Effects Of Inhalation Anesthetics Research Articles

The impact of drugs used in anaesthesia on bacteria

The impact of drugs used in anaesthesia on bacteria

Contribution of peripheral chemoreception to the depression of the hypoxic ventilatory response during halothane anesthesia in cats.

The effects of inhalational anesthetics on the hypoxic ventilatory response are complex. This study was designed to determine the contribution of peripheral chemoreception to the depression of hypoxic ventilatory response seen with halothane anesthesia. Cats were anesthetized with pentobarbital sodium and alpha-chloralose and artificially ventilated. Respiratory output was evaluated by phasic inspiratory activity of the phrenic nerve. In 12 cats, this activity was measured during inhalation of an hypoxic gas mixture with halothane, 0, 0.1, and 0.8%, with intact or denervated carotid bodies. In 10 cats, a carotid body was isolated from the systemic circulation and perfused with hypoxic Krebs-Ringer solution equilibrated with halothane, 0, 0.1, and 0.8%. The hypoxic ventilatory response was depressed in a dose-dependent manner during halothane anesthesia. In carotid body perfusion studies, the response was significantly depressed only with halothane, 0.80%. The hypoxic ventilatory response is depressed by a high dose of halothane through a peripheral effect at the carotid body.

63 Effect of inhalational anesthesia on cerebral blood flow in Moyamoya Disease

63 Effect of inhalational anesthesia on cerebral blood flow in Moyamoya Disease

Effects of inhalational anesthetics on α2-adrenergic signaling in isolated platelets

(1) The hypothesis that inhalational anesthetics affect G-protein linked α 2 adrenergic signaling pathway was investigated using human platelets as a model system. (2) α 2 receptor stimulation by UK-14304, a potent and selective agonist, inhibits cAMP production induced by prostaglandin I 2 (PGI 2). (3) Brief stimulation (30 s) with PGI 2 raised cAMP levels in platelets by 25-fold; UK-14304 suppressed the PGI 2 stimulus by 80%. (4) Halothane at fractional minimum alveolar concentration (MAC) through super physiological levels (16 MAC) had no effect on basal or prostacyclin stimulated levels of cAMP, nor did it have any effect on the inhibition of cAMP production by UK-14304. Moreover, isoflurane, enflurane and sevoflurane had no significant effect on cAMP production at 1.5 or 8 MAC. The results suggest α 2 and PGI 2 signaling pathways are not sensitive to volatile anesthetics including the α 2 or PGI 2 receptor/G-protein complex, G-protein/adenylyl cyclase complex and adenylyl cyclase itself. (5) The possibility that halothane and related anesthetics act more distally in the pathway, on cAMP-dependent protein kinase (PKA), was investigated by measuring the phosphorylation pattern of endogenous platelet proteins by PKA. (6) An increase in the [ 32P]phosphate incorporation was observed in platelets exposed to either, low doses of PGI 2 or isobutylmethylxanthine (IBMX). Halothane, isoflurane, enflurane or sevoflurane further increased the level of [ 32P]-incorporation. The apparent increase in PKA activity suggests that at least in platelets, volatile anesthetics activate PKA-dependent pathways which should antagonize α 2 adrenergic signaling.

Effect of inhalational anesthesia on cerebral circulation in Moyamoya Disease

Effect of inhalational anesthesia on cerebral circulation in Moyamoya Disease

Extreme hemodilution. Effects of inhalation anesthetics, hypoxia, and blood loss. An experimental study in pigs

Acta Anaesthesiologica ScandinavicaVolume 42, Issue 8 p. 1021-1022 Extreme hemodilution. Effects of inhalation anesthetics, hypoxia, and blood loss. An experimental study in pigs H. Schou, H. Schou Department of Anesthesia and Intensive Care, University Hospital, S-221 85, Lund ISBN91-628–2488–0Search for more papers by this author H. Schou, H. Schou Department of Anesthesia and Intensive Care, University Hospital, S-221 85, Lund ISBN91-628–2488–0Search for more papers by this author First published: 31 December 2008 https://doi.org/10.1111/j.1399-6576.1998.tb05368.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume42, Issue8September 1998Pages 1021-1022 RelatedInformation

