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PubMed1985

Sensitivity of end-tidal nitrogen in venous air embolism detection in dogs.

Embolized nitrogen appears in alveolar gas during clinical and experimental venous air embolism (VAE). Since early detection of VAE is believed to reduce morbidity and mortality, this study was done to compare the sensitivity of end-tidal nitrogen (ETN2) monitoring with other detection methods in current clinical use--precordial Doppler (PD), end-tidal CO2 (ETCO2), and pulmonary artery pressure (PAP). Ten mongrel dogs (10-17 kg) were anesthetized, placed in the supine position, immobilized, and ventilated (FIO2 1.0; PaCO2 35-40 mmHg). Anesthesia and muscle relaxation were maintained with constant infusions of thiamylal and pancuronium. Maintenance fluids were administered at 5 ml X kg-1 X h-1. Mean arterial pressure (MAP), PAP, and ETN2 and ETCO2 (Medspec II mass spectrometer) were displayed on a strip chart recorder. The dogs were divided into two equal groups and given either a step-wise sequence of 1-min air infusions (0.1-1.5 ml X kg-1 X min-1) or 5-s bolus air injections (0.25-1.0 ml X kg-1). Changes in PD sounds occurred in all animals at all air doses. Changes in cardiovascular variables and PaO2 were minimal. The threshold dose for ETCO2 and ETN2 to reach significance was 0.1 and 0.25 ml X kg-1, respectively, while PAP increases were significant at greater than 0.5 ml X kg-1 air doses. The time to maximum change (delta max) ETN2 was 30-90 s earlier than delta max ETCO2 (P less than 0.05) and 6-105 s earlier than delta max PAP. The delta max for all variables was dose related and statistically significant except for the smallest infusion VAE, where only ETCO2 was significantly changed.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1987

Anesthetic depression of myocardial contractility: a review of possible mechanisms.

The bulk of experimental evidence indicates that anesthetics do not produce their negative inotropic effect via an inhibitory action on mitochondrial electron transport. Anesthetics decrease energy need, rather than energy production. Anesthetics also decrease the rate of sequestration of Ca2+ by mitochondria, but, again, this appears not to be an important cause of reduced myocardial contractility. The role played by direct anesthetic depression of the myofibrils in reducing contractility is uncertain. Most experimental evidence now available suggests that significant myofibrillar depression, measured in terms of inhibition of actomyosin ATPase activity or inhibition of force production, occurs only at anesthetic concentrations which are high compared to concentrations employed clinically. This would seem to indicate that the myofibrils are not an important target for anesthetics in regard to the production of depressed myocardial contractility. However, the experimental act of removing myofibrils from their intracellular environment, or of removing the sarcolemma or making it hyperpermeable, appears to prevent some regulatory myofibrillar phosphorylation reactions from taking place. As stated by Winegrad, "certain forms of regulation of the cardiac myofibril are fragile and can be seen only when cellular constituents and structure are maintained." It is possible that this type of regulation is susceptible to inhibition by anesthetics. Methods for preserving this regulation are available, and will need to be employed before a depressant action of anesthetics on the myofibril can be definitely dismissed as a significant cause of the inhibition of cardiac contractility. A single study, of intracellular Ca2+ levels in the intact cell (where myofibrillar regulation was presumably preserved), has indicated that halothane may decrease myofilament Ca2+ sensitivity. However, for reasons stated above, this study cannot be taken as unequivocal proof of such an action. Despite the fact that the normal action potential is little affected by anesthetics, the sarcolemma appears to play a pivotal role in the production of anesthetic-induced contractile depression. Significant depression of the rate of upstroke of the slow (Ca2+-mediated) action potential by clinical concentrations of both inhalation and intravenous anesthetics has been demonstrated by several workers. This has been interpreted to mean that anesthetics inhibit the influx of Ca2+ through the slow channel, and such has been confirmed (to date, for halothane and thiamylal) by direct measurement of the slow inward Ca2+ current using a voltage clamp technique.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthetics↗
PubMed1991

The onset of disuse-related potassium efflux to succinylcholine.

