Hämoglobin: Interaktion mit NO während Sepsis

Nitric oxide is an endogenous vasodilator which is produced by several different NO synthases. It plays a major role in the control of vascular tone. In sepsis or after administration of endotoxin or cytokines, large amounts of NO are generated causing generalized systemic vasodilation. Free hemoglobin is able to bind NO and, thus, causes vasoconstriction in healthy and septic individuals leading to an increase in systemic blood pressure and systemic vascular resistance. It also causes pulmonary hypertension, a generally undesired effect. Free hemoglobin restores vascular reactivity which is impaired in sepsis and appears to improve the depressed myocardial contractility in sepsis. Glomerular filtration rate falls in sepsis and improves after hemoglobin administration. Urinary output increases. In healthy animals hemoglobin causes a decrease in pancreatic and renal blood flow, but in sepsis regional blood flow is not influenced by hemoglobin. The interactions between hemoglobin and the host defense system are at present incompletely understood. Infusion of large amounts of hemoglobin may cause methemoglobinemia leading to impaired oxygenation. Clinical indications of hemoglobin in the future may be its use as a blood substitute to reduce transfusion requirements and as a NO scavenger in sepsis. More studies evaluating short-term and long-term safety and efficacy are warranted prior to clinical use of hemoglobin.