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To elucidate whether interleukins are involved in vasopressin or oxytocin release during cytokine-related stressful conditions, we examined the effects of human interleukin-1 beta and interleukin-6 on plasma vasopressin and oxytocin levels in rats. Interleukin-1 beta administrated intravenously stimulated both the vasopressin and oxytocin secretion in dose-dependent manners. Neither hormone release was observed following interleukin-6 administration. Pretreatment with aspirin significantly attenuated the effects of interleukin-1 beta on both the vasopressin and oxytocin levels. SC-19220, a prostaglandin E2 receptor antagonist, did not affect the interleukin-1 beta-induced increase of plasma oxytocin levels, but almost completely abolished its effect on plasma vasopressin levels. These results suggest that under certain stressful conditions which accompany the stimulation of cytokine production, interleukin-1 is involved in the increase of plasma vasopressin and oxytocin levels and, moreover, different kinds of prostaglandins are suggested to participate in these interleukin-1-induced hormone release.

To investigate the effect of pulmonary alveolar hypoxia on the sunthesis and release of endothelin (ET)-1, ET-1-like immunoreactivity (-LI) levels of the lung and plasma were measured in conscious unrestrained rats under hypoxic conditions. Sixty-min exposure to alveolar hypoxia (10 % O2 or 5 % O2) increased the ET-1-LI level in the lung. The plasma ET-1-LI level in hypoxic rats also increased significantly. The increase of plasma and lung ET-1-LI levels were parallel to the severity of hypoxia. These results demonstrates that acute pulmonary alveolar hypoxia increases lung and plasma ET-1-LI levels in conscious unrestrained rats, suggesting a possible physiological or pathophysiological significance of ET in alveolar hypoxia.

In helical strips of dog cerebral and mesenteric arteries previously contracted with KCl or prostaglandin F2 alpha (PGF2 alpha), the addition of pentobarbital (10(-5) to 10(-3) mol.l-1) caused dose-related relaxation, whereas thiamylal and thiopental in a low concentration (10(-5) to 10(-4) mol.l-1) caused further contraction and in a high concentration (10(-3) mol.l-1) profound relaxation. Thiobarbiturate-induced contractions were greater in mesenteric than in cerebral arteries previously contracted with PGF2 alpha. In cerebral and mesenteric arteries exposed to Ca(++)-free media for 60 min and treated with KCl or PGF2 alpha, reintroduction of Ca++ produced a transient contraction, a transient relaxation and a persistent contraction. The Ca(++)-induced persistent contraction was attenuated by pretreatment with pentobarbital (10(-4) to 10(-3) mol.l-1) and thiamylal (10(-3) mol.l-1); the attenuation was greater in arteries treated with KCl than with PGF2 alpha. The Ca(++)-induced contractions of mesenteric artery treated with PGF2 alpha were potentiated by 10(-4) mol.l-1 thiamylal. It is concluded that pentobarbital possesses only a vasodilator effect, whereas thiamylal and thiopental have both constrictor and dilator effects on vascular smooth muscle. The vasodilator effect of barbiturates is associated in part with inhibition of transmembrane influx of Ca++; the inhibition is more predominant on the influx evoked by KCl-induced depolarization than by a stimulation of PGF2 alpha receptors. Thiamylal in low concentrations appears to enhance Ca++ influx through a receptor-operated Ca++ channel for PGF2 alpha.

The effects of halothane on brain amino acid contents were investigated in rat by using a gas chromatography-mass spectrometry system. The contents of glycine and glutamate did not show any consistent changes in 1% or 2% halothane, but increased in 3% or 4% halothane. The levels of gamma-aminobutyric acid were not altered in any concentrations of halothane. The levels of aspartate increased in a dose-dependent manner up to 3% halothane, but returned to the control level in 4% halothane. These findings suggest that halothane brings the alteration of brain amino acid contents by affecting their synthesis and catabolism.