Disuse atrophy of skeletal muscle produces resistance to nondepolarizing relaxants and increased potassium efflux after the administration of succinylcholine. These changes appear to be due to development of perijunctional and/or extrajunctional receptors (up-regulation). In this study, the authors searched for the earliest detectable appearance of increased potassium efflux in beagles in whom disuse atrophy was simulated. Seven beagles underwent unilateral cast immobilization of a hind limb. Between 4 and 42 days, they periodically received succinylcholine 0.25 mg/kg while anesthetized with thiamylal and nitrous oxide. Sequential bilateral femoral venous samples showed that the casted limb did not manifest potassium release greater than the upper limit of normal (1 mEq/l) until cast immobilization periods of 14 days or longer. When this occurred, the increase in the potassium concentration in the femoral venous blood of the casted limb exceeded that from the noncasted limb by at least 0.7 mEq/l (P less than 0.01). The range for the onset of this response after casting was 14-42 days, the mean 27.2 days, and the standard deviation 9.8 days. These findings imply that up-regulation of skeletal muscle receptors, associated with exaggerated potassium efflux after administration of succinylcholine, is dependent on progressive development of extrajunctional receptors over surface membrane areas beyond the endplate.

Animals↗
PubMed1993

Efficacy of oral clonidine premedication in children.

BACKGROUND: Clonidine, an alpha 2-adrenoceptor agonist, has been shown to be effective as a preanesthetic medication in adults. The current study was designed to investigate the efficacy of two doses of oral clonidine as a premedicant preceding oral atropine in children. METHODS: In a prospective, randomized, double-blind, controlled clinical trial, 105 children, aged 4-12 yr, undergoing elective ophthalmologic surgery received 0.4 mg/kg diazepam, 2 micrograms/kg clonidine, or 4 micrograms/kg clonidine orally. These agents mixed with apple juice were administered 105 min before the estimated time of induction of anesthesia, and were followed by treatment with 0.03 mg/kg oral atropine 60 min before anesthesia. A blinded observer noted the children's level of sedation, quality of separation from parents, and degree of acceptance of mask application during inhalation of nitrous oxide used for establishment of venous access. Anesthesia was induced with 5 mg/kg thiamylal, and tracheal intubation was facilitated with 0.2 mg/kg vecuronium. Hemodynamic changes after tracheal intubation were compared among the three groups. RESULTS: Clonidine produced significant sedation, and the effect was dose related. Clonidine, 4 micrograms/kg, provided better quality of separation and acceptance of mask than the two other regimens. This dose of clonidine attenuated the increases in blood pressure and heart rate after tracheal intubation. No clinically significant perioperative hypotension or bradycardia was observed. CONCLUSIONS: These data indicate that, even in pediatric surgery, the combination of 4 micrograms/kg and 0.03 mg/kg oral clonidine is an effective premedication. However, the safety and optimal dose of clonidine in this setting remain to be determined.

Administration, Oral↗
PubMed1994

Clonidine and lidocaine inhibition of isoflurane-induced tachycardia in humans.

