Background: Halothane and Isoflurane are two frequent inhalation agents used as maintenance anesthesia during surgery. After experiencing anesthesia, many patients experience decreased hemodynamic ...status as pressure blood, respiration, and pulse. Because that study this expected could determine proper anesthesia for use.
Purpose : evaluates differences in hemodynamic status post-anesthesia consequence use of halothane and isoflurane.
Method research: Study this is a study with quasi pre-post design experiment with a control group design. The sample study is all patients undergoing Installation Surgery at Sele Be Solu Hospital, Sorong City, which uses the general anesthesia technique with inhalation of halothane or isoflurane for as many as 21 people. Instrument study use sheet observation to measure pressure, blood, respiration, and pulse During surgery.
Research Results: The Wilcoxon test obtained a score of 0.157 on the pressure blood respondent after getting anesthesia halothane and respondents after getting anesthesia isoflurane, i.e., 0.007. significance of 1.000 and 0.317 on pulse respondents who got anesthesia halothane and isoflurane. Significance of 1.000 and 0.083 on respiration respondents who got anesthesia halothane and isoflurane. Mann Whitney test shows changes in blood pressure, pulse, and respiration in anesthetized respondents who used halothane and isoflurane score significance of 0.784, 0.576, and 0.307.
Conclusion: There is a difference in blood pressure at first and end anesthesia use of isoflurane. No, there is a difference in frequency pulse, initial pulse, and respiration anesthesia, and end anesthesia use isoflurane.No there is a difference in pressure blood, pulse, and respiration at the beginning and end anesthesia use halothane. There is no difference in blood pressure, pulse, and respiration after general anesthesia uses isoflurane and halothane.
Background
Sevoflurane is an inhaled volatile anaesthetic that is widely used in paediatric anaesthetic practice. Since its introduction, postoperative behavioural disturbance known as emergence ...agitation (EA) or emergence delirium (ED) has been recognized as a problem that may occur during recovery from sevoflurane anaesthesia. For the purpose of this systematic review, EA has been used to describe this clinical entity. A child with EA may be restless, may cause self‐injury or may disrupt the dressing, surgical site or indwelling devices, leading to the potential for parents to be dissatisfied with their child's anaesthetic. To prevent such outcomes, the child may require pharmacological or physical restraint. Sevoflurane may be a major contributing factor in the development of EA. Therefore, an evidence‐based understanding of the risk/benefit profile regarding sevoflurane compared with other general anaesthetic agents and adjuncts would facilitate its rational and optimal use.
Objectives
To compare sevoflurane with other general anaesthetic (GA) agents, with or without pharmacological or non‐pharmacological adjuncts, with regard to risk of EA in children during emergence from anaesthesia. The primary outcome was risk of EA; secondary outcome was agitation score.
Search methods
We searched the following databases from the date of inception to 19 January 2013: CENTRAL, Ovid MEDLINE, Ovid EMBASE, the Cumulative Index to Nursing and Allied Health Literature (CINAHL) (EBSCOhost), Evidence‐Based Medicine Reviews (EBMR) and the Web of Science, as well as the reference lists of other relevant articles and online trial registers.
Selection criteria
We included all randomized (or quasi‐randomized) controlled trials investigating children < 18 years of age presenting for general anaesthesia with or without surgical intervention. We included any study in which a sevoflurane anaesthetic was compared with any other GA, and any study in which researchers investigated adjuncts (pharmacological or non‐pharmacological) to sevoflurane anaesthesia compared with no adjunct or placebo.
Data collection and analysis
Two review authors independently searched the databases, decided on inclusion eligibility of publications, ascertained study quality and extracted data. They then resolved differences between their results by discussion. Data were entered into RevMan 5.2 for analyses and presentation. Comparisons of the risk of EA were presented as risk ratios (RRs) with 95% confidence intervals (CIs). Sevoflurane is treated as the control anaesthesia in this review. Sensitivity analyses were performed as appropriate, to exclude studies with a high risk of bias and to investigate heterogeneity.
