Effects Of Halothane Anesthesia Research Articles

Comparison of Effects of Halothane Anaesthesia in Horses with and Without Dexmedetomidine Continuous Rate Infusion

Comparison of Effects of Halothane Anaesthesia in Horses with and Without Dexmedetomidine Continuous Rate Infusion

From the Journal archives: A harbinger of modern anesthesia

From the discovery of anesthesia in 1846 until the 1960s, anesthetic investigations focused largely on the management of clinical problems. The 1960s saw increasing attention to the dose-related effects of anesthesia on the vital processes of the body. Investigators interested in anesthesia developed tools for defining anesthetic kinetics (what the body does to anesthetics) and comparative pharmacodynamic effects (the relative effects of what anesthetics do to the body). In 1968, the Canadian Journal of Anaesthesia published an article by Tsutomu Oyama (1923-2008) et al. entitled ‘‘Effects of halothane anaesthesia and surgery on adrenocortical function in man’’, which is an exemplar presaging the expansion of pharmacodynamic studies. Before the 1960s, relatively little was known of the effects of anesthetics on the body, in this case, specifically the release of free corticosteroids, such as, 17hydroxycorticosteroids (17-OHCS), especially in humans. Oyama opened a new window.

Effects of Halothane Anesthesia in Unilateral Nephrectomized Dog: Histopathological and Biochemical Findings

Effects of Halothane Anesthesia in Unilateral Nephrectomized Dog: Histopathological and Biochemical Findings

Pressor and intra-renal effects of angiotensins I and II, and noradrenaline, in anaesthetized and conscious sheep: The effects of halothane anaesthesia on pressor sensitivity and electrolyte shifts: the proposed use of angiotensin I in treating septicaemia and septic shock

The pressor and intra-renal actions and effects of octa - and deca-peptides angiotensins II and I and of the catecholamine noradrenaline, in anaesthetized and conscious sheep, are considered. The halothane anaesthetic substantially lowers pressor sensitivity to both peptides but does not influence their ability to liberate K(+) ions into the circulating plasma. In comparison with angiotensin II, both angiotensin I and noradrenaline -- with direct presentation to the kidney -- are ineffective in decreasing intra-renal blood flow. However, with left ventricular injection, both pressor compounds immediately increase the blood pressure, as does angiotensin II. Combined doses of the decapeptide and catecholamine are thus highly effective in raising the blood pressure while having a minimal effect on blood flow through the kidney. This overall situation could provide a basis for treating clinical shock, especially regarding septicaemia and septic shock. The lowered hind-limb blood flow, with administration of the pressor compounds into the femoral artery, contrasts strongly with the raised flow resulting from intravenous injection. Experimental procedures to establish, or otherwise, relevant hypothetical situations are detailed.

Halothane attenuated haloperidol and enhanced clozapine-induced dopamine release in the rat striatum

The effect of halothane anesthesia on changes in the extracellular concentrations of dopamine (DA) and its metabolites (3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA)) induced by neuroleptics was studied using in vivo microdialysis techniques. Halothane attenuated haloperidol-induced dopamine release and enhanced clozapine-induced dopamine release in the rat striatum. A microdialysis probe was implanted into the right striatum of male SD rats. Rats were given saline or the same volume of 200 μg kg −1 haloperidol (D 2 receptor antagonist), 10 mg kg −1 sulpiride (D 2 and D 3 antagonist), or 10 mg kg −1 clozapine (D 4 and 5-HT 2 antagonist) intraperitoneally with or without 1-h halothane anesthesia (0.5 or 1.5%). Halothane anesthesia did not change the extracellular concentration of DA, but increased the metabolite concentrations in a dose-dependent manner. The increased DA concentration induced by haloperidol was significantly attenuated by halothane anesthesia, whereas the metabolite concentrations were unaffected. Halothane had no effect on the changes in the concentrations of DA or its metabolites induced by sulpiride. The clozapine-induced increases in DA and its metabolites were enhanced by halothane anesthesia. Our results suggest that halothane anesthesia modifies the DA release modulated by antipsychotic drugs in different ways, depending on the effects of dopaminergic or serotonergic pathways.

Effects of halothane anaesthesia on the cryopreservation of epididymal spermatozoa in pony stallions.

Effects of halothane anaesthesia on the cryopreservation of epididymal spermatozoa in pony stallions.