BACKGROUND: A rapid increase in isoflurane concentration can induce tachycardia and hypertension and increase plasma catecholamine concentrations. To investigate a possible mechanism, we measured hemodynamic responses to isoflurane administered via mask; we also administered clonidine for premedication, lidocaine topically to the nasal mucosa, or lidocaine intravenously to evaluate the effect of these drugs on the hemodynamic responses. METHODS: Forty ASA physical status 1 patients (aged 20-30 yr) scheduled for elective oral surgery participated in the study. Thirty patients were randomly allocated to one of three groups: a control group, a group receiving 3-4 micrograms.kg-1 of oral clonidine for premedication, and a group receiving 2 ml of 4% lidocaine spray to the nasal mucosa. Ten patients were assigned nonrandomly to a group receiving intravenous lidocaine continuously (0.4 mg.kg-1 bolus followed by 30 micrograms.kg-1.min-1) after the initial randomized experiments were done to test whether systemic lidocaine blunts the responses to inhaled isoflurane. Anesthesia was induced with thiamylal, after which inhalation of 1% isoflurane in 100% oxygen via mask was begun. The inspired concentration of isoflurane was increased by 1% every 5 min to a maximum of 4%. During normocapnia and without surgical stimulation, heart rate and systolic blood pressure were measured every minute for 20 min before and during isoflurane inhalation. Plasma catecholamine concentrations were measured before and at each isoflurane concentration. RESULTS: In the control and intravenous lidocaine groups, an increase in isoflurane concentration from 2% to 3% significantly increased systolic blood pressure (peak changes of 16 +/- 5 and 15 +/- 6 mmHg, respectively) and heart rate (peak changes of 23 +/- 3 and 13 +/- 4 beats.min-1, respectively). A change in concentration to 4%, however, did not significantly alter hemodynamics. Blood pressure and heart rate responses to a change to 3% isoflurane were significantly blunted in the groups receiving clonidine (peak changes of 4 +/- 4 mmHg and 8 +/- 3 beats.min-1, respectively) or nasal lidocaine (peak changes of 2 +/- 1 mmHg and 4 +/- 2 beats.min-1, respectively) compared with the control group. In all groups, plasma epinephrine and norepinephrine concentrations increased after administration of 2% and 1% isoflurane, respectively. Plasma lidocaine concentrations were 0.3-1.3 micrograms.kg-1 in the nasal lidocaine group and 0.6-1.5 micrograms.kg-1 in the intravenous lidocaine group. CONCLUSIONS: Stepwise increases in isoflurane concentration elicited hypertension and tachycardia as well as increments in plasma catecholamine concentrations during mask anesthesia. Nasal administration of lidocaine and clonidine premedication significantly blunted the circulatory responses to isoflurane. Intravenous lidocaine did not significantly weaken the responses to changes in isoflurane concentration.

Administration, Topical↗
PubMed1995

Wheezing during induction of general anesthesia in patients with and without asthma. A randomized, blinded trial.

BACKGROUND: Patients with asthma who require general anesthesia and tracheal intubation are at increased risk for the development of bronchospasm during induction. The incidence of wheezing during induction with different intravenously administered agents is unknown. A randomized, double-blinded prospective study was undertaken to evaluate the incidence of wheezing in asymptomatic asthmatic and nonasthmatic patients receiving three commonly used intravenous anesthetic agents for induction of anesthesia. METHODS: Fifty-nine asymptomatic asthmatic and 96 nonasthmatic patients of ASA physical status 1 and 2 were studied. All patients received 1.5 micrograms/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital or 2.5 mg/kg propofol, 1.5 mg/kg succinylcholine, tracheal intubation, and inhalational anesthesia. Wheezing was assessed by an independent blinded observer, auscultating the lungs at 2 and 5 min postintubation. Data were analyzed by Pearson's chi-squared, Fisher's exact test, and multiple logistic regression with significance set at P < 0.05. RESULTS: Both asthmatic and nonasthmatic patients who received a thiobarbiturate for induction had a greater incidence of wheezing than did patients receiving propofol. In asthmatic patients, 45% (23, 67) (mean and 95% confidence interval) who received a thiobarbiturate, 26% (8, 44) who received an oxybarbiturate, and none (0, 17) who received propofol wheezed after intubation. In nonasthmatic patients, 16% (3, 28) who received thiobarbiturate and 3% (0, 9) who received propofol wheezed. CONCLUSIONS: This study suggests that propofol should be considered for induction of anesthesia in patients, particularly those with asthma, who require timely intubation.

Adolescent↗
PubMed1995

The changing pharmacodynamics of metocurine identify the onset and offset of canine gastrocnemius disuse atrophy.

BACKGROUND: Immobilization of skeletal muscle results in disuse atrophy and resistance to nondepolarizing muscle relaxants. We studied the pharmacodynamics of metocurine (MTC) to identify the development and recovery of disuse-related resistance to MTC. METHODS: Nineteen dogs underwent cast immobilization of a hind limb for as long as 3 weeks. Before, during, and after casting, dogs were intermittently anesthetized with thiamylal-N2O-fentanyl. The blood concentration of MTC and the corresponding degree of paralysis after a brief infusion were recorded and were used to characterize the pharmacokinetics and pharmacodynamics of MTC. RESULTS: Pharmacodynamic study of the response to MTC demonstrated resistance by the 4th day of casting. The effect-site concentration associated with 50% paralysis of twitch increased after 3 weeks from approximately 250 to 750 ng/ml. After cast removal, resistance persisted for 2 more weeks. Six weeks after cast removal, the effect-site concentration associated with 50% paralysis of twitch was normal in every dog. CONCLUSIONS: Within the context of this study of immobilization disuse atrophy, pharmacokinetic and pharmacodynamic characterization of antagonist responses can be used to infer muscle disuse-related changes in acetylcholine receptors.

