The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
One hundred and fifteen consecutive symptomatic patients undergoing graded exercise testing, selective coronary angiography and left ventriculography were retrospectively evaluated. The sensitivity, specificity, and false negative response rates of the exercise tests were 79%, 81%, and 21%, respectively. Although the magnitude of a positive ST-segment response was related to more extensive vascular disease, the frequency of false negative responses was nearly identical in patients with single, double, or triple vessel disease (22%, 21%, 19%). Analysis of the false negative group demonstrated significant ventriculographic and hemodynamic abnormalities when compared to the true positive responders. Five out of six patients with the most serious motion disorders in the study fell into the false negative group. There were no significant differences in the extent, distribution and severity of vascular involvement, or in the development of collateral circulation in the two groups. However, occluded vessels supplied abnormal ventricular segments more frequently in the false negative group (88% vs 38%); the absence of an "ischemic response" and the presence of segments of abnormal myocardium may be related. Left ventricular dysfunction appears to be an important reason for a false negative response to exercise.
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