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PubMedDate not supplied

Physiologic mechanisms by which local anesthetics may cause injury to nerve and spinal cord.

OBJECTIVE: Review evidence for possible physiologic mechanisms by which local anesthetics cause nerve injury was reviewed. METHODS: Published clinical case reports, and both in vivo and in vitro experimental studies in animals, were reviewed. Reports with direct bearing on possible mechanisms of local anesthetic neurotoxicity were included. RESULTS: There is basic and clinical evidence that local anesthetics can cause nerve injury. Nerve injury may result from direct toxicity to the axon or Schwann cell, or may be secondary to disruption of the nerve microenvironment. Although each of these possibilities is supported by published experiments, injury to the axon is the most likely explanation for persistent neurologic deficits, such as those believed to result from clinical use of local anesthetics. Whether the injury is direct or indirect, and the precise mechanism by which it occurs, has received only limited study. CONCLUSIONS: In rare instances, the clinical use of local anesthetics is associated with neurologic morbidity. The physiologic mechanisms of toxicity for which there is the best evidence are inhibition of fast axonal transport, disruption of the axonal cytoskeleton, axonal degeneration, and ischemic nerve injury. The effects of local anesthetics on nerve blood flow may be related to inhibition of endothelium-dependent vasodilation or interruption of the synthesis of vasodilating prostaglandins. Both the prevention and the treatment of nerve injury caused by local anesthetics requires information that is not yet available about the physiologic and molecular mechanisms for direct neural toxicity of local anesthetics.

Anesthetics, Local↗

PubMed1996

Binding of the volatile anesthetic halothane to the hydrophobic core of a tetra-alpha-helix-bundle protein.

Although volatile general anesthetics interact with several proteins, little is known about the location or characteristics of the binding sites at the molecular level. A detailed structural description of how anesthetics associate with macromolecules is necessary for understanding anesthetic mechanisms of action. The recent introduction of designed synthetic proteins provides new opportunities for obtaining structural and functional information on anesthetic-protein interactions. A synthetic tetra-alpha-helix-bundle protein was used to examine the interaction of halothane with a designed protein interior. The tetra-alpha-helix-bundle comprises 124 residues in the form of two identical 62-residue di-alpha-helical peptides, held together in an all-parallel bundle by hydrophobic forces. Steady-state and time-resolved tryptophan fluorescence and circular dichroism spectroscopy were used to study the anesthetic-protein interaction. Halothane quenches bundle tryptophan fluorescence with a dissociation constant of 2.3 +/- 0.4 mM and a Hill number of 0.9 +/- 0.1. Tryptophan fluorescence decay analysis indicates that halothane quenches the protein fluorescence by a static mechanism. Circular dichroism spectroscopy revealed no change in protein secondary structure on exposure to halothane. Dissociation of the tetra-alpha-helix-bundle into 62-residue di-alpha-helical peptides by trifluoroethanol eliminated the halothane-protein interaction. The results suggest that halothane binds to the hydrophobic interior of the tetra-alpha-helix-bundle, close to the tryptophan residues. The protein tertiary and quaternary structures are required for anesthetic binding. This study demonstrates the feasibility of using synthetic tetra-alpha-helix-bundles as model anesthetic-binding proteins. The use of de novo designed bundle proteins should allow structural, energetic and functional descriptions of anesthetic-protein interactions.

Amino Acid Sequence↗

PubMed1996

[Evaluation of vaporizers by anesthetic gas monitors corrected with a new method for preparation of calibration gases].

For resolving the discrepancy of concentrations found among anesthetic gas monitors, the author proposed a new method using a vaporizer as a standard anesthetic gas generator for calibration. In this method, the carrier gas volume is measured by a mass flow meter (SEF-510 + FI-101) installed before the inlet of the vaporizer. The vaporized weight of volatile anesthetic agent is simultaneously measured by an electronic force balance (E12000S), on which the vaporizer is placed directly. The molar percent of the anesthetic is calculated using these data and is transformed into the volume percent. These gases discharging from the vaporizer are utilized for calibrating anesthetic gas monitors. These monitors are normalized by the linear equation describing the relationship between concentrations of calibration gases and readings of the anesthetic gas monitors. By using normalized monitors, flow rate-concentration performance curves of several anesthetic vaporizers were obtained. The author concludes that this method can serve as a standard in evaluating anesthetic vaporizers.