Acetylcholine↗
PubMed1998

Skin vasomotor reflex predicts circulatory responses to laryngoscopy and intubation.

BACKGROUND: An evaluation of autonomic reactivity may help to predict circulatory responses to intubation. The relation between the magnitude of the skin vasomotor reflex (SVmR) immediately before laryngoscopy and the circulatory responses to intubation was examined. METHODS: Forty-four adult patients (classified as American Society of Anesthesiologists physical status I or II) were studied. General anesthesia was induced with fentanyl and thiamylal and maintained with nitrous oxide and sevoflurane. The SVmR was evoked by an electrostimulus to the ulnar nerve, and decreases in skin blood flow were detected using a laser-Doppler flowmeter. In study 1, two groups of patients were studied. In the monitored group (n = 14), laryngoscopy was performed when the SVmR amplitude had decreased to less than 0.1. In the control group (n = 15), intubation was performed regardless of changes in the SVmR amplitude. In study 2, after induction, the end-tidal concentration of sevoflurane was maintained at 1 MAC (n = 9) or 1.3 MAC (n = 6) for 5 min. The SVmR was tested by changing the electric intensity. RESULTS: In study 1, the blood pressure and heart rate of the control group increased significantly (P < 0.01) after laryngoscopy. The blood pressure of the monitored group did not increase. The SVmR amplitude and the systolic blood pressure changes showed a significant linear correlation (P < 0.001). In study 2, the relation between the electric intensity and the SVmR amplitude showed a weak but significant correlation (P < 0.01) in the 1 MAC group. CONCLUSION: The evaluation of the SVmR provides useful information for determining the optimal anesthetic depth for laryngoscopy and intubation in individual patients.

Adult↗
PubMed2003

Thiopental inhibits tumor necrosis factor alpha-induced activation of nuclear factor kappaB through suppression of kappaB kinase activity.

BACKGROUND: Thiopental is frequently used for the treatment of intracranial hypertension after severe head injury and is associated with immunosuppressive effects. The authors have recently reported that thiopental inhibits activation of nuclear factor (NF) kappaB, a transcription factor implicated in the expression of many inflammatory genes. Thus, it was the aim of the current study to examine the molecular mechanism of this inhibitory effect. METHODS: The authors tested gamma-aminobutyric acid (GABA), the GABA(A) antagonist bicuculline, and the GABA(B) antagonist dichlorophenyl-methyl-amino-propyl-diethoxymethyl-phosphinic acid (CGP 52432) in combination with thiopental for their influence on the activation of NF-kappaB. In addition, they investigated the direct effect of thiopental on activated NF-kappaB DNA binding activity. These experiments were conducted in Jurkat T lymphocytes using electrophoretic mobility shift assays. The presence of the phosphorylated and dephosphorylated NF-kappaB inhibitor IkappaBalpha (Western blotting) and IkappaB kinase activity were studied in Jurkat T cells and human CD3+ T lymphocytes. In addition, the authors tested the effect of the structural barbiturate analog pairs thiopental-pentobarbital and thiamylal-secobarbital and of thiopental in combination with the thio-group containing chemical dithiothreitol on the activation of NF-kappaB. RESULTS: GABA did not inhibit NF-kappaB activation, and the GABA(A) and GABA(B) antagonists bicuculline and CGP did not diminish the thiopental-mediated inhibitory effect on NF-kappaB activation. Thiopental did not inhibit activated NF-kappaB directly in a cell-free system. The phosphorylation of IkappaBalpha was prevented after incubation with 1,000 microg/ml thiopental. The same concentration of thiopental also inhibited IkappaB kinase activity in tumor necrosis factor-stimulated Jurkat T cells and human CD3+ T lymphocytes (60% suppression, P < 0.05 vs. tumor necrosis factor alpha alone). Thiobarbiturates (4 x 10(-3) m) inhibited NF-kappaB activity, whereas equimolar concentrations of the structural oxyanalogs did not. Preincubation of thiopental with dithiothreitol diminished the inhibitory effect. CONCLUSION: Thiopental-mediated inhibition of NF-kappaB activation is due to the suppression of IkappaB kinase activity and depends at least in part on the thio-group of the barbiturate molecule.