Effects of inhalation anaesthetics on the release of acetylcholine in the rat cerebral cortex in vivo

By analysing the EEG, reticular multi-unit activity and behavioural changes, we have classified general anaesthetics into three groups: central nervous system (CNS) depressant, CNS excitant and epileptogenic agents. Changes in CNS neural activity are associated with alteration in transmitter release. We have attempted to clarify the actions of widely used inhalation anaesthetics, such as isoflurane (CNS depressant), nitrous oxide (CNS excitant) and sevoflurane (epileptogenic) on acetylcholine (ACh) release in the cerebral cortex using brain microdialysis. ACh release was suppressed by isoflurane and sevoflurane in a dose-related manner but recovered on wash-out. There were no significant differences between the effects of sevoflurane and isoflurane at the same MAC values. In contrast, ACh release was enhanced significantly by nitrous oxide. These findings indicate that the response of the cortical cholinergic cells to different anaesthetics reflects their neurophysiological characteristics, that is whether they stimulate or suppress CNS neurones.

INHALATIONAL ANESTHETICS AND CONTROL OF BREATHING DURING HYPOXIA

The ventilatory response to hypoxia is an important reflex in ensuring that adequate respiratory gas exchange takes place. Knill and Gelb 22 were the first to point out how sensitive the hypoxic ventilatory response is to suppression by inhalational anesthetics in humans. More recent observations have extended and amplified their pioneering work. This article first reviews the physiology of the hypoxic ventilatory response, including the occurrence of hypoxic ventilatory decline that occurs when hypoxia is prolonged beyond approximately 5 minutes. The interaction of the hypoxic response with behavioral pathways is discussed. Secondly, the effects of inhalational anesthetics on the hypoxic response are discussed.

Effect of inhalation anaesthetics on the phase behaviour, permeability and order of phosphatidylcholine bilayers

We have used differential scanning calorimetry and fluorescence anisotropy measurements to investigate the effect of five inhalation anaesthetics of diverse chemical structure (halothane, enflurane, n-pentane, chloroform and diethylether) on the phase behaviour of liposomes prepared from dimyristoylphosphatidylcholine (DMPC) and dipalmitoylphosphatidylcholine (DPPC), respectively. The incorporation of these anaesthetics induced a decrease of the phase transition temperature and/or a broadening of the phase transition peak depending on the transverse localisation of the investigated anaesthetic. At high anaesthetic concentrations we observed the disappearance of the pretransition peak and the appearance of a shoulder on the main phase transition peak due to the domain formation of the anaesthetics. An anaesthetic induced carboxyfluorescein efflux from the vesicle lumen was completed within a few minutes after the addition of the anaesthetics, probably resulting from a transient formation of membrane holes. All results are discussed with regard to the physicochemical properties of the anaesthetics applied.

Inhalation anesthetics suppress the expression of c-Fos protein evoked by noxious somatic stimulation in the deeper layer of the spinal cord in the rat

The effects of inhalation anesthetics, nitrous oxide (N 2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat. The expression of c-Fos protein was detected by immunocytochemistry following the injection of formalin (5%, 100 μl) into the plantar surface of the left hindpaw. After 15 min of halothane (F) anesthesia, the anesthetics was switched to 40% or 70% of N 2O, 0.5% or 1.5% of F or room air (for control) immediately following the formalin injection. Two hours later the rats were sacrificed and perfused. Sections of the L4 level of spinal cord were immunostained with anti c-Fos antibody. We counted the number of Fos-like immunoreactive (FLI) cells in every specific lamina as follows; superficial layer (laminae I and II), nucleus proprius (laminae III and IV), neck of the dorsal horn (laminae V and VI) and ventral gray (laminae VII–X). Then we compared the results of each category of sample. Both N 2O and halothane suppressed the expression of c-Fos in the neck of the dorsal horn and ventral gray in a dose-dependent manner, but no effects were seen at the superficial layer or nucleus proprius. Suppression of c-Fos expression was greater under N 2O than halothane anesthesia. This finding suggests that N 2O had a stronger analgesic effect than halothane. The current study indicates that inhalation anesthetics do not act equally on every kind of spinal neurons. Both N 2O and halothane have effects on spinal neurons in the deeper layers but not on the neurons existed in laminae I–II, some of which directly receive noxious inputs. Pretreatment with 2 mg/kg of naloxone, which completely reversed the effects of morphine, did not alter the effect of 70%N 2O, suggesting that the analgesic effect of N 2O is not mediated by an intrinsic opioid mechanism at the spinal cord level. ©1977 Elsevier Science B.V. All rights reserved.