Anesthetics, Inhalation↗

PubMed1976

Influence of anesthetic agent on survival following hemorrhage.

One hundred and twenty-eight Sprague-Dawley rats were each anesthetized with one of four anaesthetics and subjected to a standard hemorrhage protocol to determine the effects of anesthetics on survival following hemorrhage. The anesthetics studied were: halothane, 1.26 vol per cent; fluroxene, 4.5 vol per cent; pentobarbital, 50 mg/kg ip; ketamine, 125 mg/kg, im. Mean arterial pressure was conrolled at 40 torr during 60 minutes of hemorrhage. Cumulative survival rates were determined at the end of hemorrhage and 24 hr, 48 hr, 72 hr, and 7 days after hemorrhage. Twenty-four-hour survival rates were: halothane, 50.0 per cent; fluroxene, 56.3 per cent; pentobarbital, 59.4 per cent; ketamine, 84.4 per cent. Seven-day survival rates were: halothane, 46.9 per cent; fluroxene, 18.7 per cent; pentobarbital, 53.1 per cent; ketamine; 81.3 per cent. Survival rates were significantly higher (P less than 0.05) in animals anesthetized with ketamine compared with survival rates associated with the other anesthetics. Long-term (72-hr and seven-day) survival rates were significantly (P less than 0.05) lower in animals anesthetized with fluroxene. Microscopic examination of livers and small intestines revealed significantly fewer (P less than 0.05) athologic changes in the splanchnic organs of hemorrhaged rats anesthetized with ketamine compared with animals anesthetized with the other drugs.

Anesthetics↗

PubMed1998

[Cardiocirculatory effects of intravenous anesthetic induction in an experimental model of acute hypovolemia].

OBJECTIVE: To evaluate the cardiovascular effects of ketamine, midazolam, thiopentone and propofol in acutely hypovolemic pigs and to determine whether the association of ketamine and midazolam offers any advantage. PATIENTS AND METHODS: Twenty-two Landrace-Large-White pigs. After monitoring was begun, acute hypovolemia was induced by means of rapid exsanguination of 30% of calculated volume. Hemodynamic variables were measured: a) at baseline; b) after exsanguination; c) 2 min after anesthetic induction; d) 10 min after anesthetic induction, and e) after reinfusion of the exsanguinated volume. RESULTS: All pressures, cardiac output, cardiac index, and mixed venous oxygen saturation fell significantly with the induction of hypovolemia. Heart rate, systemic vascular resistances and arteriovenous oxygen differential increased. Ten min after anesthetic induction, heart rate in the midazolam group was significantly lower than in the ketamine-midazolam group. Arterial pressures decreased significantly after anesthetic induction with all drugs. The decrease in systolic arterial pressure was smaller in thiopenthal-anesthetized pigs than in pigs receiving either midazolam or propofol at the 10 min recording. The decrease in mean arterial and diastolic pressure after 10 min was smaller with thiopental than with any other drug. The decrease in mean arterial pressure was less in the thiopental and ketamine-midazolam groups than in the others after reinfusion. Diastolic arterial pressure at 10 min and after reinfusion had decreased less in the thiopental and ketamine-midazolam groups than in the propofol group. After anesthetic induction, the post-hypovolemic figures for cardiac output and cardiac index held steady or changes were slightly accentuated, with no statistically significant differences among the groups. CONCLUSIONS: The intravenous anesthetics evaluated were detrimental to cardiovascular function in acute hypovolemic pigs. Low-dose thiopental and ketamine plus midazolam may be the anesthetics of choice in this setting. Propofol caused the greatest degree of hemodynamic instability.

Acute Disease↗

PubMed1992

Interactions between volatile anesthetics and dipalmitoyl phosphatidylcholine liposomes as studied by fluorometry with a thiacarbocyanine dye.

