The effect of short-term continuous epidural morphine on postoperative pain after laparoscopic cholecystectomy.

This study was undertaken to determine whether short-term continuous epidural analgesia using morphine would relieve pain after laparoscopic cholecystectomy. The authors retrospectively reviewed the clinical data of 182 cases who had undergone a laparoscopic cholecystectomy. These cases were divided into four groups according to their anesthetic modes as follows: a control group with general anesthesia only (n = 37); group I, general anesthesia combined with one shot of epidural morphine (n = 78); and group II, general anesthesia combined with continuous epidural analgesia using morphine (IIa for 12 h (n = 33); IIb for 8 h (n = 34)). The pain score on a four-category verbal scale and the frequency of analgesic use were investigated. There were no differences in the background characteristics of the patients among the groups, except for the duration of surgery (I vs IIa; P = 0.006). The pain scores were significantly different between the control group and the other groups. The frequency of analgesic use in the control group was also significantly higher than in the other groups. A tendency toward a higher frequency of analgesic use in group I, compared with that in groups IIa and IIb, was observed. These findings thus suggest that short-term continuous epidural analgesia using morphine can effectively relieve postoperative pain after a laparoscopic cholecystectomy.

[Anesthesia for a patient with heparin-induced thrombocytopenia: a case report].

A 68 year-old man underwent a femoral-popliteal bypass surgery. He was diagnosed as heparin-induced thrombocytopenia (HIT) by platelet aggregation test when he underwent CABG 4 years ago. For the present surgery we administered nafamostat mesilate and urokinase for anticoagulation during surgery instead of heparin. After the operation, laboratory studies showed no thrombocytopenia.

[The effects of preoperative drinking and H2 blocker on gastric acid secretion].

We studied the effects of preoperative drinking and H2 blocker on gastric acid secretion in 63 patients (ASA I-II, > 18yrs) scheduled for afternoon surgery. Group A (n = 20), as a control, was not permitted to eat and drink from 9 pm, the day before surgery, and was then given 500 ml of maintainance fluid before anesthesia. Group B (n = 20) fasted from 9 pm the day before surgery, and was allowed to drink clear fluids until 2hs before anesthesia. Group C (n - 23) followed the same guidelines as group B, and was given famotidine (20mg) orally at 9 pm the day before and 2hs before anesthesia. After induction, a Salem sump tube was inserted into the stomach and a gastric fluid aspiration was performed. The fluid volume and pH were measured after collection. Gastric pH was significantly higher (P < 0.001) in group C (6.4 +/- 0.9) than in groups A (3.1 +/- 1.8) and B (2.7 +/- 1.8). Fluid volume was similar in each group (A; 11 +/- 9/B; 12 +/- 9/C; 12 +/- 13ml). The dilution of gastric acid by the ingested fluid was not observed. We conclude that preoperative drinking does not affect gastric contents in elective operative patients. To reduce the risk of developing aspiration pneumonia, we recommend that every patient should receive an oral H2 blocker.

Halothane and isoflurane preferentially inhibit prostanoid-induced vasoconstriction of rat aorta.

In a previous study, we demonstrated that halothane and isoflurane inhibit binding of thromboxane A2 to its receptors on human platelets and thus inhibit prostanoid-induced aggregation strongly. The aim of this study was to determine whether volatile anaesthetics inhibit prostanoid-induced vasoconstriction preferentially. Rat isolated aortic rings were mounted in organ baths and their isometric tension was measured. They were contracted with STA2 (a stable thromboxane A2 analogue), prostaglandin F2 alpha (PGF2 alpha), phenylephrine, and 20 mM KCl, and then exposed to halothane (0.5-3%), isoflurane (0.5-3%), and sodium nitroprusside (SNP, 10(-9)-3 x 10(-7) M). Halothane (2-3%) and isoflurane (2-3%) induced greater relaxation of aortic rings precontracted with STA2 and PGF2 alpha than of those precontracted with phenylephrine (P < 0.01). Halothane induced greater relaxation of rings precontracted with KCl than phenylephrine only at 3%, whereas isoflurance relaxed rings precontracted with KCl more than those with phenylephrine at 0.5, 2 and 3% (P < 0.05). In contrast, SNP relaxed rings precontracted with PGF2 alpha. KCl and phenylephrine equally, but induced smaller relaxations of those precontracted with STA2 (P < 0.05). We conclude that halothane and isoflurane inhibit prostanoid-induced vasoconstriction preferentially, possibly by interacting with prostanoid receptors.

Halothane and enflurane constrict canine mesenteric arteries by releasing Ca2+ from intracellular Ca2+ stores.