Effects of Inhalational Anesthetics on Contractile Responses and Nitric Oxide Synthase Activity in Endotoxemic Rats

Background : Recent studies revealed that inhalational anesthetics(IA) attenuate NO production. But the hemodynamic changes produced by IA in septic syndrome patient are still sufficient to threaten patient, surgeon and anesthesiologist. So we examined which IA is proper to maintain vascular contractile force and evaluated the effects of NOS inhibitors on contractile force of septic rat aorta under IA. Methods : Aortic ring preparation was obtained from LPS-treated(1.5 mg/kg, i.p. for 18h) rats. The development of sepsis was confirmed by iNOS activity and iNOS expression using RT-PCR. Contractile responses of aorta to phenylephrine admministation in the presence or absence of halothane, enflurane and isoflurane were evaluated. We also evaluated the effects of NOS inhibitors, one is NG-nitro-L-arginine methyl ester(L-NAME) and the other is aminoguanidine. Statistical significances(p<0.05) were analyzed according to data characteristics by unpaired t-test and paired t-test. Results : The contractile responses to phenylephrine admministration were attenuated in LPS-treated rings. Isoflurane, even at the dose of 2 MAC, didn''t affect the contractile response while both halothane and enflurane decreased the contractile response even at the dose of 1 MAC. The potentiation of contractile responses by NOS inhibitors were not affected during administeration of IA. Conclusions : From these results, it is suggested that isoflurane is the safest inhalational anesthetic and NOS inhibitors, especially L-NAME, may be very useful in the therapy of septic shock patients during general anesthesia. (Korean J Anesthesiol 1997; 33: 204∼214)

Effect of inhalational anesthetics on dynorphin mRNA expression in spinal dorsal horn neurons after noxious stimuli

Our internal casein kinase 1ε lead inhibitor, compound 1 was partially cleared by the polymorphic cytochrome P450 2D6. CYP2D6 involvement in metabolism implies more extensive clinical trials. We therefore wanted to reduce the contribution to clearance by this enzyme. We utilized metabolism reports for compound 1 performed in recombinant CYP2D6 together with structure-metabolism variation in structures of closely related analogs in order to see if we could incorporate similar substitution patterns in our lead compound. In addition, we utilized a previously established docking method using a modified CYP2D6 crystal structure to see if the metabolism patterns in CYP2D6 could be reproduced to afford the metabolites in the metabolism reports as well as those for the compounds used in the structure-metabolism relationship. All three of these steps, the metabolism report, the establishment of structure-metabolism relationships and the docking, lead to compound 10 where CYP2D6 was not involved in the clearance pathways.

Pulmonary vascular effects of isoflurane anesthesia after left lung autotransplantation in chronically instrumented dogs.