Anesthetics, Intravenous↗
PubMed1987

Bronchial blood flow measured by video dilution technique in sheep.

Bronchial blood flow was studied with the video dilution technique (VDT) in seven sheep. All animals were anesthetized (thiamylal and halothane) and ventilated. A videodensitometer and a videotape replay of the fluoroscopic image of dye moving through the common bronchial artery were used to construct dye mass vs. time curves. The areas under the curves were inversely proportional to flow in the bronchoesophageal artery, the site of dye injection. At thoracotomy, an electromagnetic flow probe (EMFP) was placed on the common bronchial artery (the major branch of the bronchoesophageal artery) to measure blood flow changes simultaneously by EMFP and by VDT. These two methods of measurement of blood flow to the airways were compared to validate the use of VDT in this circulation. Common bronchial artery blood flow was increased by injection of radiocontrast dye into the fluoroscopically positioned bronchoesophageal artery catheter causing hyperosmotically induced hyperemia. In 160 simultaneous measurements in five sheep, the percent change in flow as measured by EMFP and VDT correlated closely (r = 0.96). When flow changed because of spontaneous aortic pressure changes or pharmacologic intervention (28 simultaneous measurements in five sheep), the percent change in flow by EMFP and VDT also correlated well (r = 0.98). Bronchial blood flow changes in sheep can be measured accurately using the video dilution technique.

Animals↗
PubMed1992

Effects of nicardipine on the circulatory responses to tracheal intubation in normotensive and hypertensive patients.

This study was undertaken to examine the effects of nicardipine on circulatory responses to laryngoscopy and tracheal intubation in normotensive (n = 39) and hypertensive (n = 36) patients. Laryngoscopy and tracheal intubation were performed after induction of anaesthesia with thiamylal, followed by administration of intravenous saline or nicardipine 20 or 30 micrograms.kg-1 and suxamethonium. Blood pressure and heart rate were recorded, and rate-pressure product was calculated. Nicardipine 20 and 30 micrograms.kg-1 prevented the increase in mean arterial pressure after intubation in normotensive and hypertensive patients (p less than 0.01 compared with saline). The changes in heart rate after intubation were significantly greater in normotensive patients than in hypertensive patients when 20 or 30 micrograms.kg-1 of nicardipine was given (p less than 0.05 and p less than 0.01 respectively). Rate-pressure product increased significantly (p less than 0.01) after intubation in normotensive patients whether nicardipine was administered or not, but the increase was suppressed completely by nicardipine 20 or 30 micrograms.kg-1 in hypertensive patients. We conclude that nicardipine is effective in preventing the circulatory responses to laryngoscopy and tracheal intubation in hypertensive patients.

Adult↗
PubMed1976

Jet ventilation for fiberoptic bronchoscopy under general anesthesia.

An oxygen jet method ventilating patients during laryngoscopy has been applied to fiberoptic bronchoscopy. A 3.5 mm plastic tube 24.5 cm long was inserted into the trachea through the mouth. An intermittent jet of oxygen at 3.5 atm (50 psi) was applied to this tube using a 1.5 mm ID plastic catheter to ventilate the patient. Anesthesia was accomplished with intravenous thiamylal and Innovar. The patients were paralyzed with continuous succinylcholine. The technique has subsequently been used without complications in more than 1,000 patients. A fluidic ventilator was developed for delivering and controlling the oxygen jet. The airway pressure can be monitored continuously and, by the use of fluidic devices, the jet can be set to cut off automatically if the airway pressure is too high. The above techique for laryngoscopy with the fluidic ventilator was used in 28 patients undergoing fiberoptic bronchoscopy (Olympus 5.7 mm diameter). The airway pressure was continuously monitored with a line attached to the suction port of the bronchoscope. Arterial PCO2 ranged from 23 to 42 mmHg and PO2 from 105 to 325 mmHg. The high PO2 levels were maintained even during suctioning. General anesthesia for fiberoptic bronchoscopy can be performed using an endotracheal tube not smaller than 8 mm internal diameter (ID). The advantages of the oxygen jet technique are that it can be used in smaller patients and that the upper airway can be examined.