BACKGROUND: Recent studies suggest that volatile anesthetics cause not only vasodilation but also vasoconstriction, depending on the experimental conditions. However, the mechanism of the constrictive effect of volatile anesthetics has not been clarified. The aim of this study was to evaluate the vasoconstrictor effects of halothane, enflurane, and isoflurane and to elucidate the underlying mechanism. METHODS: Vascular rings of canine mesenteric arteries were mounted in organ baths, and isometric tension changes were recorded. Changes in intracellular free Ca2+ concentration of vascular smooth muscle were examined by using the fluorescent Ca2+ indicator fura 2 and a dual-wavelength fluorometer. RESULTS: Halothane (0.75-2.3%) and enflurane (1.7-3.4%), but not isoflurane (1.2-3.5%), induced a concentration-dependent transient contraction, followed by a slight, sustained contraction. Halothane (1.5%)- and enflurane (3.4%)-induced contractions were reduced by endothelial denudation and enhanced by indomethacin (10(-5) M) treatment but were not affected by L-NG-nitroarginine (10(-5) M) or nifedipine (2 x 10(-7) M) treatment. Ryanodine (2 x 10(-5) M) treatment completely abolished the transient increases in tension and Ca2+ concentration. Even in ryanodine-treated arteries, however, both anesthetics induced a slowly developing sustained contraction, and the sustained contraction induced by enflurane (3.4%) was not accompanied by a significant increase in Ca2+ concentration. CONCLUSIONS: Halothane and enflurane, but not isoflurane, induce vasoconstriction by releasing Ca2+ from intracellular stores. Release of a vasodilating prostanoid and endothelium-derived constricting factor may also be involved in the vasoconstrictor effect. Furthermore, increased Ca2+ sensitivity of contractile machinery may be involved in the effect of enflurane.

Mechanisms of inhibition of endothelium-dependent relaxation by halothane, isoflurane, and sevoflurane.

Volatile anaesthetics inhibit endothelium-dependent relaxation, but the underlying mechanism(s) have not been clarified. In an attempt to elucidate the mechanism(s), we determined the effects of halothane, isoflurane and sevoflurane on relaxation induced by acetylcholine and sodium nitroprusside (SNP) and the cGMP formation elicited by exogenous nitric oxide (NO) and SNP in rat aortas. Acetylcholine (10(-7)-10(-5) M)-induced relaxation was attenuated by halothane (2%), isoflurane (2%) and sevoflurane (4%). SNP (10(-8) M)-induced relaxation was reduced by halothane (2%), but not by isoflurane (2%) or sevoflurane (4%). The cGMP level of NO-stimulated aorta was reduced by halothane (2%) and sevoflurane (4%), but not by isoflurane (2%). The cGMP level of SNP (10(-7) M)-stimulated aorta was reduced by halothane (2%), but not by isoflurane (2%) and sevoflurane (4%). We conclude that the mechanisms responsible for the inhibition of endothelium-dependent relaxation differ among anaesthetics. Isoflurane inhibits the relaxation mainly by inhibiting the formation of NO in the endothelium. In contrast, the effect of halothane on endothelium-dependent relaxation may be largely due to the inhibition of action of NO in the vascular smooth muscle and the effect of sevoflurane may be to inactivate NO or to inhibit the action of NO.

Direct vascular effect of ropivacaine in femoral artery and vein of the dog.

A study was conducted to examine the direct vascular effect of ropivacaine, in comparison with the effect of bupivacaine and lidocaine. Changes in tension induced by ropivacaine (10(-5)-3 x 10(-3) mol l-1) and lidocaine (10(-5)-10(-2) mol l-1) were examined cumulatively in vascular rings of dog femoral artery and vein under basal tension, or in those which had been precontracted with phenylephrine submaximally in Krebs' bicarbonate solution at 37 degrees C aerated with 95% O2 and 5% CO2 (pH 7.4). The change in tension induced by 10(-2) mol l-1 ropivacaine was tested under basal tension in vascular rings bathed in HEPES buffer (pH 6.8). Ropivacaine induced greater constriction than bupivacaine at concentrations over 10(-3) mol l-1 in vascular rings under basal tension (P < 0.01). The maximal contraction was induced by ropivacaine at 10(-3) mol l-1, averaging 51.5 +/- 2.8% (n = 11) and 27.0 +/- 3.7% (n = 12) of the maximal contraction induced by epinephrine in the artery and vein, respectively, and the contractions induced by ropivacaine at 10(-2) mol l-1 were 16.3 +/- 2.0% (n = 11) and 5.5 +/- 1.1% (n = 9), respectively. Phenylephrine (10(-6) mol l-1)-precontracted artery was contracted significantly by ropivacaine at 3 x 10(-4) mol l-1 and 10(-3) mol l-1, and by bupivacaine at 3 x 10(-4) mol l-1, whereas the phenylephrine (10(-6) mol l-1)-precontracted vein was relaxed by these anesthetics. Lidocaine did not exert constricting effects.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of enflurane, isoflurane, and sevoflurane on renal tubular functions].

