The use of antifibrinolytics in cardiac surgery is a well-accepted technique to reduce perioperative blood loss and to minimize blood transfusions . Since profound hypothermia induces coagulopathy by kinin and kallikrein activation, platelet dysfunction and fibrinolysis, and since circulatory arrest causes an increase of activated protein C and the endothelial release of tissue-type plasminogen activator, the administration of antifi-brinolytics in these conditions seems to be appropriate.
Unfortunately, concern about the potential prothrom-botic properties of antifibrinolytics, specifically aproti-nin, has provoked controversy about their use. In earlier studies aprotinin was related to adverse outcomes, including mortality, renal dysfunction, and thrombotic complications [60, 62]. It is generally accepted that these complications were due to inadequate hepariniza-tion. In later retrospective studies, in which the heparin dose was optimized, aprotinin had no deleterious effect on organ function, and mostly diminished blood loss and transfusions . Since aprotinin has additional anti-inflammatory properties, its use in DHCA surgery is even more attractive since DHCA causes a profound form of vascular endothelial injury and apoptosis in various organs . Larger, multicenter studies should be initiated to end the controversy.
Anesthetics, including inhalation agents and opioids, and potent intravenous sedatives, such as etomidate and propofol, all diminish CMR02, and in doing so may exert neuroprotective properties. In animal models most anesthetics suppress brain concentrations of catechola-mines and glutamine during incomplete ischemia .
Similar to the experiences with thiopentone, propofol did not show protection against neuropsychiatric dysfunction following cardiac surgery in humans .
An exciting new development is the so-called preconditioning effect of inhalation agents. Ischemic preconditioning of the myocardium was first described by Murry et al. , who described the protective effect of brief periods of previous ischemia against a subsequent, more prolonged period of myocardial ischemia. Isch-emic stimuli cause the release of adenosine, bradykinin, noradrenaline, and free radicals. Through intracellular messenger systems, such as protein kinase C, ATP-sensi-tive potassium (K+) channels on the sarcolemma and mitochondria are activated, preventing the influx of calcium into the cytosol.
Halogenated agents, such as isoflurane and sevoflu-rane, have been shown to mimic this preconditioning effect and to protect the myocardium during ischemic episodes and reperfusion . In a recent study sevo-flurane also showed renal protective properties, although the mechanism behind this observation is not yet clear . It is tentative to assume that similar preconditioning effects by inhalation agents may be true during brain ischemia. In animal studies isoflurane and sevoflurane pretreatment protected the brain against ischemia , with an identical underlying mechanism as in myocardial tissues [31, 66].
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...