The effects of volatile anesthetics on the properties of dipalmitoyl phosphatidylcholine liposome were investigated by fluorescence spectroscopy with a thiacarbocyanine dye (3,3"-dioctadecyl-2,2"-thiacarbocyanine) which is sensitive to the viscosity and the dielectric constant of the environment. Seven volatile anesthetics, halothane, enflurane, isoflurane, methoxyflurane, sevoflurane, diethylether and chloroform were used. All anesthetics decreased the phase transition temperature of the liposome and increased the effective dielectric constant of the water-liposome interface. The increase of the effective dielectric constant was attributed to the release of the hydrated water molecules from the membrane surface. The increment of the effective dielectric constant depended on the thermodynamic activity of anesthetics in the solution, and was not affected seriously by the kind of anesthetics. On the other hand, the degree of the depression of the phase transition temperature depended on the molar concentrations of anesthetics. Considering from the Ferguson's report, which is dealt with the relationship between the physiological effect and the thermodynamic activity, the effect of anesthetics on the effective dielectric constant of the membrane surface is more correlated to the anesthetic action than the effect on the phase transition temperature.

Journal Article↗

PubMed1988

Interactions of the local anesthetic tetracaine with membranes containing phosphatidylcholine and cholesterol: a 2H NMR study.

The interactions of the local anesthetic tetracaine with multilamellar dispersions of 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and cholesterol have been investigated by deuterium nuclear magnetic resonance of specifically deuteriated tetracaines, DMPC and cholesterol. Experiments were performed at pH 5.5, when the anesthetic is primarily charged, and at pH 9.5, when it is primarily uncharged. The partition coefficients of the anesthetic in the membrane have been measured at both pH values for phosphatidylcholine bilayers with and without cholesterol. The higher partition coefficients obtained at pH 9.5 reflect the hydrophobic interactions between the uncharged form of the anesthetic and the hydrocarbon region of the bilayer. The lower partition coefficients for the DMPC/cholesterol system at both pH values suggest that cholesterol, which increases the order of the lipid chains, decreases the solubility of tetracaine into the bilayer. For phosphatidylcholine bilayers, it has been proposed [Boulanger, Y., Schreier, S., & Smith, I. C. P. (1981) Biochemistry 20, 6824-6830] that the charged tetracaine at low pH is located mostly at the phospholipid headgroup level while the uncharged tetracaine intercalates more deeply into the bilayer. The present study suggests that the location of tetracaine in the cholesterol-containing system is different from that in pure phosphatidylcholine bilayers: the anesthetic sits higher in the membrane. An increase in temperature results in a deeper penetration of the anesthetic into the bilayer. Moreover, the incorporation of the anesthetic into DMPC bilayers with or without cholesterol results in a reduction of the lipid order parameters both in the plateau and in the tail regions of the acyl chains, this effect being greater with the charged form of the anesthetic.

Cholesterol↗

PubMed1981

Anesthetic doses blocking adrenergic (stress) and cardiovascular responses to incision--MAC BAR.

The reaction to stress, while vital to the conscious animal, may be detrimental to the surgical patient. To assess the stress-ablating action of different anesthetics (halothane, enflurane, morphine, and spinal) and anesthetic doses, we studied the responses in plasma norepinephrine, muscle movement, pupil diameter, heart rate, and blood pressure to induction of anesthesia and incision in 170 unpremedicated healthy adults. The age-adjusted dose (mean +/- SD) of anesthesia that blocked the adrenergic response in 50 per cent of individuals who had a skin incision (MAC BAR) was 1.45 +/- 0.08 MAC for halothane, 1.60 +/- 0.13 MAC for enflurane, or 1.13 +/- 0.09 +/- mg/kg for morphine sulfate (each anesthetic was given with 60 per cent nitrous oxide). No patient with a level of spinal anesthesia that blocked the pain of incision had an adrenergic response to incision. Increasing doses of halothane and morphine were associated with less of a cardiovascular response to incision (as measured by rate-pressure product); this was not true for enflurane. No patient with an adequate level of spinal anesthesia had a cardiovascular response to skin incision. The changes in heart rate, blood pressure, rate-pressure product, and plasma norepinephrine content that occurred with induction of anesthesia tended to equalize these values between patients, regardless of anesthetic dose, and for all individual and combined anesthetics. That is, if a patient's heart rate while awake was below 63 beats/min, heart rate tended to rise 58 per cent of the difference between heart rate while awake and 63 beats/min, and vice versa. Similarly, the change in blood pressure with induction averaged 75 per cent of the difference between systolic blood pressure while awake and 88 torr. The average for the change in rate-pressure product with induction was 79 per cent of the difference between rate-pressure product while awake and 5917 torr.beats/min. It was concluded that all the anesthetics tested can prevent the neuroendocrine response to skin incision at clinically attainable doses. Thus, comparisons of neuroendocrine stress during surgery require quantitation of anesthetic dose. If adverse effects of surgery are related to the neuroendocrine stress that surgical manipulations induce, the hypothesis "the less anesthetic the better" may be wrong.

