Pulmonary vascular injury

U1. Uchiba, M., Okajima, K Murakami, K., Nawa, K., Okabe, H and Takatsuki, K., Recombinant human soluble thrombomodulin reduces endotoxin-induced pulmonary vascular injury via protein C activation in rats. Thromb. Haemost. 74, 1265-1270 (1995). 

Rat models of monocrotaline-induced pulmonary vascular injury-inflammation (120,121) and chronic bronchitis, with their appropriate controls have been used in exposures of groups of 16 animals to CAPs and groups of 16 normal or diseased animals exposed to filtered air at the same temperature, pressure, and flow, as a control. The concentration factor of outdoor air particles was approximately 30-fold. Exposures to CAPs resulted in significant mortality with monocrotaline-induced inflammation and significant mortality in animals with chronic bronchitis. Table 2 lists concentration, mortality, and pathological findings in these studies (21). 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

Kim H, Chen X, Gillis N. (1992). Ginsenosides protect pulmonary vascular endothelium against free radical-induced injury. Biochem Biophys Res Community. 189 670-72. 

During lung transplantation, pulmonary vascular pressure and an intrapulmonary shunt have been shown to respond to inhaled nitric oxide and inhaled aerosolized prostacyclin [149,150]. Aerosolized prostacyclin has also been described as an alternative to nitric oxide in the management of reperfusion injury after lung transplantation [150]. 

Right ventricular function frequently is impaired, presumably as a result of preservation injury and elevated pulmonary vascular resistance. A restrictive hemodynamic pattern may be present initially, but it usually improves over the 6 weeks following transplantation. Donor-recipient size mismatch may contribute to early posttransplantation hemodynamic abnormalities characterized by higher right and left ventricular end-diastolic pressures. Supraventricular arrhythmias in the early posttransplant period usually are transient and may result from overvigorous use of catecholamines or milrinone later, they should raise suspicion for acute rejection. 

The vasoconstrictor action of shed blood tested by perfusion of the rabbit ear is markedly decreased by heparin and this was known long before the identification of the vasoconstrictor activity as serotonin (5-hydroxytryp-tamine). Heparin inhibits the release of both 5-hydroxytryptamine and a polypeptide from platelets into plasma, and in vitro there is mutual antagonism between heparin and 5-hydroxytryptamine . Heparin effectively antagonizes the effect of serotonin on pulmonary vascular bed and bronchial wall musculature and prevents the symptoms of 5-HT release in pulmonary embolism, in the cardiopulmonary by-pass, in experimental burn injuries and in carcinoid tumour. 

Benzing, A., and Geiger, K. (1994). Inhaled nitric oxide lowers pulmonary capillary pressure and changes longitudinal distribution of pulmonary vascular resistance in patients with acute lung injury. Acta Anaesthesiol. Scand. 38, 640-645. 

The effectiveness of nitric oxide as a pulmonary vasodilator, together with the diminished response to acetylcholine in a variety of patients in whom endothelial injury is postulated, begs the question as to whether a deficiency of endogenously released nitric oxide is responsible for the elevation in pulmonary vascular tone. Nitric oxide is thought to be released continuously under basal conditions, and inhibition of basal release may lead to an increase in systemic vascular resistance. The perfusion of isolated human lungs with methylene blue, an inhibitor of nitric oxide-mediated vessel relaxation, leads to an increase in pulmnary vascular resistance. Thus, endothelial damage with a reduction in endogenous nitric oxide could account for pulmonary vasoconstriction. 

Pulmonary Complications of Systemic Disease, edited by J. F. Murray Lung Vascular Injury Molecular and Cellular Response, edited by A. Johnson and T. J. Ferro Cytokines of the Lung, edited by J. Kelley... 

Aromatic Hydrocarbons Aromatic hydrocarbons are characterized by one or more six-carbon ring structures with one hydrogen atom per carbon atom. The name aromatic comes from the solvent s aroma. On the whole, aromatic hydrocarbons are local irritants and vasodilators that cause severe pulmonary and vascular injury when absorbed into the body in sufficient concentrations. They can cause dermatitis and can be potent narcotics, with effects on the central nervous system. Of this group, benzene—with its link to leukemia—is strongly regulated and appears to be the most toxic aromatic hydrocarbon. Examples of aromatic hydrocarbons and their respective TLVs are benzene (0.5 ppm), toluene (50 ppm), and xylene (100 ppm). 

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