Effect of Halothane Anesthesia on Glucose Utilization and Production in Adolescents

SBAI, D.; JOUVET, P.; SOULIER, A.; PÉNICAUD, L.; MERCKX, J.; BRESSON, J. L.; Zarmsky, Roxanne M.D. Author Information

Halothane anesthesia and serum electrolytes

The disparate observations on the effect of halothane anesthesia on the serum electrolyte levels in humans prompted us to carry out this work. In this study the levels of sodium, potassium, magnesium, calcium, chloride and inorganic phosphorus were determined in serum of 25 male and 15 female patients, with an age range of 15 to 40 years, who had various pathologies requiring surgery and who were given halothane anesthesia. Significant difference were detected in the concentrations of sodium, potassium, calcium and inorganic phosphorus between presurgical and post-anesthesia induction samples. The truly striking finding in the present study was the significant increase in serum inorganic phosphorus in the intra-operative period. It is suspected that this increase is due to a defect in phosphorylating mechanisms which leads to a rapid hydrolysis of stored and preformed ATP.

Liver function and halothane‐diethyl‐ether azeotrope anaesthesia

A general anaesthetic drug that fulfils requirements for use under difficult circumstances is the inhalation agent halothane-diethyl-ether (HE) azeotrope. Although both halothane and diethyl ether have been described in detail, their effect on the liver when given together as an azeotrope has not been systematically characterised. The effect on liver function was evaluated and compared with the effects of halothane anaesthesia (H) and spinal anaesthesia with tetracaine (S), the last named serving as controls. The series consisted of 33 healthy men (ASA 1-2) receiving no medication and scheduled for inguinal hernia repair. The patients were randomly allocated to receive HE, H or S. The following parameters were estimated the day before surgery and on the first postoperative day: liver cell metabolism (bile acids, unconjugated bilirubin), cell integrity (aminotransferases), synthesizing capacity (Prothrombin complex), cholestasis (conjugated bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase), and global liver function (chenodeoxycholic load test). No major differences emerged between the groups. Unconjugated bilirubin was increased in all groups. Prothrombin complex activity was reduced in all groups. Conjugated bilirubin was increased in the H group. The oral bile acid load test and the fasting bile acid were unaltered by anaesthesia in all groups. No major impact on liver cell function was seen in the early post-operative period after HE azeotrope anaesthesia. The findings support our view that HE azeotrope could be considered as an alternative anaesthetic agent under field conditions.

Effects of anaesthesia and recent surgery on diastolic function

The aims were to determine the effects and the extent to which halothane anaesthesia affects diastolic function both immediately after and remote from surgery and to investigate whether the effect is due to alterations in loading conditions. Eight mongrel dogs were studied under halothane anaesthesia (0.5-1.5 end tidal vol%) with the chest closed, after acute instrumentation with left ventricular pressure transducers, left atrial and aortic catheters, and left ventricular diameter and wall thickness crystals. The same dogs were then studied in the fully conscious state, 2-3 weeks later. An additional four dogs were studied in the conscious state and then again under halothane anaesthesia remote from acute instrumentation. The left ventricular isovolumetric relaxation time constant, tau, as well as myocardial and chamber stiffness constants were used as indices of diastolic function. Following halothane anaesthesia and recent surgery, tau was prolonged significantly compared to the conscious state, at 30(SEM 1) v 22(1) ms (p < 0.01), but there were no changes in either myocardial or chamber stiffness. While tau remained sensitive to increased heart rate and enhanced contractility and was prolonged by increasing afterload in both the anaesthetised and conscious states, it was consistently prolonged following halothane anaesthesia and recent surgery even at matched levels of contractile states, heart rates and loading conditions, compared to the conscious state, at 26(1) v 19(1) ms (p < 0.01). When the effects of halothane anaesthesia were examined after full recovery from surgery, tau was still prolonged under halothane anaesthesia, at 29(2) v 20(1) ms (p < 0.01), compared to the conscious state, but in contrast to the findings following halothane anaesthesia and recent surgery, it was fully normalised [19(1) v 19(1) ms] when contractile state and loading conditions were matched. Left ventricular diastolic function is influenced markedly by halothane anaesthesia and recent surgery, and to a degree comparable to many pathological states. The effects of halothane anaesthesia and recent surgery appear to prolong the isovolumetric relaxation time constant independently of heart rate, contractility, and loading conditions and are most likely to be due to the combined direct effects of anaesthetics and acute instrumentation.