Main results
We included 158 studies involving 14,045 children. Interventions to prevent EA fell into two broad groups. First, alternative GA compared with sevoflurane anaesthesia (69 studies), and second, use of an adjunct with sevoflurane anaesthesia versus sevoflurane without an adjunct (100 studies). The overall risk of bias in included studies was low. The overall Grades of Recommendation, Assessment, Development and Evaluation Working Group (GRADE) assessment of the quality of the evidence was moderate to high. A wide range of EA scales were used, as were different levels of cutoff, to determine the presence or absence of EA. Some studies involved children receiving potentially inadequate or no analgesia intraoperatively during painful procedures.
Halothane (RR 0.51, 95% CI 0.41 to 0.63, 3534 participants, high quality of evidence) and propofol anaesthesia were associated with a lower risk of EA than sevoflurane anaesthesia. Propofol was effective when used throughout anaesthesia (RR 0.35, 95% CI 0.25 to 0.51, 1098 participants, high quality of evidence) and when used only during the maintenance phase of anaesthesia after sevoflurane induction (RR 0.59, 95% CI 0.46 to 0.76, 738 participants, high quality of evidence). No clear evidence was found of an effect on risk of EA of desflurane (RR 1.46, 95% CI 0.92 to 2.31, 408 participants, moderate quality of evidence) or isoflurane (RR 0.76, 95% CI 0.46 to 1.23, 379 participants, moderate quality of evidence) versus sevoflurane.
Compared with no adjunct, effective adjuncts for reducing the risk of EA during sevoflurane anaesthesia included dexmedetomidine (RR 0.37, 95% CI 0.29 to 0.47, 851 participants, high quality of evidence), clonidine (RR 0.45, 95% CI 0.31 to 0.66, 739 participants, high quality of evidence), opioids, in particular fentanyl (RR 0.37, 95% CI 0.27 to 0.50, 1247 participants, high quality of evidence) and a bolus of propofol (RR 0.58, 95% CI 0.38 to 0.89, 394 participants, moderate quality of evidence), ketamine (RR 0.30, 95% CI 0.13 to 0.69, 231 participants, moderate quality of evidence) or midazolam (RR 0.57, 95% CI 0.41 to 0.81, 116 participants, moderate quality of evidence) at the end of anaesthesia. Midazolam oral premedication (RR 0.81, 95% CI 0.59 to 1.12, 370 participants, moderate quality of evidence) and parental presence at emergence (RR 0.91, 95% CI 0.51 to 1.60, 180 participants, moderate quality of evidence) did not reduce the risk of EA.
One or more factors designated as high risk of bias were noted in less than 10% of the included studies. Sensitivity analyses of these studies showed no clinically relevant changes in the risk of EA. Heterogeneity was significant with respect to these comparisons: halothane; clonidine; fentanyl; midazolam premedication; propofol 1 mg/kg bolus at end; and ketamine 0.25 mg/kg bolus at end of anaesthesia. With investigation of heterogeneity, the only clinically relevant changes to findings were seen in the context of potential pain, namely, the setting of adenoidectomy/adenotonsillectomy (propofol bolus; midazolam premedication) and the absence of a regional block (clonidine).
Authors' conclusions
Propofol, halothane, alpha‐2 agonists (dexmedetomidine, clonidine), opioids (e.g. fentanyl) and ketamine reduce the risk of EA compared with sevoflurane anaesthesia, whereas no clear evidence shows an effect for desflurane, isoflurane, midazolam premedication and parental presence at emergence. Therefore anaesthetists can consider several effective strategies to reduce the risk of EA in their clinical practice. Future studies should ensure adequate analgesia in the control group, for which pain may be a contributing or confounding factor in the diagnosis of EA. Regardless of the EA scale used, it would be helpful for study authors to report the risk of EA, so that this might be included in future meta‐analyses. Researchers should also consider combining effective interventions as a multi‐modal approach to further reduce the risk of EA.