Adolescent↗

PubMed1986

Actions of general anesthetics on acetylcholine receptor-rich membranes from Torpedo californica.

The molecular mechanisms by which general anesthetics act on postsynaptic membranes can only be worked out in a highly purified, homogeneous system. The nicotinic acetylcholine receptor-rich membranes from the electric tissue of Torpedo californica are currently the only postsynaptic membranes that fulfill this condition. Is this peripheral synapse acted on with a pharmacologic specificity similar to that for general anesthesia, and how much less sensitive is it to anesthetic action than the unknown central site? To answer these questions, the authors studied the effects of 13 anesthetic compounds, including volatile general anesthetics, alkanols, and urethane, on the equilibrium binding of 3H-acetylcholine to these nicotinic receptors. As the anesthetic concentration was raised, all the agents first increased acetylcholine binding steeply and then, with few exceptions, decreased it again at higher concentrations. Anesthetics increased acetylcholine binding by decreasing acetylcholine's dissociation constant without changing the Hill coefficient or the number of sites. To a first approximation, the relative ability of these agents to increase 3H-acetylcholine binding parallels that of anesthesia in vivo as predicted by the Meyer-Overton lipid solubility rule. On average, they produced half maximal increases in acetylcholine binding (EC50) at about four times the concentration that causes loss of righting reflex in one-half of a group of animals (ED50). However, a few agents deviated from this relationship. They were the agents with greatest general anesthetic potency in both the volatile anesthetic series (thiomethoxyflurane) and the normal alcohol series (octanol), and required up to 17 times their ED50s to achieve a half effect on acetylcholine binding. Although the concentrations required were high, these effects were reversible.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Octanol↗

PubMed1988

Ca2+ uptake and Ca2+ release by skeletal muscle sarcoplasmic reticulum: differing sensitivity to inhalational anesthetics.

The effects of halothane, enflurane, and isoflurane were measured on two different mechanisms of Ca2+ regulation by isolated skeletal muscle sarcoplasmic reticulum (SR) membranes. A 100,000-dalton Ca2+-ATPase protein transports Ca2+ from outside to inside the SR membrane. At concentration ranges representing anesthetic levels of 0.06 to 2.3 times MAC, halothane, enflurane, and isoflurane each increased rate of Ca2+ uptake by SR. Each concentration of isoflurane produced a greater rate of Ca2+ uptake, whereas halothane and enflurane produced maximum stimulation of Ca2+ uptake at 1 and 1.6 times MAC, respectively. The second Ca2+ regulation mechanism studied was a Ca2+ release channel in the SR membrane. The release of Ca2+ via this mechanism requires a critical threshold Ca2+ load (nmol Ca2+/mg SR protein) for Ca2+-induced Ca2+ release to occur. Each anesthetic tested effectively lowered the critical Ca2+ load threshold for Ca2+ release, i.e., the Ca2+ channel was more readily induced to an open state in the presence of anesthetic. The concentrations of anesthetics having this effect on the putative Ca2+ channel were between 0.0026 and 0.078 MAC equivalents for each agent, and these concentrations are much lower than the anesthetic concentrations affecting Ca2+ uptake. These data show that in isolated skeletal muscle SR membranes a Ca2+ channel release function is altered at anesthetic concentrations far below those that change Ca2+ uptake function by a Ca2+-ATPase and below concentrations of the volatile agents producing clinical anesthesia. The Ca2+ channel effect may represent protein-anesthetic interaction, whereas the Ca2+-ATPase effect may occur by a generalized SR membrane perturbation by the anesthetics.

Anesthesiology↗

PubMed1990

Volatile anesthetic effects on left ventricular relaxation in swine.

