussed.

The changes in right and left heart pressures during exercise and recovery in rheumatic heart disease

The variations in pulmonary artery mean pressure, pulmonary artery pulse pressure, right ventricular end-diastolic and left atrial mean pressures, and the mean diastolic left atrial-left ventricular gradients at rest, and during exercise and recovery have been analyzed. Several distinct patterns of change in these pressures have emerged. The reason for these patterns is not clearly understood. Several possibilities are proposed to explain the observed changes.

Some effects of partial pulmonary valvectomy.

Partial pulmonary valvectomy was performed in 19 dogs. No change in pulmonary arterial pulse pressure was seen when less than one valvular cusp was removed; frequently no change was observed when an entire cusp was removed. Widening of the pulmonary arterial pulse pressure could be produced by removal of more than one cusp or by inducing pulmonary hypertension after removal of only one cusp. Observation as long as six months postoperatively revealed no evidence of right ventricular failure resulting from the operation.

THE RELATION OF PULMONARY ARTERIAL PRESSURE VARIATIONS TO THE ACTIVITY OF AFFERENT PULMONARY VASCULAR FIBRES

1. A method of recording pulmonary arterial pressure in animals with closed chests and spontaneous respiration is described.2. The activity of pulmonary vascular fibres is shown to bear a direct relationship to the pulmonary arterial pulse pressure. Some evidence is put forward for the belief that the receptors of these fibres are situated on the arterial side of the pulmonary vascular bed.