Vascular pharmacology
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Vascular pharmacology · Aug 2007
Clinical TrialDoes Sildenafil produce a sustained benefit in patients with pulmonary hypertension associated with parenchymal lung and cardiac disease?
Sildenafil may be of benefit for selected patients with pulmonary hypertension associated with parenchymal lung and cardiac diseases. However the medium term benefits of this treatment for such patients is unclear. ⋯ Sildenafil may have a role for selected patients with pulmonary hypertension associated with cardiac and pulmonary diseases. The medication seems well tolerated and for some patients is effective within 8 weeks and results in a sustained long term improvement in haemodynamics and exercise capacity.
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Vascular pharmacology · Aug 2007
Comparative StudyCaffeic acid phenethyl ester (CAPE) protects rat skeletal muscle against ischemia-reperfusion-induced oxidative stress.
Oxygen-derived free radicals have been implicated in the pathogenesis of skeletal muscle injury after ischemia-reperfusion. Caffeic acid phenethyl ester, an active component of propolis extract, exhibits antioxidant properties. The aim of this study was to assess the effects of caffeic acid phenethyl ester (CAPE) and alpha-tocopherol (vit E) on ischemia/reperfusion (I/R) injury in a rat hind limb ischemia/reperfusion model. ⋯ No differences were noted in muscle tissue SOD in three I/R groups, but SOD activity were increased in the plasma of I/R+CAPE and I/R+vit E groups compared with I/R group. Whereas tissue CAT activity was not changed among groups. Our results indicate that CAPE has antioxidant properties similar to those of vit E in this model and may attenuate the harmful effects of hind limb I/R in skeletal muscle.
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Vascular pharmacology · Jun 2007
Clinical TrialAcute haemodynamic responses to inhaled nitric oxide and intravenous sildenafil in distal chronic thromboembolic pulmonary hypertension (CTEPH).
Although surgery is the treatment of choice for CTEPH, it is not appropriate for patients with surgically inaccessible distal disease. These patients are traditionally managed supportively, but may benefit from newer, more specific vasoactive therapies. This study examines the acute haemodynamic responses to inhaled nitric oxide (iNO) and intravenous sildenafil in this patient population. ⋯ Although all but one patient failed to fulfil the formal haemodynamic response criteria typically used in idiopathic pulmonary arterial hypertension (IPAH), subjects displayed significant acute responses to both iNO and sildenafil suggesting that increased vascular tone forms an important component of distal CTEPH. It is possible that these acute haemodynamic responses may translate to improved clinical outcomes, and thus further long term trials of sildenafil in distal CTEPH are warranted.
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Vascular pharmacology · Jun 2007
Potential effects of PKC or protease inhibitors on acute pancreatitis-induced tissue injury in rats.
Acute pancreatitis (AP) is still one of the severe diseases, that cause the development of multiple organ dysfunction with a high mortality. Effective therapies for AP are still limited, mainly due to unclear mechanisms by which AP initiates both pancreatic and extrapancreatic organ injury. ⋯ Inhibition of proteases in AP may be helpful in ameliorating the inflammatory reaction in both pancreatic and extrapancreatic tissues, where neutrophil involvement may be regulated by PKC and proteases.
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Vascular pharmacology · May 2007
Vascular endothelium summary statement V: Pulmonary hypertension and acute lung injury: public health implications.
Although relatively rare, pulmonary hypertension can be devastating for those individuals who are affected and has significant societal implications. The 2003 WHO classification separates PAH (idiopathic, specific disease linked) from pulmonary hypertension related to lung disease, thromboembolic disease, and pulmonary venous hypertension. Another form of pulmonary hypertension, persistent pulmonary hypertension (PPHN), occurs in the newborn. ⋯ They are usually related to direct lung injury or indirect injury from sepsis, trauma, and other disorders. Although these pulmonary disorders reflect distinct pathophysiologic mechanisms, current evidence strongly suggests that a common denominator underlying many of the established molecular and cellular elements is endothelial cell activation and dysfunction. This summary statement briefly summarizes the state of the science and suggests future avenues of public health research.