The effects of halothane (0.5, 1.0, and 1.5%; n = 10), enflurane (1.0, 2.0, and 3.0%; n = 8), and isoflurane (0.75, 1.5, and 2.25%; n = 8) on isovolumic relaxation were studied in open-chest swine. The time constant for isovolumic left ventricular pressure decline, T, was determined at each anesthetic concentration at the intrinsic heart rate and during atrial pacing to 150 beats per min. The effect of increased left ventricular afterload on T was investigated by partial occlusion of the thoracic aorta to raise the left ventricular systolic pressure to baseline in the presence of volatile anesthetics, and 20% above baseline in the absence of volatile anesthetics. Heart rate and left ventricular systolic pressure decreased substantially with all three anesthetics, whereas left ventricular end-diastolic pressure increased (by 3-4 mmHg). Relaxation time constants increased with all three anesthetics at the intrinsic heart rate; when the heart rate was controlled by pacing, T increased in the halothane and enflurane, but not in the isoflurane, experiments. T was significantly prolonged (by 30-100%) by partial aortic occlusion in the presence of anesthetic, but not in the control measurements. T did not change significantly in the isoflurane experiments when atrial pacing was employed with partial aortic occlusion. The volatile anesthetics, particularly halothane, seem to impair the relaxation process of the left ventricle; further investigation of the mechanisms of this interference, such as anesthetic effects on intracellular calcium movement and total left ventricular load, is warranted.

Animals↗

PubMed1994

Humans anesthetized with sevoflurane or isoflurane have similar arrhythmic response to epinephrine.

BACKGROUND: Anesthetics can alter the dose of exogenously administered epinephrine that causes cardiac arrhythmias. The purpose of this study was to test the hypothesis that in humans anesthetized with sevoflurane, the arrhythmic response to epinephrine is not different from the response in humans anesthetized with isoflurane. METHODS: We determined the arrhythmogenicity of submucosally administered epinephrine in 40 ASA physical status 1 or 2 patients who were to undergo transsphenoidal surgery. Patients were assigned randomly to be given 1.0-1.3 minimum alveolar concentration sevoflurane or isoflurane. A surgeon, blinded to the anesthetic and the concentration of epinephrine, injected into the nasal submucosa epinephrine 10, 13.3, or 20 micrograms/ml in saline of volume sufficient for surgical need. We defined a "positive" response as three or more premature ventricular contractions within 5 min after initiation of injection. Responses between anesthetic groups within each dose range of epinephrine were compared by chi-squared analysis. RESULTS: No patient given either anesthetic developed premature ventricular contractions with doses of epinephrine less than 5 micrograms/kg. At larger doses of epinephrine (5-9.9 and 10-14.9 micrograms/kg), the frequency of arrhythmias did not differ between patients given sevoflurane and patients given isoflurane. Patients anesthetized with 1.2 minimum alveolar concentration sevoflurane had blood pressure similar to and heart rate less than those of patients anesthetized with similar concentrations of isoflurane. Blood pressure and heart rate were increased similarly in both groups after laryngoscopy and tracheal intubation and after epinephrine injection. CONCLUSIONS: Sevoflurane and isoflurane do not differ in their sensitization of the human myocardium to the arrhythmogenic effect of exogenously administered epinephrine.

Adult↗

PubMed1995

Volatile anesthetic actions on contractile proteins in membrane-permeabilized small mesenteric arteries.

