The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (Qs/Qt) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. Qs/Qt significantly increased (p less than 0.005) from 5.19% to 8.81%, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr (p less than 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes . sec/cm5 (p less than 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased Qs/Qt from 5.13% to 6.19% (p less than 0.005), whereas PAP decreased from 18 to 10 torr (p less than 0.005) and PVR decreased from 237 to 162.6 dynes . sec/cm5 (p less than 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in Qs/Qt, PAP, or PVR. Cardiac output remained unchanged in both groups of patients. Various mechanisms to explain these results can be postulated. When hypotension is induced in patients with normal pulmonary function. PAP decreases and the effect of gravity puts more blood through dependent areas where most of the shunt units are. In patients with COPD, destructive vascular changes increase PAP, preventing vasodilators from decreasing PVR. In addition, dilation of hypoxic pulmonary vasoconstriction (if present) by SNP and TNG will occur independent of the two previously mentioned mechanisms. These results provide evidence that SNP- and TNG-induced hypotension may cause significant impairment in pulmonary gas exchange in patient with normal lung function. In patients with COPD pulmonary gas exchange is not affected after deliberate hypotension with SNP or TNG.