Anesthesia, General↗
PubMed1989

Isoflurane or halothane for cesarean section: comparative maternal and neonatal effects.

The maternal and neonatal effects of isoflurane and halothane combined with 50% N2O - 50% O2 were compared in 60 healthy parturients undergoing primary or repeat cesarean section. All patients had rapid sequence induction of anesthesia with sodium thiamylal 4 mg/kg followed by succinylcholine for tracheal intubation. Patients were randomly assigned to one of three groups of 20 each (inspired 0.5% isoflurane, 1% isoflurane or 0.5% halothane), combined with 50% N2O and O2. After delivery, 67% N2O in O2 was used, supplemented by butorphanol. Maternal blood loss did not differ significantly among the three groups and none of the patients developed intraoperative awareness. At the time of delivery, maternal plasma epinephrine levels were significantly above preinduction levels in the 0.5% isoflurane group but unchanged in the other two groups. Neonatal status as ascertained by Apgar scores, cord acid base status and the Neurologic and Adaptive Capacity Scores (NACS) was equally good in the three groups of patients. Serum inorganic fluoride concentrations in the mother after anesthesia were not significantly above preanesthetic levels in any of the groups and there was no biochemical evidence of renal toxicity. In all neonates fluoride ion concentrations in the first voided urine sample were less than 7 mumol/l, a value well below that associated with nephrotoxicity. It is concluded that isoflurane is a safe supplement to N2O - O2 mixture for cesarean section and is a safer alternative to halothane in situations when patients receiving beta-adrenergic therapy require cesarean section since halothane might potentiate arrhythmias caused by beta adrenergic agonists.

Adult↗
PubMed1994

Effects of induced hypotension on arterial blood-gases under spontaneous breathing.

The effects of deliberate hypotension on both PaO2 and PaCO2 were investigated under isoflurane anaesthesia with spontaneous breathing from a laryngeal mask. Lumbar epidural block was introduced; anaesthesia was induced with thiamylal (4 mg.kg-1) and maintained with 0.5% isoflurane in nitrous oxide (4 l.min-1) and oxygen (2 l.min-1) under spontaneous breathing. After that nitroglycerin, trimetaphan or prostaglandin E1 were used to induce a hypotension of 70% of control. All three drugs significantly decreased PaO2, from 19.9 +/- 3.3, 19.2 +/- 2.7, and 19.6 +/- 3.1 kPa to 14.6 +/- 1.9, 16.6 +/- 2.2, and 16.2 +/- 2.4 kPa (mean +/- s.d.), respectively; none of them increased PaCO2. In spite of the sparing of functional residual capacity under spontaneous breathing, the levels of reduction of PaO2 were the same as levels reported in paralyzed and mechanically ventilated subjects. In conclusion, under deliberate hypotension PaO2 decreases to a considerable degree, even under spontaneous breathing, presumably not because of alveolar hypoventilation, but because of the suppression of hypoxic pulmonary vasoconstriction by the drugs used in this study.

Adult↗
PubMed1998

In vitro study on antioxidant potential of various drugs used in the perioperative period.

