Pulmonary vascular system

Because of the presence of anionic sites on the endothelium and on the glycocalyx layer, anionic macromolecules show a significantly slower rate of extravasation compared with neutral and cationic macromolecules. Kern and Swanson [39] found a threefold increase in the permeability of the pulmonary vascular system to cationic albumin, compared with native albumin of the same molecular weight and hydrodynamic radius. 

Teflon injected in a young woman for urinary incontinence migrated to the pulmonary vascular system (5). 

Tolazoline dilates the pulmonary vascular system by stimulating both Hp and H2-receptors. Cimetidine and ranitidine block H2-receptors so that at least part of the effects of tolazoline are abolished. It has been suggested that this interaction is confined to children. ... 

Wielopolski P, Oudkerk M, van Ooijen P. Magnetic resonance imaging and angiography of the pulmonary vascular system. In Oudkerk M, van Beek E, ten Cate I, eds. Pulmonary Embolism. Berlin Blackwell Science, 1999 250-329. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

The relationship for pulmonary vascular resistance is very non-linear owing to the effect of recruitment and distension of vessels in the pulmonary vascular bed in response to increased pulmonary blood flow. The PVR is usually around 10 times lower than the systemic vascular resistance, at 50-150 dyne.s.cm-5. 

Pharmacoiogy The major pharmacologic actions of treprostinil are direct vasodilation of pulmonary and systemic arterial vascular beds and inhibition of platelet aggregation. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

This xanthine derivative is an only a modest bron-chodilator in COPD, and because of its narrow therapeutic range, frequently seen adverse effect and drug interactions, it is becoming less frequently used, some patients experience side effects even within the therapeutic range. The non-bronchodilator effects of theophylline such as systemic and pulmonary vascular dilatation, central nervous system stimulation, improvement of the strength and effectiveness of respiratory muscles and possibly anti-inflammatory effects are of disputed clinical significance at usual therapeutic levels. 

Ideally, the distribution of osmotic diuretics should be largely confined to the vascular system, although this can lead to excessive expansion of the vascular compartment. Such an overexpansion could precipitate pulmonary edema or increase cardiac work or both. This is largely the result of rapid transfer of fluid from the interstitial to the vascular compartment. Practically speaking, however, few osmotic diuretics are available for therapeutic use. These agents, therefore, should be given cautiously to patients with compromised cardiac function. 

Mechanism of Action An antihypertensive that directly dilates pulmonary and systemic arterial vascular beds and inhibits platelet aggregation. Therapeutic Effect Reduces right and left ventricular afterload increases cardiac output and stroke volume. 

Mecfianism of Action A prostaglandin that dilates systemic and pulmonary arterial vascular beds, alters pulmonary vascular resistance, and suppresses vascular smooth muscle proliferation. Therapeutic Effect Improves symptoms and exercise tolerance in patients with pulmonary hypertension delays deterioration of condition. Pharmacokinetics Protein binding 60%. Metabolized in liver. Primarily excreted in urine minimal elimination in feces. Half-life 20-30 min. 

Mechanism of Action An antiplatelet that directly dilates pulmonary and systemic arterial vascular beds, inhibiting platelet aggregation. Therapeutic Effect Reduces symptoms of pulmonary arterial hypertension associated with exercise. Pharmacokinetics Rapidly, completely absorbed after subcutaneous infusion 91% bound to plasma protein. Metabolized by the liver. Excreted mainly in the urine with a lesser amount eliminated in the feces. Half-life 2-4 hr... 

There is a dose-dependent decrease in systemic blood pressure during isoflurane anaesthesia. This is mainly the result of a marked reduction in peripheral vascular resistance. In contrast, the decrease in arterial blood pressure during halothane anaesthesia appears to be mainly the result of a reduction in myocardial contractility. Isoflurane, in common with other volatile agents, has little effect on pulmonary artery pressure or pulmonary vascular resistance. 

Adenosine A3 Receptor and Its Role in Modulation of Systemic and Pulmonary Vascular Tone... 

A possible explanation for the differences observed in rat could be the use of animals under basal conditions vs electrically-driven systems and/or different receptor densities for different strains. Certainly, histamine H3-receptors are not homogeneously distributed along the rat vascular system, as they were found in some districts, like pulmonary microvessels (Danko et al., 1994), portal vein (Smit et al., 1997) or tail artery (Godlewski et al., 1997b), but not in vena cava (Schneider et al., 1991). 

Smooth muscles and vascular smooth muscles Prostaglandins E2 and I2 cause arteriolar dilation in the systemic and pulmonary vascular beds. Prostaglandins and E2, as well as thromboxane B2, constrict the human umbilical cord. Leukotrienes C4 and D4, which release prostaglandin E, decrease peripheral vascular resistance. 

For the vascular system, Lagana et al. [261] employed a hierarchical methodology for multiscale modeling of pulmonary and coronary perfusions in the cardiovascular system. Essentially, they studied different shunt size effect on the pressure of blood within the vessels. 

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