Single lung transplantation has become a viable therapy for treatment of end-stage pulmonary disease. We previously observed that left lung autotransplantation (LLA) results in a chronic increase in pulmonary vascular resistance and enhanced pulmonary vascular reactivity to sympathetic alpha adrenoreceptor activation. The effects of inhalational anesthetics on the pulmonary circulation after lung transplantation have not been investigated. In the current study, the authors tested the hypothesis that isoflurane anesthesia, known to cause systemic vasodilation, would exert a vasodilator influence on the baseline pulmonary circulation after LLA. In addition, they tested the hypothesis that isoflurane anesthesia, known to attenuate the systemic vasoconstrictor response to sympathetic alpha adrenoreceptor agonists, would reduce the magnitude of the pulmonary vasoconstrictor response to sympathetic alpha adrenoreceptor activation after LLA. Left pulmonary vascular pressure-flow (LPQ) plots were generated in chronically instrumented dogs by measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during inflation of a hydraulic occluder implanted around the right main pulmonary artery. Left pulmonary vascular pressure-flow plots were generated in 8 dogs 2-5 weeks after LLA in the conscious and isoflurane-anesthetized states at baseline, after beta adrenoreceptor block with propranolol, and during the cumulative administration of the alpha agonist, phenylephrine. Left pulmonary vascular pressure-flow plots also were generated in eight conscious, sham-operated control dogs at baseline, after beta block, and during phenylephrine administration. Compared with conscious control dogs, LLA resulted in a leftward shift (P < 0.01) in the baseline left pulmonary vascular pressure-flow relation, indicating chronic pulmonary vasoconstriction. Despite the enhanced level of pulmonary vasomotor tone after LLA, isoflurane did not exert a vasodilator influence on the baseline left pulmonary vascular pressure-flow relation. The pulmonary vasoconstrictor response to phenylephrine was enhanced (P < 0.01) after LLA compared with the response measured in conscious control dogs. The magnitude of the pulmonary vasoconstrictor response to phenylephrine after LLA was not attenuated during isoflurane anesthesia. Isoflurane anesthesia does not exert a vasodilator influence on the pulmonary circulation in the setting of increased pulmonary vascular resistance after LLA. In addition, in contrast to previous studies of the systemic circulation, isoflurane does not attenuate the enhanced pulmonary vasoconstrictor response to sympathetic alpha adrenoreceptor activation after LLA.

Sevoflurane anesthesia maintains reflex tachycardia on position change from supine recumbent to head-up tilt.

This study evaluated the effects of inhalational anesthetics on hemodynamic changes in response to head-up tilt in humans. Twenty-four patients were randomly divided into three groups that received either halothane, isoflurane, or sevoflurane. Changes in heart rate, blood pressure, and plasma norepinephrine concentrations were determined before and during head-up tilt position in the awake and anesthetized state. Head-up tilt caused a significant increase in the heart rate, concomitantly with a decrease or no significant changes in systolic blood pressure in the awake state. However, under 2 minimum alveolar concentrations (MAC) of halothane and isoflurane anesthesia, the heart rate did not significantly change during head-up tilt in spite of significant decreases in systolic blood pressure. In contrast, under 2 MAC of sevoflurane anesthesia, the heart rate significantly increased during head-up tilt. Plasma norepinephrine did not significantly alter during head-up tilt in the awake as well as the anesthetized state. These results suggest that sevoflurane maintains an increase in heart rate in response to head-up tilt, whereas halothane and isoflurane attenuate the response.

Effects of inhalation anesthetics on kainate-induced glutamate release from cerebellar granule cells

The mechanisms of inhalation anesthesia may include inhibiting non-NMDA excitatory amino acid neurotransmission. This possibility was addressed by measuring the effect of three anesthetics at clinically relevant concentrations on kainate-induced glutamate release from cerebellar granule cells. Cerebellar granule cells were obtained from 8-day-old SD rats and maintained in vitro for 9–14 days. Medium glutamate concentrations were measured by HPLC after 90 minutes incubation with kainate or NMDA. Inhalation anesthetics were introduced by holding the cells under a continuous flow of air/anesthetic mixtures. All anesthetics tested did not effect NMDA-induced glutamate release. Halothane (1 MAC), isoflurane (1 MAC) inhibited kainate-induced glutamate release from the cultured cells whereas enflurane (1 MAC) had no effect on kainate-induced glutamate release. The difference between enflurane and the other anesthetics tested suggests that anesthesia is dependent on more than one process and the extent at which each function is perturbed is dependent on the specific anesthetic used. Halothane inhibition of kainate-induced glutamate release was not reversible by increasing kainate concentration, indicating halothane does not directly compete with kainate at its receptor.