Time required for the cannulation of right internal jugular vein (IJV) under ultrasonographic guidance with a Valsalva maneuver was investigated in surgical patients. The degree of distension of the IJV and the changes in blood pressure (BP) during the maneuver were also examined. The required time for the cannulation was 11 +/- 5 sec (mean +/- SD, n = 21), and there was no failure in the cannulation. The mean BP decreased significantly during the maneuver, while the vessels enlarged approximately twofold, which facilitated the cannulation. The decrease in BP and the enlargement of the vessels during a Valsalva maneuver were confirmed in the left side, which indicated the feasibility of left IJV cannulation under ultrasonographic guidance.

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.

In order to assess the usefulness of oxygen-17, a stable isotope of oxygen, oxygen-17, was administered to rats for studying cerebral oxygen utilization, and the produced metabolic water was detected by 17O-NMR spectroscopy in vitro and an 1H-NMR imaging system in vivo. In the vitro study, the increment in signal amplitude of oxygen-17 was observed in the brain extracted from rats that inhaled oxygen-17 gas. The in vivo study demonstrated that there were changes in the 1H-NMR image intensity of brain of rats that inhaled oxygen-17 gas. These facts indicate that oxygen-17 can serve as a tracer in the study of cerebral oxygen utilization.

The anticonvulsant action of nitrous oxide and its time course were studied in rats. Bicuculline, a GABA-receptor antagonist, was administered intravenously at a rate of 0.2 mg.kg(-1).min(-1) during exposure to air (n = 60) or 75% nitrous oxide in oxygen (n = 80). The convulsant dose of bicuculline was determined. The rats were divided into subgroups according to the duration of exposure to air or nitrous oxide, from 0 to 120 min at 15 min intervals. Although the convulsant dose of bicuculline was consistent in the air group (1.03 +/- 0.06 mg.kg(-1), mean +/- SEM), it showed two peaks at 30- and 90 min exposures to nitrous oxide. The threshold dose in the nitrous oxide group was significantly higher than in the air group at only 15- and 30 min exposures (1.50 +/- 0.16, 2.15 +/- 0.25 mg.kg(-1), respectively, P0.05). We conclude that nitrous oxide has an anticonvulsant action against bicuculline-induced seizure, and that a cyclic nature exists in its action.

The internal jugular vein (LTV) can provide an extremely reliable site for correct placement of central venous catheter. The average success rate using this approach is more than 95 percent l. However, percutaneous cannulation of the IJV has not been recommended in pediatric age group because of the low success rate in children under age 2 • Monitoring of central venous pressure (CVP) is quite useful in the management of children undergoing major surgery, so that a safe and sure approach to percutaneous cannulation is mandatory. We describe an improved technique for the .percutaneous IJV cannulation which, in our experience, has proven very reliable when attempting to identify the IJV.

In order to evaluate the role of prostacyclin in d-tubocurarine-induced hypotension in human, the authors examined the relationship of changes of arterial blood pressure and plasma 6-keto-PGF1 alpha level following iv administration of d-tubocurarine (dTc), with or without prior administration of aspirin and H1 antagonist. The bolus injection of dTc 0.6 mg/kg caused a significant decrease in mean arterial pressure (MAP) that was associated with a significant increase in plasma 6-keto-PGF1 alpha (P less than 0.05 in both). The maximum MAP decrease and plasma 6-keto-PGF1 alpha increase were noted at 2 min after dTc administration. Pretreatment with aspirin DL-lysine (25 mg/kg) or diphenhydramine (1 mg/kg) significantly attenuated the responses of MAP (P less than 0.05 in both) and plasma 6-keto-PGF1 alpha level (P less than 0.01 for aspirin group, P less than 0.05 for diphenhydramine group). There was a significant correlation between the changes in plasma 6-keto-PGF1 alpha and those in MAP (Kendall tau (tau) = -0.504, P less than 0.01). These findings suggest that a bolus injection of dTc induces a release of prostacyclin through H1 receptor, which is responsible for the dTc-induced transient decrease of blood pressure in humans.

