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[Pulmonary circulation in patients with different types of "hypertensive heart"].

The comparison of clinical and instrumental findings of the state of pulmonary hemodynamics with respect to the type of "hypertensive heart" as determined by ultrasonic location of heart chambers, suggested that, in the absence of left-ventricular hypertrophy or in the presence of concentric myocardial hypertrophy combined with hyperfunction of this heart chamber and normal left ventricular size, increased diastolic pressure in pulmonary artery does not reflect left ventricular decompensation; rather, it is a consequence of increased vascular resistance in the pulmonary arterial system irrespective of its pathogenesis.

Adult↗

Analysis of endotoxin effects on pulmonary circulation in terms of pressure-flow characteristics.

The purpose of the present work was to explore the hypothesis that pulmonary vasoconstriction secondary to endotoxin insult results mainly from an increase in the critical closing pressure of the pulmonary vessels. Specifically, we reasoned that in the face of a Starling resistor located between pulmonary arteries and left atrium, upstream transmission of increased left atrial pressure (Pla) would be inversely related to the level of the pressure intercept (Pi) obtained by extrapolation from the linear pulmonary arterial pressure (Ppa)--flow (Q degrees) plot. Six dogs (group E) were infused with Escherichia coli endotoxin (0.25 microgram/kg/min) for 2 hr, whereas six additional dogs (group C) served as control. During baseline conditions, Pi approximated LAP in both groups. In group C dogs, increasing LAP at constant Q degrees led to a proportional augmentation of Ppa. In group E dogs, endotoxin resulted in a shift of the Ppa-Q relationships to higher pressures due to both increases in Pi and slope. In addition, changes in Pla over the same range as in control dogs affected Ppa only at the highest levels of Pla. We conclude that endotoxin insult increases the critical closing pressure that exceeds Pla and induces the occurrence of a Starling resistor responsible for the production of an effective vascular waterfall.

Animals↗

[Effects of urapidil by intravenous injection on pulmonary circulation and cardiac function in left ventricular failure].

The hemodynamic effects of urapidil were studied in 10 patients with secondary pulmonary hypertension investigated for the purpose of possible inclusion on a heart transplant waiting list. All patients gave their consent to participate. Nine patients had a dilated cardiomyopathy and 1 three-vessel coronary disease with diffuse hypokinesia. All were treated with digitalis, diuretics, converting enzyme inhibitors or calcium antagonists. Hemodynamic effects were measured 5 and 25 minutes after the slow intravenous injection of 50 mg of urapidil. Urapidil caused a significant decrease in pulmonary pressures (-20%) and total pulmonary resistance (-42.5%). The fall in systemic arterial resistance was of the same degree (41.5%). The fall in pulmonary arterial resistance was also significant (-26%). The increase in cardiac output was +35%, with no change in left ventricular myocardial function indices. Thus, in patients with congestive left ventricular failure and secondary pulmonary hypertension already treated with vasodilators, urapidil resulted in a hemodynamic improvement after intravenous administration, demonstrating a synergistic action with that of other vasodilators. This synergistic action could be used to test pulmonary arteriolar vasodilatation reserves during the hemodynamic assessment of patients in whom a heart transplant is contemplated.

Antihypertensive Agents↗