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METHODS Pulmonary hypertension may increase pulmonary capillary pressure and exacerbate pulmonary edema in acute respiratory failure. The effects of pulmonary hypertension on pulmonary capillary pressure depend on the longitudinal distribution of pulmonary vascular resistance. Since pulmonary hypertension occurs during acute respiratory failure, we hypothesized that acute respiratory failure may produce time-dependent changes in the longitudinal distribution of pulmonary vascular resistance. Therefore, we measured pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in an animal model of acute respiratory failure. Escherichia coli endotoxin (2.5 to 5.0 micrograms/kg) was administered over a 1-hr period in eight anesthetized sheep. Pulmonary and systemic hemodynamics, including pulmonary artery occlusion pressure (PAOP), pulmonary capillary pressure, and the longitudinal distribution of pulmonary vascular resistance, were measured over the next 5 hrs. Pulmonary capillary pressure was estimated by analysis of the pressure decay following pulmonary artery balloon inflation. RESULTS Endotoxin administration resulted in sustained pulmonary hypertension for the subsequent 5 hrs of the study. Pulmonary capillary pressure was increased 7 mm Hg above baseline at 0.5 and 0.75 hrs during the infusion of endotoxin but returned to baseline values at 1.5 hrs. Despite sustained pulmonary hypertension, pulmonary capillary pressure remained at baseline values for the duration of the study. Similar to pulmonary capillary pressure, pulmonary venous (or postcapillary) resistance was increased approximately four-fold over baseline at 0.5 and 0.75 hrs after initiating endotoxin administration, but returned to baseline values by the end of endotoxin administration and remained at baseline values throughout the remainder of the study. In contrast, pulmonary arterial (or precapillary) resistance remained at values approximately three times baseline during the infusion and throughout the duration of the study. CONCLUSIONS In this experimental model of acute respiratory failure, the effects of endotoxin on the longitudinal distribution of pulmonary vascular resistance are time-dependent. If these data from animals can be extrapolated to humans, we speculate that the importance of pulmonary venoconstriction in exacerbating pulmonary edema may vary over time in patients with acute respiratory failure.
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
January 1992,
Anesthesiology,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
March 1989,
Anesthesiology,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
January 1987,
Journal of applied physiology (Bethesda, Md. : 1985),
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
December 1977,
Journal of applied physiology: respiratory, environmental and exercise physiology,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
April 1978,
Journal of applied physiology: respiratory, environmental and exercise physiology,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
September 1979,
Journal of applied physiology: respiratory, environmental and exercise physiology,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
April 1968,
The Journal of clinical investigation,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
February 1993,
Der Anaesthesist,
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
April 1986,
Journal of applied physiology (Bethesda, Md. : 1985),
R G Pearl, and
E R Baer, and
L C Siegel, and
G V Benson, and
S A Rice
December 1987,
The American journal of physiology,
