Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1998
Clinical TrialIncreased anticoagulation during cardiopulmonary bypass by prostaglandin E1.
Prostaglandin E1 (PGE1) inhibits tissue factor/factor VIIa-dependent thrombin formation and platelet procoagulant activity. These pathways may trigger thrombin generation during cardiopulmonary bypass (CPB). We hypothesized that the therapeutic combination of PGE1 and heparin increases the degree of anticoagulation as measured by reduced thrombin generation during CPB. Patients undergoing primary coronary artery bypass grafting using CPB were anticoagulated with unfractionated porcine heparin and 12.5 ng x kg(-1) x min(-1) PGE1 (n = 20) or placebo (n = 20). Plasma markers that reflect thrombin generation (prothrombin fragment F1+2, thrombin-antithrombin complex) were determined, and postoperative bleeding was documented. Thrombin generation gradually increased in both groups during and after CPB but was lower in the PGE1 group. After CPB, the difference between mean levels of prothrombin fragment F1+2 was 1.9 nmol/L (95% confidence interval for difference 1.1 to 2.8; P = 0.001). The difference between mean levels of thrombin-antithrombin complex was 43.6 ng/mL (21.2 to 66.1; P = 0.001). A trend in reduced postoperative bleeding was observed in the PGE1 group with a difference of sample means of 183 mL (-5 to 371; P = 0.056). Adding PGE1 to unfractionated heparin enhances anticoagulation during CPB. The results suggest that reduced thrombin generation during surgery may decrease postoperative bleeding. ⋯ Cardiopulmonary bypass is associated with extensive thrombin generation even in the presence of clinically sufficient heparin anticoagulation. The addition of prostaglandin E1 to heparin enhances the degree of anticoagulation as measured by reduced thrombin formation during cardiopulmonary bypass.
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Anesthesia and analgesia · Nov 1998
The effect of fibrin glue patch in an in vitro model of postdural puncture leakage.
We studied the possibility of stopping a continuing transdural leakage with fibrin glue, a biologic adhesive, in an in vitro model. The model was made by sealing the bottom of a tube filled with saline to a height of 50 cm with a human lyophilized dural specimen. Dural punctures were performed with a 17-gauge Tuohy needle. The needle was then withdrawn, and 0.8 mL of fibrin glue was injected through the same needle to seal the defect. The column was refilled 3 min after sealing. The pressure in the intrathecal chamber was measured during the procedure. Macroscopic and microscopic histological studies of the dura and the fibrin plug were performed. In the five cases studied, the leak was sealed by the fibrin plug at closing pressures of 25-35 cm H2O, and no further leakage was detected after refilling. The dural specimens showed a fibrin glue plug stuck at the edges of the hole. We conclude that fibrin glue stops leakage of fluid from dural holes created by a 17-gauge Tuohy needle in an in vitro pressurized model. ⋯ We explored the possibility of repairing a cerebrospinal fluid leak produced by an accidental dural puncture during epidural anesthesia by percutaneously injecting tissue adhesive in vitro. This technique seems promising for the prophylaxis and treatment of the headache associated with this leakage but requires further study in vivo.
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Anesthesia and analgesia · Nov 1998
The effects of milrinone and its mechanism in the fatigued diaphragm in dogs.
We studied the effects of milrinone and its mechanism in nonfatigued and fatigued diaphragms in dogs. In Group Ia (n = 5), animals without fatigue, defined as the inability to sustain muscle force, received only maintenance fluids. In Group Ib (n = 5), dogs without fatigue were given a bolus injection (50 microg/kg) followed by continuous infusion (0.5 microg x kg(-1) x min(-1)) of milrinone. In Groups IIa, IIb, and IIc (n = 8 in each), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. After producing fatigue, only maintenance fluids were administered (Group IIa); milrinone (50 microg/kg loading dose plus 0.5 microg x kg(-1) x min(-1) maintenance dose) was administered (Group IIb); or nicardipine 5 microg x kg(-1) x min(-1) was infused simultaneously with milrinone (Group IIc). Diaphragmatic contractility was assessed with transdiaphragmatic pressure (Pdi). No differences in Pdi were observed in Groups Ia and Ib. After the fatigue-producing period, Pdi at low-frequency (20-Hz) stimulation decreased from the prefatigued values in Groups IIa, IIb, and IIc (P < 0.05), whereas the decrease was minimal at high-frequency (100-Hz) stimulation. Compared with Group IIa, Pdi to each stimulus increased during milrinone infusion in Group IIb (P < 0.05). In Group IIc, the augmentation of Pdi in the fatigued diaphragm by milrinone was not abolished with an administration of nicardipine. In conclusion, milrinone improves contractility in the fatigued canine diaphragm but not via its effect on transmembrane calcium movement. ⋯ Diaphragmatic fatigue may contribute to the development of respiratory failure. Milrinone increases contractility in the fatigued diaphragm and thereby may have an inotropic action on the improvement of diaphragmatic fatigue.