Decrease In Pulmonary Capillary Pressure Research Articles

The intracerebroventricular injection of rimonabant inhibits systemic lipopolysaccharide-induced lung inflammation

We investigated the role of intracerebroventricular (ICV) injection of rimonabant (500ng), a CB1 antagonist, on lipopolysaccharide ((LPS) 5mg/kg)-induced pulmonary inflammation in rats in an isolated perfused lung model. There were decreases in pulmonary capillary pressure (Ppc) and increases in the ((Wet–Dry)/Dry lung weight)/(Ppc) ratio in the ICV-vehicle/LPS group at 4h. There were decreases in TLR4 pathway markers, such as interleukin receptor-associated kinase-1, IκBα, Raf1 and phospho-SFK (Tyr416) at 30min and at 4h increases in IL-6, vascular cell adhesion molecule-1 and myeloperoxidase in lung homogenate. Intracerebroventricular rimonabant attenuated these LPS-induced responses, indicating that ICV rimonabant modulates LPS-initiated pulmonary inflammation.

Hemodynamic Effects of Enoximone in Cardiac Surgery Patients

Enoximone belongs to a new class of inotropic drugs that are not related either to digitalis or to catecholamines. It acts primarily through selective inhibition of phosphodiesterase III (PDE-III) and has additional vasodilating properties. Hemodynamic effects of intravenously administered enoximone (0.5 mg/kg) were investigated in patients undergoing aortocoronary bypass grafting before and during anesthesia as well as during extracorporeal circulation (ECC). Patients who were impossible to be weaned off ECC without pharmacological support were investigated also. A significant increase in cardiac index and dp/dtmax, a decrease in pulmonary capillary pressure, and a small decrease in mean arterial pressure were the major hemodynamic effects. Heart rate was not changed and no signs of arrhythmia were seen during the entire investigation period. Interactions with the anesthetics used could not be observed in this study. In patients with impaired myocardial performance during weaning from ECC, enoximone seems to be helpful in stabilizing cardiac output and decreasing filling pressure. The mechanism for improvement appears to be enhanced contractility due to its positive inotropic effects, as well as a decrease in left ventricular outflow resistance resulting from peripheral vasodilation.

The acute hemodynamic effects of ethacrynic acid and furosemide in patients with chronic postcapillary pulmonary hypertension.

The acute hemodynamic effects of either ethacrynic acid or furosemide were studied in 27 patients who underwent diagnostic right and transseptal left heart catheterization. Twenth-three patients had postcapillary pulmonary hypertension secondary to isolated or predominant mitral stenosis. Of these, 21 patients were in New York Heart Association functional class III, and one each in class II and IV. In the remaining four patients pulmonary artery pressures were normal. Two patients had aortic stenosis and one each coronary artery disease and nonobstructive cardiomyopathy. All four patients were in class II. Cardiac index, pressures, and pulmonary blood volume (PBV) were measured in the control state and 20, 40, and 60 min after diuretic administration. Pulmonary extravascular fluid volume (PEV) was measured in the control state and at 60 min post drug infusion. A similar hemodynamic response was observed for each drug. Significant reductions in pulmonary artery and left atrial mean pressures, cardiac index, and plasma volume occurred over the one hour observation period and were accompanied by a significant duiresis. However, despite recutions in central pressures and blood flow, PBV, ev, and PEV/PBV remained unchanged, as did systemic arterial pressure. Since 23 of the subjects had postcapillary pulmonary hypertension it is postulated that the failure of PBV to decrease significantly despite significant decreases in pulmonary artery mean pressure is related to altered pressure volume characteristics in the pulmonary vascular bed in which the lung is operating on a steep portion of its pressure volume curve. The failure of the PEV to decrease supports the concept that the pulmonary extravascular space is relatively resistant to early decreases in pulmonary capillary pressure induced acutely. The failure of the pulmonary extravascular fluid volume to decrease despite a fall in plasma volume and pressures corresponds to the well recognized delay in resolution of radiologic evidence of pulmonary congestion.

Role of the autonomous nervous system in the genesis of pulmonary hypertension in heart disease

The extent of neurogenic contribution to the genesis of chronic pulmonary hypertension appears to depend on the particular form of the underlying disease. It seems considerable in mitral stenosis and may be totally absent in idiopathic pulmonary hypertension. The other forms of the syndrome lie between these two extremes. Neurogenic pulmonary vasoconstriction in some cases seems to contribute to the maintenance of circulatory homeostasis in the lungs. In other cases its extent appears unreasonably high and attempts should be made to relieve it. Neuroplegic drugs are not only beneficial in relieving this vasoconstriction, but also by being capable of inducing a rapid decrease in pulmonary capillary pressure. This renders their use advisable in cases of imminent or manifest lung edema due to engorgement of the lungs.