Twenty-seven patients without renal disease were divided randomly into three groups of each nine patients. Each group received either enflurane, isoflurane or sevoflurane. The renal tubular functions were examined during anesthesia and on the first postoperative day. By inhalation of 1.49 MAC hours of enflurane, 2.17 MAC hours of isoflurane or 1.29 MAC hours of sevoflurane, creatinine clearance, Na excretion rate, urine beta 2-microglobulin and urine N-acetyl-beta-D-glucosaminidase showed no significant changes during anesthesia and the during postoperative period among anesthetic agents used. These results indicate that enflurane, isoflurane or sevoflurane does not affect renal tubular function specifically under anesthesia when each was given for less than four hours.

Halothane and isoflurane inhibit endothelium-dependent relaxation elicited by acetylcholine.

The purpose of this study was to determine whether volatile anesthetics modify the release of endothelium-derived relaxing factor. We examined the effects of halothane and isoflurane on endothelium-dependent relaxation and 3',5'-cyclic guanosine monophosphate formation elicited by acetylcholine and ionophore A23187 in isolated rat aorta. Halothane and isoflurane (1%-2%) significantly attenuated acetylcholine-induced relaxation of the phenylephrine-contracted aorta but had no significant effect on relaxation induced by A23187, nitroprusside, and nitroglycerin. Basal and A23187 (10(-7) M)-stimulated levels of 3',5'-cyclic guanosine monophosphate were slightly lowered by halothane and isoflurane (2%). In contrast, the increase of 3',5'-cyclic guanosine monophosphate elicited by acetylcholine (10(-5) M) was significantly attenuated by halothane (2%) and abolished by isoflurane (2%). These findings indicate that halothane and isoflurane strongly inhibit the release of endothelium-derived relaxing factor elicited by acetylcholine.

Direct vasoconstrictor and vasodilator effects of propofol in isolated dog arteries.

We have measured the direct effects of propofol 10(-7)-10(-4) mol litre-1 on isolated canine cerebral, coronary, mesenteric, femoral and renal arteries. In arterial strips precontracted submaximally with potassium chloride or prostaglandin F2 alpha (PGF2 alpha), propofol induced further contractions at low concentrations (10(-6)-10(-5) mol litre-1) and relaxation at high concentrations (10(-4) mol litre-1). Intrafat, which contains soya bean oil, egg phosphatide and glycerol in similar concentration to the emulsion formulation of propofol, had a small relaxant effect at a concentration corresponding to propofol 10(-4) mol litre-1. In humans, clinically relevant plasma concentrations of propofol have been reported to be 1-5 x 10(-5) mol litre-1, 97-99% of which is bound to plasma proteins. Therefore, the results obtained in this study demonstrated that clinically relevant concentrations of propofol did not have direct vasodilator effects.

The relaxing effects of barbiturates in vascular smooth muscle of rat aorta.

The effects of thiamylal and pentobarbital on contractions mediated through the influx of extracellular Ca(++) and the release of intracellularly stored Ca(++) were compared in rat aortic strips. Thiamylal (3 x 10(-5) M to 10(-3) M) and pentobarbital (10(-4) to 10(-3) M) significantly attenuated the contraction induced by KCl (20 mM), and shifted the dose-response curve for Ca(++) of KCl (20 mM)-treated strips downwards and to the right. Caffeine (10(-2) M)-induced contraction was significantly attenuated by thiamylal at concentrations greater than 10(-4) M and by pentobarbital at 3 x 10(-4) M. Only a high concentration (10(-3) M) of these barbiturates significantly inhibited the contractions induced by norepinephrine (NE, 10(-6) M) in Ca(++)-free medium. Contraction of strips without endothelium by a Ca(++) ionophore, A23187 (5 x 10(-6) M), in the presence of a Ca channel blocker, was relaxed by high concentrations of thiamylal (3 x 10(-4) M to 10(-3) M) and pentobarbital (10(-3) M). It is concluded that thiamylal inhibits contraction through an intracellular action as well as a Ca channel-blocking action in vascular smooth muscle of rat aorta. However, the intracellular action of pentobarbital is less potent than that of thiamylal.

The vasodilator effect of thiamylal in dog mesenteric artery: contribution of intracellular action.

The effects of thiamylal on contractions induced by various mechanisms were investigated in mesenteric arteries isolated from dogs. Thiamylal (10(-4) to 10(-3) M) significantly inhibited contractions induced by KCl (20 mM) in normal media, and those induced by norepinephrine (10(-5) M) in normal and Ca(2+)-free media. Caffeine-induced contraction was significantly inhibited by thiamylal in the concentrations greater than 3 x 10(-5) M in intact fibers and 10(-5) M in chemically skinned fibers. Chemically skinned fibers that were precontracted with Ca2+ were relaxed by thiamylal in concentrations lower than those required to relax intact fibers that were precontracted with KCl (20 mM); the ED50 was 1.52 x 10(-5) M in skinned fibers and 5.50 x 10(-4) M in intact fibers. These results suggest that intracellular mechanisms are involved in thiamylal-induced vasodilatation of dog mesenteric artery.

