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1.
Korean Journal of Anesthesiology ; : 90-97, 1997.
Article in Korean | WPRIM | ID: wpr-22012

ABSTRACT

Backgronud : Postoperative pain control became anesthesiologist's familiar yield, so many anesthesiologists are very interested in opioid and local anesthetic's characterestics and there cardiovascular effects. It's important which anesthetic has the best pain killing and the least cardiovascular effect. We used epidural opioid and local anesthetics and intravenous opioid to investigate their pain killing and cardiovascular effects. METHODS: We studied 50 patients undergoing gastrectomy. An epidural catheter was placed via the T8-9 or L1-2 interspace. Epidural fentanyl group (Ep-F) received fentanyl 2 microgram/kg in 10ml saline, epidural bupivacaine group (Ep-B), 10 ml 0.25% bupivacaine, and epidural lidocaine group (Ep-L), 10 ml 1.5% lidocaine, epidurally; intravenous fentanyl group (IV-F) received fentanyl, 2 microgram/kg. 50% of the original dose was repeated every hour until the operation ended. Control group was given nothing before general anesthesia. Cardiovascular data was compared between those before and those at 1hour after skin incision. The time interval between end of the operation and the time of first analgesic requirement and the total number of intramuscular analgesic requirements during the first 48hours postoperatively were compared. RESULTS: Urinary output during surgery was significantly larger in group Ep-F. Group Ep-L developed more frequent episodes of hypotension. Group Ep-F, group IV-F and control group required higher enflurane concentrations. CONCLUSIONS: Group Ep-F was accompanied less hypotension and postoperative analgesic requirements were reduced.


Subject(s)
Humans , Anesthesia, General , Anesthetics, Local , Bupivacaine , Catheters , Enflurane , Fentanyl , Gastrectomy , Homicide , Hypotension , Lidocaine , Pain, Postoperative , Skin
2.
Korean Journal of Anesthesiology ; : 591-603, 1997.
Article in Korean | WPRIM | ID: wpr-33365

ABSTRACT

BACKGROUND: When used to reverse the anticoagulant effect of heparin, protamine administration after cardiovascular bypass often can lead to systemic hypotension. During the reversal of heparin-induced anticoagulation, the effects of protamine on both a heparin-protamine complex and free protamine on the cardiovascular system should be considered. METHOD: To determine whether the hypotensive effect of heparin-protamine and/or protamine could be caused by endothelium-dependent and-independent component, we studied rings of the arotic arteries in rats suspended in organ chambers containing Tris Tyrode solution at 37oC and 100% O2. Arterial rings with or without endothelium were contracted with 40 mM KCl or 3 +/- 10-6M phenylephrine and then exposed to increasing concentrations of protamine (final organ bath concentration, 40~400 g/ml) both in the absence and presence of heparin (200 U/ml). RESULTS: Protamine induced concentration-dependent relaxation in arterial rings with endothelium, which were significantly greater than in rings without endothelium. The endothelium-dependent relaxation induced by protamine was inhibited by NG-monomethyl-L-arginine (L-NMMA) (10-5M) pretreatment, but was not inhibited by indomethacin (3x10-6M) pretreatment on rings with endothelium. Furthermore, the contractile inhibition was enhanced by superoxide dismutase (100 U/ml). Also, such vasodilating actions were not influenced in the presence of heparin (200 U/ml). In endothelium-denuded strips, protamine (400ug/ml) inhibited Ca++ induced contraction, which was evoked in Ca++-free solution containing 40 mM K+, and also inhibited the norepinephrine (NE)-induced contraction. Protamine inhibited on the NE-induced contraction, but not the caffein-induced contration in Ca++ free, 2 mM EGTA solution. Also, such inhibition of contracions were not inluenced in the presence of heparin (40 U/ml). CONCLUSION: This study demonstrates that protamine (in the presence or absence of heparin) acts on endothelial cell receptors to stimulate the production of nitric oxide and inhibits both Ca++-influx and the NE-induced Ca++ release from intracellular stores.


Subject(s)
Animals , Rats , Arteries , Baths , Cardiovascular System , Egtazic Acid , Endothelial Cells , Endothelium , Heparin , Hypotension , Indomethacin , Nitric Oxide , Norepinephrine , omega-N-Methylarginine , Phenylephrine , Relaxation , Superoxide Dismutase , Vasodilation
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