An analysis of the pulsatile hemodynamic responses of the pulmonary circulation to acute and chronic pulmonary venous hypertension in the awake dog.

In this study we measured high fidelity pulsatile pressure and flow waveforms at the inlet to the pulmonary vascular bed to assess the differences in adaptation to acute and chronic pulmonary venous hypertension in awake dogs. Acute elevations in left atrial pressure (P1a) were effected by inflation of left atrial balloons, while chronic elevations were accomplished by placement of aorta to left atrial shunts. Pulmonary artery hydraulic impedance was calculated and analysis of these data revealed marked differences between the responses to acute and chronic elevations of left atrial pressure. The acutely stressed dogs (n = 12) had significantly decreased pulmonary vascular resistance (when P1a = 16.9 +/- 1.0 mm Hg, PVR = 212 +/- 57 dynes sec/cm5; when P1a = 28.6 +/- 1.4 mm Hg PVR = 18 +/- 115 dynes sec/cm5; control P1a = 6.1 +/- 1.5 mm Hg, and PVR = 355 +/- 69 dynes sec/cm5) and normal characteristic impedances (ZO) (210 +/- 36, 227 +/- 39, 178 +/- 14 dynes sec/cm5, respectively), indicating recruitment of arteriolar-capillary perfusion density and no change in proximal pulmonary arterial physical properties. The chronic pulmonary venous hypertension group (n = 11) retained normal PVR (496 +/- 30 dynes sec/cm5) but demonstrated a markedly higher characteristic impedance, ZO = 361 +/- 11 dynes sec/cm5 (P < 0.001). This indicated a measurably different and extremely potent effect of chronic venous hypertension on the physical properties of the pulmonary vessels with an apparently increased arterial stiffness correlating with a 4-fold increase in Young's elastic modulus. These changes were not reversed by alpha-adrenergic blockade or acute lowering of left atrial pressures.