Age-dependent alterations in the response of isolated rat aortas to thiobarbiturates.

Responses to thiamylal and thiopental were compared in helical strips of rat thoracic aortas of different ages (5-6, 10-12 and 20-22 weeks old), precontracted partially with phenylephrine or prostaglandin F(2alpha) (PGF(2alpha)). Thiamylal and thiopental, in concentrations of 3 x 10(-5) to 10(-4) M, produced a dose-dependent relaxation in aortas at 5-6 weeks of age, no significant change of tension in those at 10-12 weeks of age, and a marked constriction in those at 20-22 weeks of age. These thiobarbiturates, in a high concentration of 10(-3) M, produced a profound relaxation in aortas at any age studied. It is concluded that the responses to thiobarbiturates of thoracic aorta precontracted with phenylephrine or PGF(2alpha) alter with age.

Halothane-induced relaxation of vascular smooth muscle: a possible contribution of increased cyclic GMP formation.

Halothane (0.75 to 2.25%) dose-dependently relaxed the vascular smooth muscle of endothelium-denuded rat aortae previously contracted with KCl, and the relaxing effect was not significantly affected by indomethacin nor dexamethasone, but partly inhibited by methylene blue. The cyclic GMP levels were increased by treatment with halothane (2.25%). It was suggested that halothane-induced relaxation of vascular smooth muscle is partly mediated by cyclic GMP formation.

Comparison of the direct effects of halothane and isoflurane on large and small coronary arteries isolated from dogs.

Relaxant responses to halothane and isoflurane were compared in helical strips of dog epicardial coronary arteries of different sizes: proximal large coronary arteries with outside diameters (OD) larger than 2.5 mm and distal small arteries with 0.7-0.9 mm OD. Responses to pharmacologic vasodilators, including nitroglycerin (NTG) and adenosine, were also studied for comparison. The relaxation induced by halothane in concentrations of 0.8-2.3% and by NTG (10(-9)-10(-5) M) was greater in proximal large coronary arteries than in distal small ones contracted with 20 mM KCl. In contrast, the relaxation by isoflurane (1.2-3.5%) and by adenosine (10(-8)-10(-4) M) was greater in small coronary arteries than in large ones. These results suggest that isoflurane is, like adenosine, preferentially a small artery dilator.

[Intraoperative anoxic spells in patients with tetralogy of Fallot].

We experienced 5 cases of intraoperative anoxic spell in 48 patients with tetralogy of Fallot (TOF). One of 5 cases had tetralogy with pulmonary atresia (Type A), and the others had tetralogy alone (Type D). The patient of type A who had anoxic spells during preoperative period had been on chronic propranolol therapy. However, the patients of type D had no anoxic spells during preoperative period and one in this type had not been on beta-adrenergic blocking drugs preoperatively. One patient was anesthetized with fentanyl-diazepam-O2, and the others were anesthetized with morphine-diazepam-O2. We used mainly alpha-adrenergic drugs and sodium bicarbonate for the therapy of intraoperative anoxic spells. Concerning the intraoperative anoxic spell, we have to be aware in the management of the patients with TOF, whether the patient had anoxic spells during preoperative period or not.

Effects of thiobarbiturates on smooth muscle reactivity in isolated aortas from spontaneously hypertensive rats.

The direct effects of thiobarbiturates on helical strips of aortas from spontaneously hypertensive (SH) rats were compared with those from Wistar-Kyoto (WKY) rats. At 5-6 wk of age, the arterial pressure of SH and WKY rats did not differ, and the effects of thiobarbiturates on aortic strips from SH and WKY rats were similar. By contrast, at the age of 10-12 or 20-21 wk arterial pressure was higher in SH than in WKY rats, and responses to thiobarbiturates differed in aortic strips from SH and WKY rats: contractile responses were greater in WKY than in SH rats, and relaxing effects were greater in SH than in WKY rats. Responses to sodium nitroprusside did not differ in the aortas of SH and WKY rats, but the effects of nifedipine were greater in strips from SH rats than from WKY rats at the age of 10-12 wk. Ca2(+)-induced contractions of strips exposed to Ca2(+)-free media and depolarized by high K+ were inhibited by treatment with thiamylal; the inhibition was greater in SH than in WKY rats. The increase in smooth-muscle relaxation induced by thiobarbiturates in strips from SH rats may be due to increased sensitivity to the Ca2(+)-channel blocking action of thiobarbiturates.