Halothane, a commonly used anesthetic can simultaneously function as a hydrogen‐bond and a halogen‐bond donor in the solid state and in solution, as shown by S. V. Rosokha, G. Resnati, and co‐workers ...in their Communication on page 12456 ff. Both interactions involve moieties commonly present in cell membranes, probable target structures of halothane in the human body. The ability of the agent to act as a polydentate tecton gives a molecular rationale for its eudismic ratio.
The α7 nicotinic acetylcholine receptor (nAChR), assembled as homomeric pentameric ligand-gated ion channels, is one of the most abundant nAChR subtypes in the brain. Despite its importance in ...memory, learning and cognition, no structure has been determined for the α7 nAChR TM domain, a target for allosteric modulators. Using solution state NMR, we determined the structure of the human α7 nAChR TM domain (PDB ID: 2MAW) and demonstrated that the α7 TM domain formed functional channels in Xenopus oocytes. We identified the associated binding sites for the anesthetics halothane and ketamine; the former cannot sensitively inhibit α7 function, but the latter can. The α7 TM domain folds into the expected four-helical bundle motif, but the intra-subunit cavity at the extracellular end of the α7 TM domain is smaller than the equivalent cavity in the α4β2 nAChRs (PDB IDs: 2LLY; 2LM2). Neither drug binds to the extracellular end of the α7 TM domain, but two halothane molecules or one ketamine molecule binds to the intracellular end of the α7 TM domain. Halothane and ketamine binding sites are partially overlapped. Ketamine, but not halothane, perturbed the α7 channel-gate residue L9′. Furthermore, halothane did not induce profound dynamics changes in the α7 channel as observed in α4β2. The study offers a novel high-resolution structure for the human α7 nAChR TM domain that is invaluable for developing α7-specific therapeutics. It also provides evidence to support the hypothesis: only when anesthetic binding perturbs the channel pore or alters the channel motion, can binding generate functional consequences.
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•The NMR structure of the human α7 nAChR TM domain (TMD) was determined.•Intra-subunit anesthetic binding sites were found at the IC end of the TMD by NMR.•Ketamine but not halothane binding perturbed the channel gate residue L9′.•Whether binding perturbs the channel gate correlates with the functional effect.•The α7 structure is invaluable for designing α7-specific therapeutics.
The objective of this study was to determine if ractopamine (RAC) impacts postmortem muscle metabolism and subsequent pork quality in Halothane (HAL) and Rendement Napole (RN) mutant pigs. All RAC ...fed pigs had increased (P < 0.04) L* values. HAL and RN mutants muscle had lower (P < 0.01) pH values but RAC feeding had no effect. RN mutants had higher and lower (P < 0.05) muscle pH and temperatures, respectfully at 15 min and RN mutant pigs had greater (P < 0.0001) glycogen initially but lactate levels similar to wild type (WT) pigs at 24 h. RAC lowered (P < 0.05) glycogen in RN mutants but not in HAL mutated or WT pig muscle. These data show RAC feeding changes postmortem energy metabolism but does not change pH and pork quality hallmark of two major pig gene mutations and supports our contention that ultimate meat quality traits and their biochemical drivers may be more complex than originally reasoned.