BACKGROUND: Since surgical trauma not only intensifies the oxidative stress by generating reactive oxygen species (ROS), but also weakens the biological defense system against ROS attack, the antioxidant activity of drugs used during the perioperative period, which possibly normalizes the impaired redox state in the patient, is of fundamental importance and great clinical interest. METHODS: We have applied the phycoerythrin fluorescence-based assay, in which 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-generated peroxyl radical attacks B-phycoerythrin (B-PE) to lead to a sensitive decrease in its fluorescence intensity linearly, to evaluate the antioxidant activity of major drugs in anesthetic practice. RESULTS: By the protective effect on B-PE fluorescence decay, the antioxidant activities of the drugs were classified into three groups: Group I drugs, which only slowed B-PE fluorescence decay (nicardipine, verapamil, diltiazem, ephedrine, aminophylline, vecuronium, lidocaine, mepivacaine, midazolam, thiamylal, droperidol, ketamine, hydroxyzine, butorphanol, prednisolone, hydrocortisone, betamethasone, dexamethasone, methylprednisolone, and furosemide); Group II drugs, which protected B-PE oxidation completely and stopped fluorescence decay in a certain duration (dopamine, epinephrine, norepinephrine, dobutamine, isoproterenol, and buprenorphine); and Group III drugs, which had no protective effect on B-PE oxidation (nitroglycerin, prostaglandin E1, neostigmine, pancuronium, suxamethonium, atropine, bupivacaine, pentazocine, and heparin). CONCLUSION: These results indicate that Group I and II drugs exert some antioxidant activity in vitro, as measured by their protection of fluorescence decay of B-PE. Careful consideration of these properties might, then, serve to facilitate more efficient drug application.

Adjuvants, Anesthesia↗
PubMed1992

Assessment of an extracorporeal liver assist device in anhepatic dogs.

We have used an anhepatic dog model to demonstrate the efficacy of a bioartificial liver assist device. Six dogs underwent total hepatectomy. Three received only medical care (controls) while the remainder were connected to an extracorporeal liver assist device (ELAD). The control dogs failed to regain consciousness after anesthesia although all lived 4-5 h postoperatively. Plasma ammonia concentration increased by an average of 250 mumol/L between the end of surgery and the demise of the animals. The treated dogs lived 3-12.5 h, and 2 of them required repeated doses of thiamylal sodium to maintain sedation. Plasma ammonia concentration was unchanged after connection to the ELAD except in the longest survivor, whose ammonia began to rise after 8 h on the ELAD. The short survival in the other 2 treated dogs was the result of uncontrolled intraabdominal bleeding. This device is capable of replacing the metabolic function of the liver, and might provide hepatic support in patients awaiting transplantation or in fulminant hepatic failure.

Ammonia↗
PubMedDate not supplied

Postural influence on systemic blood pressure in large full-term pregnant bitches during general anesthesia.

Effects of positioning on systemic blood pressure were evaluated in six full-term pregnant golden retriever bitches during general anesthesia. Two positions (dorsal and left lateral recumbency) were examined. Anesthesia was induced with thiamylal sodium and maintained with halothane in oxygen. Direct arterial blood pressures were recorded from the bitches in each position. Effects of positioning for each bitch during general anesthesia were reexamined after the bitch weaned its pups; thus, each bitch served as its own control. Maternal posture had no significant effect (p greater than 0.05) on systemic blood pressure. Pregnancy had no significant effect (p greater than 0.05) on systemic blood pressure. Supine hypotension did not occur in anesthetized large, full-term pregnant bitches. Dorsal recumbency was an acceptable position for cesarean sections performed with the patient under general anesthesia.

Anesthesia, General↗
PubMedDate not supplied

Hemodynamic function during neurectomy in halothane-anesthetized horses with or without constant dose detomidine infusion.

Nine horses were premediated with acepromazine, and anesthesia was induced with guaifenesin and thiamylal. Anesthesia was maintained in four horses with halothane in oxygen, and in five horses with halothane in oxygen plus a constant dose infusion of detomidine. Both maintenance regimens produced a MAC equivalent of 1.4 at the ambient barometric pressure. Hemodynamic and respiratory measurements were made after the horses were anesthetized, during surgical manipulations involving skin or tissues other than nerves, during manipulation and transection of digital nerves, and after surgery while the limbs were being bandaged. Heart rate was significantly higher in horses anesthetized with halothane only than in horses that also received detomidine; there were no other differences in hemodynamic function or recovery characteristics. Respiratory rate was significantly higher than baseline during soft tissue and nerve manipulations; arterial blood pressure was significantly higher after surgery began and highest during neurectomy; cardiac output and cardiac index were significantly decreased during surgery; systemic vascular resistance was significantly increased during neurectomy and bandaging and highest during neurectomy. The data suggest that the increase in blood pressure often associated with surgical stimulation is caused by increased vascular resistance and may be accompanied by a decrease in cardiac output.

Analgesics↗