各種吸入麻酔薬による犬の縮胞性免疫機能への影響

各種吸入麻酔薬による犬の縮胞性免疫機能への影響

Patch clamp techniques to study effects of anesthetics on airway smooth muscle cells

Inhalation anesthetics have a direct relaxant effect on airway smooth muscle. Recent research has done much to clarify the cellular mechanisms for contraction and relaxation in airway smooth muscles and has suggested a possible mechanism of action for inhalation anesthetics in these muscles [1,2]. As in other muscle cells, the free intracellular concentration of CaZ+([Ca2+]i ) plays a central role in regulation of airway smooth muscle tone [3]. Yamakage [1] demonstrated that relaxation of precontracted tracheal smooth muscle by halothane was associated with a decrease in [Ca2+]i . Because sustained contraction of this tissue requires the continued entry of e x t r a c e l l u l a r Ca 2+, a possible mechanism for the airway relaxant effect of inhalation anesthetics is inhibition of voltage-dependent Ca > channels (VDC) [4]. Patch clamp techniques provide a means for directly studying properties of membrane ion channels [5]. Applications of these methods to airway smooth muscle cells have demonstrated a variety of K + and Ca 2+ channels that are likely of functional importance [6,7]. One patch clamp method, whole-cell recording, is particularly useful for quantifying Ca 2+ current (Ic,) through VDC. In this report, we describe the results of a preliminary study that demonstrates inhibition by enflurane of Ica in isolated airway smooth muscle cells. Porcine tracheal smooth muscle, dissected free of epithelium and connective tissue, was minced. The tissue fragments were digested in Ca2+-free Tyrode's solution containing 0.1% collagenase, 0.05% trypsin

Effects of Inhalation Anesthetics on Myocardial and Hepatic Energy Metabolism in Normotensive and Spontaneously Hypertensive Rats Subjected to Hemorrhage

Forty spontaneously hypertensive rats (SHRs) and forty normotensive Wistar-ST rats (NRs) were used to assess the influence of anesthetics on myocardial and hepatic energy metabolism after hemorrhage. They were divided into five pairs of groups: a control group (pentobarbital 6 mg.100 g BW-1 ip), and four others which received 1.2% halothane, 2.2% enflurane, 1.4% isoflurane, and 3.3% sevoflurane, respectively. Following a 10 min stabilization period, blood (2 ml.100 g BW-1) was gradually withdrawn over a 5 min period from a femoral artery. Thirty min after the induction of hemorrhage, the heart and liver were removed and myocardial and hepatic metabolites (ATP, lactate, pyruvate and glycogen) were measured by enzymatic methods. There were no significant differences in myocardial metabolites among either the anesthetic groups or between SHRs and NRs. However, hepatic ATP levels in all SHR groups were significantly lower than those in NR groups. Moreover, ATP levels in the inhalation anesthetic groups of SHRs were significantly higher than that in the control group of SHRs. All inhalation anesthetics, especially isoflurane, may reduce metabolic deterioration of the liver during hemorrhage when compared to barbiturate anesthesia.

Effects of inhalation anesthetics on myocardial and hepatic energy metabolism in normotensive and spontaneously hypertensive rats subjected to hemorrhage

Forty spontaneously hypertensive rats (SHRs) and forty normotensive Wistar-ST rats (NRs) were used to assess the influence of anesthetics on myocardial and hepatic energy metabolism after hemorrhage. They were divided into five pairs of groups: a control group (pentobarbital 6 mg.100 g BW-1 ip), and four others which received 1.2% halothane, 2.2% enflurane, 1.4% isoflurane, and 3.3% sevoflurane, respectively. Following a 10 min stabilization period, blood (2 ml.100 g BW-1) was gradually withdrawn over a 5 min period from a femoral artery. Thirty min after the induction of hemorrhage, the heart and liver were removed and myocardial and hepatic metabolites (ATP, lactate, pyruvate and glycogen) were measured by enzymatic methods. There were no significant differences in myocardial metabolites among either the anesthetic groups or between SHRs and NRs. However, hepatic ATP levels in all SHR groups were significantly lower than those in NR groups. Moreover, ATP levels in the inhalation anesthetic groups of SHRs were significantly higher than that in the control group of SHRs. All inhalation anesthetics, especially isoflurane, may reduce metabolic deterioration of the liver during hemorrhage when compared to barbiturate anesthesia.

The Effects of Inhalational Anesthetics on Memory and Cognitive Function

The Effects of Inhalational Anesthetics on Memory and Cognitive Function