Anesthesia and analgesia
-
Anesthesia and analgesia · Mar 2001
Thromboelastography for monitoring prolonged hypercoagulability after major abdominal surgery.
Despite clinical and laboratory evidence of perioperative hypercoagulability, there are no consistent data evaluating the extent, duration, and specific contribution of platelets and procoagulatory proteins by in vitro testing. We tested the hypothesis that the parallel use of standard and abciximab-cytochalasin D-modified thromboelastography (TEG) can assess 7 days' postoperative hypercoagulability and can estimate the independent contribution of procoagulatory proteins and platelets. Thromboelastograms were performed before surgery, at the end of surgery, 6 h after surgery, and on postoperative days 1, 2, 3, and 7; they were analyzed for the reaction time and the maximal amplitude (MA). We calculated the elastic shear modulus of standard MA (G(t)) and modified MA (G(c)), which reflect total clot strength and procoagulatory protein component, respectively. The difference was an estimate of the platelet component (G(p)). There was a 10% perioperative increase of standard MA, corresponding to a 50% increase of G(t) (P < 0.0001) and an 86%-90% contribution of the calculated G(p) to G(t). We conclude that serial standard and modified thromboelastography may reveal prolonged postoperative hypercoagulability and the independent contribution of platelets and procoagulatory proteins to clot strength. ⋯ Postoperative hypercoagulability, occurring for at least 1 wk after major abdominal surgery, may be demonstrated by standard and modified thromboelastography. This hypercoagulability is not reflected by standard coagulation monitoring and seems to be predominantly caused by increased platelet reactivity.
-
Anesthesia and analgesia · Mar 2001
Morphine enhances myofilament CA(2+) sensitivity in intact guinea pig beating hearts.
We investigated whether morphine alters intracellular Ca(2+) concentration ([Ca(2+)](i)), left ventricular pressure (LVP), and myofilament Ca(2+) sensitivity under physiologic conditions in intact guinea pig beating hearts and whether delta(1), delta(2), and kappa opioid stimulations are related to the direct cardiac effects of morphine. Transmural LV phasic [Ca(2+)](i) was measured from fluorescence signals at 385 nm and 456 nm. The Ca(2+) transients during each contraction were defined as available [Ca(2+)](i). The hearts were perfused with modified Krebs-Ringer solution containing morphine in the absence and presence of delta(1) (BNTX), delta(2) (NTB), and kappa (nor-BNI) antagonists, while developed LVP and available [Ca(2+)](i) were recorded. Morphine (1 microM) decreased available [Ca(2+)](i) by 44 +/- 12 nM without decreasing developed LVP at 2.5 mM of [CaCl(2)](e) (P < 0.05). Morphine (1 microM) caused a leftward shift in the curve of developed LVP as a function of available [Ca(2+)](i) (P < 0.05). BNTX (1 microM), but not nor-BNI (1 microM) or NTB (0.1 microM) blocked morphine (1 microM) effects to decrease available [Ca(2+)](i). Morphine decreases available [Ca(2+)](i) but not LVP, and it enhances myofilament Ca(2+) sensitivity under physiologic conditions at clinical concentrations in intact isolated beating guinea pig hearts. The delta(1) opioid stimulation modifies the effects of morphine on Ca(2+) transients and myofilament Ca(2+) sensitivity. ⋯ Morphine modifies myofilament Ca(2+) sensitivity and Ca(2+) transients in guinea pig hearts at concentrations that are clinically relevant.
-
Anesthesia and analgesia · Mar 2001
The effects of olprinone (a phosphodiesterase III inhibitor) on hepatic vascular bed in a porcine model of endotoxemia.
Decreased hepatic blood flow, and impaired hepatic oxygen delivery caused by endotoxin, result in hepatic metabolic deterioration followed by liver dysfunction and multiple organ failure. Among phosphodiesterase III inhibitors, only olprinone increases hepatosplanchnic blood flow. We evaluated the effects of olprinone on systemic hemodynamics, hepatic circulation, and hepatic oxygen delivery in a porcine model of endotoxemia. Fifteen pigs received a continuous infusion (1.7 microg. kg(-1). h(-1)) of endotoxin (lipopolysaccharide [LPS]) via the portal vein for 240 min. Seven of these pigs received olprinone infusion (0.3 microg. kg(-1). min(-1)) via a central vein from t = 150 min to t = 240 min, whereas the eight remaining pigs served as LPS controls. Continuous infusion of LPS caused significant reductions in hemodynamic variables and a significant increase in arterial lactate. After the administration of olprinone during the LPS infusion, portal venous flow and hepatic oxygen delivery were increased and were higher than in the LPS group. Furthermore, olprinone prevented any further increase in arterial lactate. We conclude that the administration of olprinone halted the disturbances in the hepatic circulation, especially in portal venous flow and hepatic oxygen delivery, in a porcine model of endotoxemia. ⋯ Endotoxin is a causative factor in peripheral vascular failure, resulting in a hemodynamic depression that includes a reduction in liver blood flow. The administration of olprinone (phosphodiesterase III inhibitor) improves the liver blood flow circulation in a porcine model of endotoxemia.