BACKGROUND: Volatile anesthetics have been shown to have vasodilating or vasoconstricting actions in vitro that may contribute to their cardiovascular effects in vivo. However, the precise mechanisms of these actions in vitro have not been fully elucidated. Moreover, there are no data regarding the mechanisms of volatile anesthetic action on small resistance arteries, which play a critical role in the regulation of blood pressure and blood flow. METHODS: With the use of isometric tension recording methods, volatile anesthetic actions were studied in intact and beta-escin-membrane-permeabilized smooth muscle strips from rat small mesenteric arteries. In experiments with intact muscle, the effects of-halothane (0.25-5.0%), isoflurane (0.25-5.0%), and enflurane (0.25-5.0%) were investigated on high K(+)-induced contractions at 22 degrees C and 35 degrees C. All experiments were performed on endothelium-denuded strips in the presence of 3 microM guanethidine and 0.3 microM tetrodotoxin to minimize the influence of nerve terminal activities. In experiments with membrane-permeabilized muscle, the effects of halothane (0.5-4.0%), isoflurane (0.5-4.0%), and enflurane (0.5-4.0%) on the half-maximal and maximal Ca(2+)-activated contractions were examined at 22 degrees C in the presence of 0.3 microM ionomycin to eliminate intracellular Ca2+ stores. RESULTS: In the high K(+)-stimulated intact muscle, all three anesthetics generated transient contractions, which were followed by sustained vasorelaxation. The IC50 values for this vasorelaxing action of halothane, isoflurane, and enflurane were 0.47 vol% (0.27 mM), 0.66 vol% (0.32 mM), and 0.53 vol% (0.27 mM), respectively, at 22 degrees C and were 3.36 vol% (0.99 mM), 3.07 vol% (0.69 mM), and 3.19 vol% (0.95 mM), respectively, at 35 degrees C. Ryanodine (10 microM) eliminated the anesthetic-induced contractions but had no significant effect on the anesthetic-induced vasorelaxation in the presence of high K+. In addition, no significant differences were observed in the dose dependence of the direct vasodilating action among these anesthetics with or without ryanodine at either the low or the high temperature. However, significant differences were observed in the vasoconstricting actions among the anesthetics, and the order of potency was halothane > enflurane > isoflurane. The Ca(2+)-tension relation in the membrane-permeabilized muscle yielded a half-maximal effective Ca2+ concentration (EC50) of 2.02 microM. Halothane modestly but significantly inhibited 3 microM (approximately the EC50) and 30 microM (maximal) Ca(2+)-induced contractions. Enflurane slightly but significantly inhibited 3 microM but not 30 microM Ca2+ contractions. Isoflurane did not significantly inhibit either 3 microM or 30 microM Ca2+ contractions. CONCLUSIONS: Halothane, isoflurane, and enflurane have both vasoconstricting and vasodilating actions on isolated small splanchnic resistance arteries. The direct vasoconstricting action appears to result from Ca2+ release from the ryanodine-sensitive intracellular Ca2+ store. The vasodilating action of isoflurane in the presence of high K+ appears to be attributable mainly to a decrease in intracellular Ca2+ concentration, possibly resulting from inhibition of voltage-gated Ca2+ channels. In contrast, the vasodilating actions of halothane and enflurane in the presence of high K+ appears to involve inhibition of Ca2+ activation of contractile proteins as well as a decrease in intracellular Ca2+ concentration in smooth muscle.

Animals↗

PubMed1991

Does the anesthetic technique influence the postoperative analgesic requirement?

In order to determine the effect of two standard general anesthetic techniques on the postoperative analgesic requirement, 53 adults undergoing elective intra-abdominal surgery were randomly assigned to one of two anesthetic treatment groups according to an open parallel protocol design. One of the groups received an opioid-based anesthetic; the other group was administered an inhaled anesthetic. The postoperative analgesic requirement was quantified using a Baxter PCA device. The group receiving the opioid-based anesthetic required significantly less morphine in the recovery room (5.7 +/- 5.5 mg; mean +/- SD) compared with those receiving the conventional inhaled anesthetic (16.6 +/- 7.1 mg). During the first 8 hours after discharge from the recovery room there was a trend toward higher PCA morphine usage in the inhaled anesthetic group (25.6 +/- 15 mg vs. 18.6 +/- 13 mg); however, this difference was not statistically significant (p = 0.08). From 8 to 40 hours after surgery, the morphine usage was nonsignificantly higher in the opioid group (64 +/- 30 mg vs. 56 +/- 38 mg, p = 0.43). In conclusion, the general anesthetic technique used during an elective operation appeared to have little if any effect on the postoperative analgesic requirement after discharge from the recovery room.

Abdomen↗

PubMed2005

Anesthetics and brain toxicity.

PURPOSE OF REVIEW: Recent experimental data from rodent studies have demonstrated accelerated neurodegeneration in rat pups exposed to commonly used anesthetic drugs. These provocative findings certainly question and undermine the safe use of anesthetic drugs, particularly in pediatric anesthesia, and have prompted many to investigate the neurotoxic effect of anesthetic drugs on the developing brain. This review will address the scientific evidence for the anesthetic-induced neurotoxicity and its applicability in humans. RECENT FINDINGS: Several investigators have shown that prolonged administration of anesthetic drugs, including ketamine, isoflurane, nitrous oxide and midazolam, produced increased neurodegeneration in 7-day-old rat pups. The combination of the latter three drugs led to altered learning behavior in adulthood. Despite these unequivocal findings in rodents, similar changes cannot be reproduced in other species. Furthermore, withholding anesthesia during painful procedures in neonatal rats resulted in significant long-term aberrant responses to sensory stimulation and pain thresholds. SUMMARY: Taken together, these studies question the applicability of these data to the anesthetic management of the neonate. Further investigations in this area are needed before withholding anesthetics in the anesthetic management of pediatric surgical patients.

