Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current therapies for acute heart failure syndromes (AHFS) target hemodynamics by decreasing congestion or increasing myocardial contraction. Several new agents for AHFS use novel mechanisms of action that focus on new treatment targets, such as those providing anti-ischemic and anti-stunning effects, blocking vasopressin receptors, or blocking endothelin-1 receptors. For example, levosimendan acts as a calcium sensitizer and adenosine triphosphate-dependent potassium (K(ATP)) channel opener that increases contraction, causes vasodilation, and provides cardioprotective effects. This is accomplished by its dual mechanism of action. Levosimendan binds to cardiac troponin C, thereby enhancing calcium myofilament responsiveness and increasing myocardial contraction without increasing intracellular calcium levels. Thus, contraction is increased with no significant increase in myocardial oxygen consumption. The opening of K(ATP) channels by levosimendan causes vasodilation and exerts anti-ischemic and anti-stunning effects on the myocardium. Other new agents target neurohormonal pathways. Tezosentan is an antagonist of endothelin-1 receptors A and B. By inhibiting endothelin-1 receptors, tezosentan may counteract the activities of endothelin-1, which include vasoconstriction, proarrhythmic activities, potentiation of other neurohormones, and mediation of increased vascular permeability. Tolvaptan is a vasopressin V2-receptor antagonist that functions as an aquaretic (ie, it increases urine volume and serum sodium with little or no sodium loss). Therefore, by using novel mechanisms of action, these agents may provide new opportunities for helping patients with AHFS.
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PMID:Pharmacology of new agents for acute heart failure syndromes. 1618 25

Acute right ventricular (RV) failure has until recently received relatively little attention in the cardiology, critical care or anaesthesia literature. However, it is frequently encountered in cardiac surgical cases and is a significant cause of mortality in patients with severe pulmonary hypertension who undergo non-cardiac surgery. RV dysfunction may be primarily due to impaired RV contractility, or volume or pressure overload. In these patients, an increased pulmonary vascular resistance (PVR) or a decreased aortic root pressure may lead to RV ischaemia, resulting in a rapid, downward haemodynamic spiral. The key aspects of 'RV protection' in patients who are at risk of perioperative decompensation are prevention, detection and treatment aimed at reversing the underlying pathophysiology. Minimising PVR and maintaining systemic blood pressure are of central importance in the prevention of RV decompensation, which is characterised by a rising central venous pressure and a falling cardiac output. Although there are no outcome data to support any therapeutic strategy for RV failure when PVR is elevated, the combination of inhaled iloprost or intravenous milrinone with oral sildenafil produces a synergistic reduction in PVR, while sparing systemic vascular resistance. Levosimendan is a promising new inotrope for the treatment of RV failure, although its role in comparison to older agents such as dobutamine, adrenaline and milrinone has yet to be determined. This is also the case for the use of vasopressin as an alternative pressor to noradrenaline. If all else has failed, mechanical support of the RV should be considered in selected cases.
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PMID:Anaesthesia and right ventricular failure. 1949 56