The induction of ischemic stroke in the experimental model requires general anesthesia. One of the factors that can be effective in the size of ischemic brain lesions and neurological outcomes is the ...type of anesthesia. So, the current study was designed to compare the impacts of the most important and widely used anesthetics including halothane, isoflurane, and chloral hydrate on the transient middle cerebral artery occlusion (MCAO) outcomes. Adult Male Sprague-Dawley rats were randomly divided into three groups as follows: (1) MCAO + halothane group, (2) MCAO + isoflurane group, and (3) MCAO + chloral hydrate group. After 24 h, the mortality rate, infarct size, tissue swelling, neurological function, hemodynamic, and arterial blood gas parameters were assessed. Our finding showed that 60 min MCAO rats anesthetized with chloral hydrate significantly increased mortality rate, infarct size, tissue swelling, and neurological deficits compared with halothane and isoflurane anesthetics after 24 h of MCAO. Also, chloral hydrate caused a significant decrease in mean arterial pressure and arterial pO2 compared to halothane and isoflurane anesthetics. On the basis of the current data, we concluded that chloral hydrate increased cerebral infarct volume and neurological outcomes and reduced hemodynamic and metabolic parameters compared with halothane and isoflurane-anesthetized rats temporal MCAO.
The halothane hepatitis that was not Mizobe, Toshiki
British journal of anaesthesia,
January 2020, 2020-01-00, Letnik:
124, Številka:
1
Journal Article
General anesthetic drugs have been associated with various unwanted effects including an interference with mitochondrial function. We had previously observed increases of lactate formation in the ...mouse brain during anesthesia with volatile anesthetic agents. In the present work, we used mitochondria that were freshly isolated from mouse brain to test mitochondrial respiration and ATP synthesis in the presence of six common anesthetic drugs. The volatile anesthetics isoflurane, halothane, and (to a lesser extent) sevoflurane caused an inhibition of complex I of the electron transport chain in a dose-dependent manner. Significant effects were seen at concentrations that are reached under clinical conditions (< 0.5 mM). Pentobarbital and propofol also inhibited complex I but at concentrations that were two-fold higher than clinical EC
50
values. Only propofol caused an inhibition of complex II. Complex IV respiration was not affected by either agent. Ketamine did not affect mitochondrial respiration. Similarly, all anesthetic agents except ketamine suppressed ATP production at high concentrations. Only halothane increased cytochrome c release indicating damage of the mitochondrial membrane. In summary, volatile general anesthetic agents as well as pentobarbital and propofol dose-dependently inhibit mitochondrial respiration. This action may contribute to depressive actions of the drugs in the brain.
BACKGROUND:The degree to which different volatile anesthetics depress carotid body hypoxic response relates to their ability to activate TASK potassium channels. Most commonly, volatile anesthetic ...pairs act additively at their molecular targets. We examined whether this applied to carotid body TASK channels.
METHODS:We studied halothane and isoflurane effects on hypoxia-evoked rise in intracellular calcium (Cai, using the indicator Indo-1) in isolated neonatal rat glomus cells, and TASK single-channel activity (patch clamping) in native glomus cells and HEK293 cell line cells transiently expressing TASK-1.
RESULTS:Halothane (5%) depressed glomus cell Cai hypoxic response (mean ± SD, 94 ± 4% depression; P < 0.001 vs. control). Isoflurane (5%) had a less pronounced effect (53 ± 10% depression; P < 0.001 vs. halothane). A mix of 3% isoflurane/1.5% halothane depressed cell Cai response (51 ± 17% depression) to a lesser degree than 1.5% halothane alone (79 ± 15%; P = 0.001), but similar to 3% isoflurane alone (44 ± 22%; P = 0.224), indicating subadditivity. Halothane and isoflurane increased glomus cell TASK-1/TASK-3 activity, but mixes had a lesser effect than that seen with halothane alone4% halothane/4% isoflurane yielded channel open probabilities 127 ± 55% above control, versus 226 ± 12% for 4% halothane alone (P = 0.009). Finally, in HEK293 cell line cells, progressively adding isoflurane (1.5 to 5%) to halothane (2.5%) reduced TASK-1 channel activity from 120 ± 38% above control, to 88 ± 48% (P = 0.034).
CONCLUSIONS:In all three experimental models, the effects of isoflurane and halothane combinations were quantitatively consistent with the modeling of weak and strong agonists competing at a common receptor on the TASK channel.
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