Nitroprusside is frequently employed to lower blood pressure in a variety of situations where precise control over systemic hemodynamics is imperative. In the normal lung, this vasodilator does not produce any significant change in gas exchange. In contrast, a significant deterioration in gas exchange is produced when the drug is infused during pulmonary edema in [...]
There are a group of diverse, unrelated clinical states where alteration of the normal AHPR is observed, but the mechanisms remain unclear. The influence of lung inflation on the response is controversial. An increase in lung inflation is associated with a decrease in the magnitude of the response. Pulmonary hypertension and elevations of left atrial [...]
The pathophysiologic role of the AHPR in patients with acute cor pulmonale presenting with right ventricular failure, increased right ventricular afterload, and an elevated pulmonary vascular resistance is well known. A more controversial subject is whether hypoxic vasoconstriction is a stimulus for the vascular changes that occur during chronic hypoxic exposure. Chronic hypoxia is associated [...]
The clinical implications of alterations of the AHPR are not widely appreciated. Our discussion of modification of the normal response will be arbitrarily divided into three areas: loss of the response in lung injury states; alteration of the response after chronic hypoxic exposure; and the alteration of the response in a diverse set of clinical [...]
Direct effects of hypoxia on the vasculature are often discussed using a three-part model: sensor, transducer, and effector. The key questions for the oxygen sensor are its location and what specific cell or cell organelle plays this role. The likely site for the sensor is the precapillary arteriole, but the specific identity of the sensor [...]
Mechanism Two main hypotheses underlie most investigations of the mechanism of the AHPR. The first is that the response is dependent on the release of a vasoactive mediator from some site within the lung. The opposing view states that acute hypoxia elicits vasoconstriction via a direct effect on pulmonary vascular smooth muscle without the involvement [...]
Several important factors modify hypoxic vasoconstriction (Table 1). While the effects of many of these factors have been repeatedly substantiated, the mechanisms of action remain largely unexplained. Although the AHPR is present in the lungs of all mammalian species examined, there is considerable species variation in the magnitude of the response. Pigs and cows have [...]