Although a large number of studies on pulmonary aspiration have been reported [1,2] and precautions are being taken to prevent this complication [3], all of these studies and precautions involve patients with a normal upper gastrointestinal (GI) tract. As far as we know, there is currently no documentation in the literature, including major textbooks, of studies investigating whether standard precautions are sufficient to prevent pulmonary aspiration in patients with a history of esophageal or gastric surgery. Here we would like to report a case of pulmonary aspiration in a postesophagectomy patient during induction of anesthesia, because this case is valuable to clarify the risks of aspiration in patients who have undergone upper GI tract surgery.

To investigate the clinical significance of endothelin (ET), a potent and long-acting vasoconstrictor peptide in anesthesia and surgery, we measured plasma ET-like immunoreactivity (ET-LI) levels by using radioimmunoassay in patients undergoing various kinds of surgery under general anesthesia. No significant changes in plasma ET-LI levels were observed in patients undergoing relatively minor surgery under general anesthesia with nitrous oxide and halothane (n=6), enflurane (n=6), or isoflurane (n=5). Although plasma ET-LI levels after surgery in patients undergoing total knee replacement (12.4±0.9 [mean±SEM] pg/mL, n=7), hysterectomy (11.4±0.6 pg/mL, n=8) or cholecystectomy (14.8±1.2 pg/mL, n=9) were no different from those before surgery, plasma ET-LI levels after surgery in patients undergoing gastrectomy (20.4±1.9 pg/mL, n=15), esophagectomy (24.7±2.5 pg/mL, n=12), hepatectomy (27.5±3.4 pg/mL, n=12), or heart surgery (43.1±4.1 pg/mL, n=18) were higher than those before surgery (P

The role of sensorimotor cortex (anterior and posterior sigmoid gyri) as the origin of enflurane-induced generalized seizures was examined and compared to that of lidocaine-induced seizures in cats. The inhaled enflurane concentration was adjusted at 3.5% in oxygen, the maximum potency to induce generalized seizures. Repetitive electrical stimulation with supramaximum intensity at a forepaw (2 Hz, 0.5 ms, 10 V) induced generalized seizures, which ended with a sudden appearance of isoelectricity in the electroencephalogram (EEG), the so-called "postictal depression." Repetitive auditory stimuli also induced similar grand mal-type EEGs. Unilateral ablation of the sensorimotor cortex completely blocked the induction of generalized seizures by contralateral somatosensory stimuli. However, it had little effect on the induction of seizures by ipsilateral somatosensory stimuli or bilateral auditory stimuli. In contrast, bilateral ablation of the sensorimotor cortex did not have a significant effect on the lidocaine-induced seizures. These findings indicate that the involvement of the sensorimotor cortex is essential for the development of enflurane-induced but not lidocaine-induced seizures.

Nitric oxide (NO) synthase inhibitor (N”-nitro-Larginine methyl ester [L-NAME]) has been reported to reduce minimum alveolar anesthetic concentration (MAC) of halothane when administered intravenously (IV) and to reduce thermal hyperalgesia, or produce antinociception in the formalin test, when administered intracerebroventricularly (ICV) or intrathecally (IT). This study attempts to identify the site(s) in the central nervous system (CNS) where L-NAME acts to reduce the halothane MAC. For this purpose, we examined the effects of IV, ICV, and IT administration of L-NAME on the halothane MAC in rats. In contrast to an earlier study, we did not observe any decrease in the halothane MAC after IV (10-30 mg/kg) administration of L-NAME. ICV (100 pg) and IT (100 pg and 1 mg) administration of L-NAME also did not alter the halothane MAC. These findings indicate that the L-arginine-NO pathway is not involved in the mechanism of action of halothane to suppress mechanical nociceptive response or in the nociceptive neural mechanism of mechanical stimulation. (Anesth Analg 1994;78:1154-7)

