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To analyze the effects of acute elevations in arterial blood pressure on pulmonary blood volume (PBV) and left ventricular function, eight normal controls and ten patients with previous myocardial infarctions were studied using equilibrium radionuclide angiography during the infusion of phenylephrine. Radionuclide estimates of PBV did not change significantly in the control subjects (48 ± 20 units at rest, 53 ± 28 units after administration of atropine, and 47 ± 20 units at the peak elevation of pressure), though cardiac output rose and pulmonary transit time declined (P < .05). In infarct patients, resting PBV was similar to that of normals at rest (44 ± 12 vs. 48 ± 20, P=not significant). However, it rose significantly at the peak elevation of arterial pressure (55 ± 12 units, P < .05 vs. control). Transit time was greater in the patients at rest (22 ± 15 units vs. 14 ± 7 units in controls, P < .01), and, unlike transit time of normals, did not decline with pressure overload. At any level of afterload-induced increases in end-diastolic volume or decreases in ejection fraction, PBV was greater in the patients than in normals. This suggests that, while the absolute response of cardiac volume and ejection fraction to pressure overload may be quantitatively similar in normals and infarct patients, this is not mirrored by changes in PBV and transit time. In all likelihood, elevations in cardiac filling pressures and pulmonary distending pressures occur in the infarct patients. Increases in PBV may be a noninvasive reflection of both the development of incipient congestive heart failure and reduced myocardial compliance in infarct patients. In this way, pressure overload stress may be a useful technique to prospectively categorize patient populations subject to higher incidences of congestive failure.