Hypoxic Pulmonary Vasoconstriction

Hypoxic Pulmonary Vasoconstriction

The pulmonary circulation responds to acute hypoxia with increases in pulmonary artery pressure and vascular resistance. This acute hypoxic pressor response (AHPR) is a unique physiologic feature distinguishing the pulmonary from the systemic cir­culation which dilates in response to hypoxia. Since Von Euler and Liljestrand described the phenomenon of acute hypoxic pulmonary vasoconstriction within the feline pulmonary circulation, it has fascinated vascular physiologists and stimulated a substantial number of studies aimed at defining the mechanism of this response.

Airway hypoxia is a consequence of many lung diseases. In addition, abnormalities of the pulmonary vasculature are prominent features of the pathophysi­ology of acute and chronic respiratory failure. In this context, the AH PR occupies a unique position at the interface between the normal and abnormal pulmo­nary circulation in transition from health to disease.

We will review the major features of the AH PR, and summarize the important aspects of investigations aimed at defining the mechanism of this response. In addition, we will discuss the known factors which modify the response in the clinical setting. We will place special emphasis on information obtained within the last five years, especially recent findings concern­ing the vascular endothelium.

Physiologic Characteristics of the Response

The AH PR has a long evolutionary history. It is present in fish, amphibia, reptiles, birds, and mam­mals. Figure 1 illustrates the major features of the response shared by all species in which it has been studied. The response begins within seconds of ven­tilation with hypoxic gas, reaches a maximum within minutes, and can be sustained for hours. Graded decreases in Pa02 produce similar increases in pul­monary vascular resistance with a threshold for vaso­constriction at Pa02 of 60 mm Hg. In both human subjects and animal preparations, alveolar hypoxia increases pulmonary artery pressure, does not consis­tently change left atrial pressure and heart rate, but has a variable effect on cardiac output. Although alveolar, or airway, hypoxia alone is sufficient to stimulate hypoxic vasoconstriction, an additional con­tribution to the initiation of the response comes from the Po2 of mixed venous blood. cialis 20 mg

FIGURE 1. Characteristics of acute hypoxic pulmonary vasoconstric-tion. Lungs were isolated from rats, ventilated with 21 percent O,- 5 percent C02, balance N2 and perfused with whole blood. When the lungs were ventilated with 10 percent 02-5 percent C02, balance N2, mean pulmonary arterial pressure (Ppa) promptly increased, returning to baseline upon ventilation with air.