Halothane as an Anesthetic for Fetal Surgery

Halothane has become the preferred anesthetic agent during fetal surgery because it can be administered via maternal inhalation and it improves surgical exposure by relaxing the uterus. However, the effects of halothane anesthesia on fetal cardiovascular homeostasis during fetal surgery have not been documented. In 10 pregnant ewes, inhalation halothane anesthesia was administered and their fetuses were instrumented for cardiovascular evaluation. During a 1-hour period we evaluated the acute effects of halothane anesthesia on fetal hemodynamics, arterial blood gases, cardiac output, placental blood flow, total vascular resistance, systemic vascular resistance, and placental vascular resistance. Fetal cardiac output and placental blood flow were determined by the radiolabelled microsphere technique and resistances were calculated using pressure and flow data. These findings were compared to both the results we obtained in 15 fetal sheep anesthetized with the maternal administration of intravenous ketamine, and to the accepted values found in nonanesthetized, chronically instrumented fetal sheep. Our findings indicate that with halothane anesthesia during fetal surgery fetal cardiac output and placental blood flow significantly decrease, and total vascular resistance increases. Placental vascular resistance increases out of proportion to systemic vascular resistance, resulting in the shunting of blood away from the placenta. The combination of decreased cardiac output and increased shunting of blood away from the placenta causes depressed respiratory gas exchange. These findings are not present with other anesthetic agents. Halothane has significant negative effects on both the fetal heart and the peripheral vasculature which disrupt fetal cardiovascular homeostasis. Halothane is a poor anesthetic during fetal intervention.

Tyrosine hydroxylase activity in the locus coeruleus of conscious rats: Differences with the anesthetized rats

Microdialysis was used to estimate in vivo tyrosine hydroxylase (TH) activity in locus coeruleus (LC) of conscious rats. An aromatic amino acid decarboxylase inhibitor, difluoromethyl-DOPA (DFMD), was perfused through the dialysis probe and the DOPA accumulating in dialysates was measured. A 3 h perfusion of a 6 × 10 −4 mol/ l DFMD solution was needed to obtain measurable levels of DOPA in LC dialy sates: a linear increase in DOPA concentrations was first observed and, then, a steady state. DOPA disappeared completely after inhibition of TH by α-methyl-p-tyrosine, showing that it reflects TH activity. The DFMD perfusion needed in this study was six times higher in concentration and three times longer in duration than the one required in a previous study we performed in LC of anesthetized rats. Furthermore, TH activity was found lower than the one we previously reported. We conclude that these differences could be explained by the effects of halothane anesthesia on DFMD and DOPA degradation and/or on LC neurons TH activity itself.

Effects of halothane anesthesia on vasoconstrictor response to NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthesis, in sheep.

This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in chronically instrumented, halothane-anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P < 0.05) in both groups. However, L-NAME produced a sharp increase in mean arterial and pulmonary artery pressures only in the control group, whereas the pressor response in the halothane group was attenuated. Cardiac output, which was significantly lower after L-NAME administration in both groups, increased after L-arginine. The results suggest that halothane does not significantly alter the EDRF/NO-mediated effects on the vasculature but potentiates the cardiac depressant effect of L-NAME.

Halothane-associated enhancement of the secondary immune response to sheep erythrocytes in mice: cell transfer studies.

The effect of halothane anesthesia on the humoral immune response to sheep red blood cells was studied in mice immunized twice, with a 15-day interval. On both occasions, mice were exposed to 1.5% halothane for 40 min immediately after sensitization. Halothane reexposure resulted in increased numbers of IgG-secreting cells (IgG-SC) as well as circulating 7S-serum agglutinins. To examine further whether this effect could be obtained in syngeneic recipients, adoptive transfer experiments employing spleen cells were performed. While mice receiving cells from unimmunized and anesthetized donors displayed significantly higher levels of IgG-SC, recipients of cells from normal, immunized and immunized-anesthetized donors showed a depressed response when compared to control counterparts. Besides the possibility of an enhancing effect of halothane reexposure on the humoral response, this procedure may counteract normal physiological immunoregulatory processes during the generation of the immune response.

Halothane Inhibits the Intraalveolar Recruitment of Neutrophils, Lymphocytes, and Macrophages in Response to Influenza Virus Infection in Mice