We have demonstrated previously, using dog epicardial arteries of different sizes, that isoflurane, like adenosine, is preferentially a small coronary artery dilator, whereas halothane, like nitroglycerin, is a large artery dilator. The present study was designed to compare the direct effects of sevoflurane with those of isoflurane and halothane. Proximal large coronary arteries with an outer diameter (o.d.) of 2.5-3.2 mm and distal small arteries of 0.6-0.9 mm o.d. were isolated from dogs and then cut into vascular rings. They were precontracted with KCl (20 mM), and their relaxant responses to anaesthetics were compared relative to the maximal responses induced by papaverine. Sevoflurane, halothane and isoflurane (1-3 human MAC) induced dose-dependent relaxation of these arteries. The relaxant response to sevoflurane did not differ between large and small arteries. However, the relaxant response of the large arteries to halothane (1.5-2.3%) was greater than that of small arteries (P0.01) and the response of small arteries to isoflurane (3.5%) was greater than that of large arteries (P0.05). In large arteries, the potency of the relaxant effect at equivalent human MAC could be ranked as halothaneor = sevofluraneisoflurane, and, in small epicardial arteries as isofluranesevofluranehalothane. We conclude that, unlike isoflurane, sevoflurane is not a preferential dilator of small coronary arteries.

To investigate the possible role of atrial and brain natriuretic peptides (ANP and BNP) in the renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP), we measured changes in plasma ANP and BNP levels during PEEP in patients undergoing subtotal esophagectomy. Application of 15 cm of H2O PEEP for 1 h decreased the levels of plasma ANP and BNP from 24.4 +/- 5.5 (mean +/- SEM) and 19.0 +/- 3.5 fmol/mL to 14.4 +/- 2.1 and 15.3 +/- 3.0 fmol/mL, respectively (P < 0.05). The level of plasma cyclic guanosine monophosphate, an intracellular second messenger of ANP and BNP, also decreased from 8.4 +/- 1.5 to 5.7 +/- 0.8 pmol/mL (P < 0.05). PEEP increased the levels of plasma arginine vasopressin from 2.0 +/- 0.5 to 4.2 +/- 1.2 pg/mL, aldosterone from 36.1 +/- 4.9 to 65.3 +/- 12.7 pg/mL, and plasma renin activity from 1.4 +/- 0.5 to 2.7 +/- 0.7 ng.mL-1.h-1. During PEEP ventilation, urine output, urinary sodium and potassium excretion, osmolar clearance, and cardiac index all decreased. PEEP increased free water clearance, right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. The level of plasma endothelin, mean blood pressure, and heart rate did not change significantly. These results suggest that not only hemodynamics and the vasopressin and renin-angiotensin-aldosterone system, but also the natriuretic peptide system (ANP and BNP), are involved in the renal effects of PEEP.

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.

The possibility of acute tolerance to nitrous oxide was examined during halothane anesthesia in humans. Nitrous oxide was added to the inspired gas twice. The first admixture induced three successive stages of electroencephalogram (EEG): delta-waves lasting for 13 +/- 12 min, theta-waves lasting for 41 +/- 21 min, and, finally, spindle-type waves. The spindle-type EEG was similar to that of halothane anesthesia in configuration, but smaller in amplitude and faster in frequency than that seen during halothane anesthesia. The second admixture, given after a 20-30-min interval, induced a continuous delta-wave EEG in one patient, theta-waves followed by spindle EEG in eight patients, and spindle-type EEG in four patients. The successive changes of electroencephalographic response during the first admixture indicate that an alteration of central nervous system function occurred. The altered state was maintained in the absence of nitrous oxide: responses to a second admixture were characteristic of the later, altered, stages of responses seen after the first admixture. These findings support the view of acute tolerance to nitrous oxide.

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.