Journal Article↗

PubMed2006

Anesthetic management of morbidly obese and super-morbidly obese patients undergoing bariatric operations: hospital course and outcomes.

BACKGROUND: Although the implications for the anesthetic and perioperative care of severely obese patients undergoing weight loss operations are considerable, current anesthetic management of super-obese (SO) patients (BMI > or =50 kg/m(2)), including super-super-obese (BMI > or =60) derives from experience with morbidly obese (MO) patients (BMI 40-49.9 kg/m(2)). We compared anesthetic and perioperative data of SO patients and MO patients undergoing weight loss operations to evaluate if anesthetic management influenced outcome. METHODS: A retrospective analysis was performed on data from 150 consecutive patients (119 MO, 31 SO) undergoing bariatric surgery between May 2000 and March 2005. Data analyzed included preoperative anesthetic assessment, anesthetic management, postoperative care, and intra- or postoperative complications. RESULTS: There were no differences in anesthetic management or in postoperative course or outcome between MO and SO patients. Intraoperative surgical complications occurred in 26% (n=8) in the SO group and 14% (n=15) in the MO group (P<0.01). CONCLUSIONS: No differences in outcome occurred between MO and SO patients undergoing bariatric operations under similar anesthetic management. Anesthesia for weight loss surgery can be safely performed on SO patients with the understanding that these patients are not at risk per se due to their higher BMI. The degree of obesity influenced only the incidence of intraoperative surgical complications.

Adult↗

PubMed1992

[Comparison of anesthetic morbidity and mortality before and after the implementation of quality assurance in Tri-Service General Hospital].

The desire to improve anesthetic outcome is a cornerstone in modern anesthesia. There are many means to reach this goal, such as enforcement in personal training, elevation of monitoring standards, constant vigilance and stern quality assurance (QA). The department of Anesthesiology, Tri-Service General Hospital, has adopted the QA program and implemented it since March 1, 1990. Because there were no significant differences in terms of personnel training, monitoring standards and types of anesthesia and surgery before and after the application of QA program, we investigated the effects of QA on anesthetic major morbidity and coma/mortality. We analyzed the anesthetic results obtained in two separate periods respectively spanning from Jan. 1, 1989 to Dec. 31, 1989 and from Mar. 1, 1990 to Feb. 28, 1991. During the first two months of 1990, the department's personnel were trained to be familiar with the QA program. We compared the anesthetic major morbidity and coma/mortality of one year before the implementation of QA with those in a one-year period after its implementation. Before and after enforcement of QA, there were no significant differences (p greater than 0.05) regarding major morbidity and coma/mortality, but the rates of anesthetic complications were lower after the practice of QA program. Since the functions of QA was aimed at alerting the anesthetic personnel to keep constant vigilance over the act of anesthesia, QA in theory could reduce anesthetic accidents and mishaps related jointly to surgery and anesthesia. The reason why QA did not decrease anesthetic major morbidity and coma/mortality in this study may be due to limited number of anesthesia in relatively short period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

[Psychopathology of endogenous anesthetic depression].

Studies of the psychopathological structure of anesthetic depressions in 60 patients with attack-like progressive schizophrenia made it possible to distinguish three types of depressive conditions: anxious-anesthetic with agitation, melancholic-anesthetic with a characteristic depressive triad, self-accusation ideas and adynamic disorders and pure-anesthetic ones where psychic anesthesia was the most significant manifestation of the depressive condition with immaterial intensity of other symptoms of depression. In anxious-anesthetic depressions, psychic anesthesia was characterized by primarily sensual character (little differentiated sensation of internal emptiness), whereas in pure-anesthetic depressions, it was marked by primarily ideational character (sensation of inferiority of different sides of emotional life); in melancholic-anesthetic depressions, psychic anesthesia was sensual-ideational in nature and was the main plot for self-accusation ideas. A number of regularities were revealed in the dynamics of anesthetic depression attacks to establish that the types of depressive conditions described previously were stages in the development of an attack.

Adult↗