The effect of halothane anesthesia on the influenza A specific immune response and the pathogenesis of infection was evaluated in mice. Three-wk-old CD-1 mice were anesthetized with either 2% halothane for 2 h or ketamine (100 mg/kg intraperitoneally) and subsequently inoculated intranasally with a sublethal dose of influenza type A/PR/8/34 virus. Bronchoalveolar lavage was performed on animals from each group at 4 h postinoculation and daily thereafter for 14 days. Total and differential white blood cell counts were measured in the lavage fluid and the lungs were examined histologically for evidence of injury. Infected mice anesthetized with halothane had lower daily cell counts in the lung than animals anesthetized with ketamine and a marked change in cell type distribution. On Days 4 and 11 postinoculation, there were significantly (P < 0.05) more white blood cells in the lavage fluid of animals anesthetized with ketamine than halothane (mean/mL, 738,000 +/- SEM, 128,000 vs 196,000 +/- 51,400, respectively, and 1,020,000 +/- 227,000 vs 117,000 +/- 34,600, respectively). Differential counts were significantly higher (P < 0.05) in the ketamine group compared to the halothane for neutrophils on Day 4 (452,000 +/- 77,900 vs 72,000 +/- 46,000, respectively) and on Day 11 for lymphocytes (340,000 +/- 59,000 vs 33,000 +/- 17,000, respectively) and macrophages (480,000 +/- 120,000 vs 130,000 +/- 61,000). Infected mice that were given ketamine were qualitatively "sicker" than the halothane-treated group as evidenced by the appearance of ruffled fur, tachypnea, and cachexia. Animals anesthetized with ketamine demonstrated a greater degree of pulmonary histopathology including diffuse infiltration of macrophages, neutrophils, hemorrhage, and fibrin deposition.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Halothane Anesthesia on Lower Esophageal Contractility

The Effect of Halothane Anesthesia on Lower Esophageal Contractility

An Experimental Study on the Effects of Halothane Anesthesia on the Hepatic Function of Rats Pretreated with Ethyl Alcohol

An Experimental Study on the Effects of Halothane Anesthesia on the Hepatic Function of Rats Pretreated with Ethyl Alcohol

Effects of Halothane Anesthesia on Radial Arterial Waveform : A power spctral approach

Effects of Halothane Anesthesia on Radial Arterial Waveform : A power spctral approach

An in vivo microdialysis characterization of extracellular dopamine and GABA in dorsolateral striatum of awake freely moving and halothane anaesthetised rats

This study describes the results of a systematic characterization of extracellular dopamine (DA) and γ-aminobutyric acid (GABA) recovered from dorsolateral striatum using in vivo microdialysis in rats following acute (2.5 h) and chronic (1 day, 2 day and 4 day) implantation of the probe. The voltage and calcium dependence of DA and GABA overflow was characterised by perfusion with the sodium channel blocker tetrodotoxin (TTX 10-6M) and with Ca 2+-free Ringers perfusion medium. In addition, the effect of halothane anaesthesia on the responsiveness of these neurotransmitter substances to TTX and Ca 2+-free perfusion medium was investigated. Perfusion with TTX decreased basal DA levels by at least 60% in all groups. The TTX-induced decrease was most profound in halothane-anaesthetised rats, 24 h after implantation of the probe. Responsiveness of GABA to TTX infusion was different between the groups. In acutely implanted halothane-anaesthetised rats basal GABA levels were unaltered by perfusion with TTX while in the remaining groups at least a 35% reduction was observed. In awake rats 2 days following implantation of the probe removal and replacement of the Ca 2+ from the perfusion medium resulted in a reversible reduction of basal DA by 87%. In addition, basal GABA levels were decreased by 52%. This decrease was delayed and was not reversed 1.5 h after the Ca 2+-free perfusion medium was replaced with normal perfusion medium although basal GABA levels returned to pre-experimental levels by the following day. The present study demonstrates that the responsiveness of striatal DA and GABA to manipulations of both voltage-dependent (TTX) and vesicular release (Ca 2+-free perfusion) is influenced by the length of time elapsed after the implantation of the dialysis fiber and the conscious state of the animal.

Effects of halothane anaesthesia on extracellular levels of dopamine, dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindolacetic acid in rat striatum: a microdialysis study

The effects of halothane anaesthesia on striatal extracellular levels of dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5HIAA) were investigated in microdialysis experiments. Induction of anaesthesia was accompanied by a rapid increase in dopamine levels and a slower increase in DOPAC and HVA. 5HIAA was not affected. The reduction of dopamine levels induced by apomorphine 0.05 mg/kg appeared with a shorter latency in conscious rats than in anaesthetised rats but the maximum decrease was unaffected by anaesthesia. The decreases in dopamine and DOPAC induced by alpha-methyl-p-tyrosine 50 mg/kg were affected in opposite directions by halothane: the dopamine reduction was more pronounced while the DOPAC reduction was less pronounced in anaesthetized than in conscious animals. In no case was a qualitative shift in the response observed. It is concluded that halothane may influence the levels of dopamine as well as the response to dopaminergic drugs.