The long-term goals are a better understanding of how the volatile anesthetic agents, halothane and isoflurane, attenuate the sympathetic vasoconstrictor tone in splanchnic and cutaneous capacitance veins. Increases in sympathetic tone to these vessels is a major mechanism by which large volumes of blood are shifted to the heart to produce rapid increases la cardiac output. Interestingly, these very veins are among the first to dilate following induction of anesthesia with halothane or isoflurane. Thus, anesthetics impair an important mechanism normally used to enhance venous return and to maintain cardiac output. This anesthetic action is an important consideration in selecting anesthetics for patients who are hypovolemic or for patients whose cardiac out-put is being maintained through increased activity of the sympathetic nervous system. Because the portal venous system starts and ends with capillaries, direct measurement of pressures via catheter during anesthesia cannot be achieved noninvasively; thus information on the effects of anesthetics in this system lags behind that in other vascular systems. To study this system, in vitro techniques are needed and can provide much information on the action of anesthetics on vessels. Studies proposed are: (1) to measure levels of two cotransmitter peptides, neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP), along with the transmitter, norepinephrine (NE), in cutaneous and mesenteric veins and in intestinal and peripheral arteries; (2 to explore whether NPY or VIP may influence NE dynamics at neuroeffector units in saphenous and portal veins. NPY typically enhances vasoconstrictor responses, whereas VIP enhances vasoconstrictor responses. Both VIP and NPY are present in portal vein and NPY in saphenous vein. They are released. along with NE, during electrical stimulation (ES); and (3) to ?study the effects of anesthetic agent on release of NE and NPY and/or VIP (and the resulting contractile response) in superfused segments of saphenous and portal veins during resting conditions and during ES. Techniques to be used include: superfusion of helically cut strips of vein in the presence and absence of halothane and isoflurane; determination of endogenous NE in superfusate in the presence and absence of anesthetic using liquid chromatography with electrochemical detection and quantitation of NPY and VIP by radioimmunoassay.
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