Role of Anesthetic Agents on Cardiac and Immune Systems

Yu, Huang-Ping

doi:10.1097/shk.0b013e3182357054

Cited by 6 publications

(4 citation statements)

References 136 publications

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“…Topical antiseptic solutions often contain chlorhexidine which is a potent antibacterial compound and is known to inactivate HIV-1 and HSV [10]. Because the immune and nervous systems communicate with each other, anesthetics are known to dampen the immune response [11]. Collectively, these procedures could impact the ex vivo challenge assay by interfering with HIV-1 infection of the tissue.…”

Section: Discussionmentioning

confidence: 99%

HIV-1 Infection of Female Genital Tract Tissue for Use in Prevention Studies

Dezzutti

Uranker

Bunge³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Objective Ex vivo HIV-1 challenge has been proposed as a bio-indicator of microbicide product effectiveness. The objective of this study was to establish optimal parameters for use of female genital tract tissue in this model. Design Ex vivo challenge involves in vivo product use, followed by tissue biopsy, and exposure of the tissue to HIV-1 in the laboratory. Methods Paired ectocervical and vaginal biopsies were collected from 42 women and 28 had additional biopsies from each site collected after 5% lidocaine (n=14) or chlorhexidine (n=14) treatment. Tissues were transported immediately to the laboratory and exposed to HIV-1. HIV-1 infection was followed by p24 ELISA on culture supernatants and at study end after weighing and fixing the tissue for immunohistochemistry (IHC) to detect p24 expressing cells. Results While both tissue types were equally infected with HIV-1 based on IHC results, ectocervical tissues had significantly higher HIV-1 replication than vaginal tissues (P < .005). Lidocaine and chlorhexidine had minimal impact on HIV-1 infection and replication. Point estimates for p24 levels were defined for 95% probability of p24-positive tissues and were 3.43 log10 for ectocervical tissue and 2.50 log10 for vaginal tissue based on weight-adjusted cumulative p24 endpoints. Conclusions While similar proportions of ectocervical and vaginal tissues support HIV-1 infection, higher levels of HIV-1 replication were observed in ectocervical tissues. Defining point estimates for HIV-1 infection in fresh ectocervical and vaginal tissues provides valuable information for the evaluation of HIV-1 preventative treatments during early clinical studies.

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Section: Discussionmentioning

confidence: 99%

HIV-1 Infection of Female Genital Tract Tissue for Use in Prevention Studies

Dezzutti

Uranker

Bunge³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…The immunomodulatory effects of propofol have been reported in a variety of experimental and functional research over the years (29). However, very little is known about the pharmacologic mechanisms of propofol, especially in impairing neutrophil functions.…”

Section: Discussionmentioning

confidence: 99%

Propofol Inhibits Superoxide Production, Elastase Release, and Chemotaxis in Formyl Peptide–Activated Human Neutrophils by Blocking Formyl Peptide Receptor 1

Yang

Chung

et al. 2013

The Journal of Immunology

172

200

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Neutrophils play a critical role in acute and chronic inflammatory processes, including myocardial ischemia/reperfusion injury, sepsis, and adult respiratory distress syndrome. Binding of formyl peptide receptor 1 (FPR1) by N-formyl peptides can activate neutrophils and may represent a new therapeutic target in either sterile or septic inflammation. Propofol, a widely used i.v. anesthetic, has been shown to modulate immunoinflammatory responses. However, the mechanism of propofol remains to be established. In this study, we showed that propofol significantly reduced superoxide generation, elastase release, and chemotaxis in human neutrophils activated by fMLF. Propofol did not alter superoxide generation or elastase release in a cell-free system. Neither inhibitors of γ-aminobutyric acid receptors nor an inhibitor of protein kinase A reversed the inhibitory effects of propofol. In addition, propofol showed less inhibitory effects in non-FPR1–induced cell responses. The signaling pathways downstream from FPR1, involving calcium, AKT, and ERK1/2, were also competitively inhibited by propofol. These results show that propofol selectively and competitively inhibits the FPR1-induced human neutrophil activation. Consistent with the hypothesis, propofol inhibited the binding of N-formyl-Nle-Leu-Phe-Nle-Tyr-Lys-fluorescein, a fluorescent analog of fMLF, to FPR1 in human neutrophils, differentiated THP-1 cells, and FPR1-transfected human embryonic kidney-293 cells. To our knowledge, our results identify, for the first time, a novel anti-inflammatory mechanism of propofol by competitively blocking FPR1 in human neutrophils. Considering the importance of N-formyl peptides in inflammatory processes, our data indicate that propofol may have therapeutic potential to attenuate neutrophil-mediated inflammatory diseases by blocking FPR1.

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“…These findings indicate that the changes in p-eNOS, Bcl-2, and p-Bad expression induced by hypercholesterolemia may not be severe enough to influence IR injury in hypercholesterolemic rats; the exact reason needs further exploration. Nevertheless, myocardial eNOS activity is crucial in acute protection against cardiac IR injury (26,27). In addition, the Bcl-2 family, including Bcl-2 and Bad, is regulated by NOS and affects myocardial cell death (2).…”

Section: Discussionmentioning

confidence: 99%

Hypercholesterolemia Abrogates Sevoflurane-Induced Delayed Preconditioning Against Myocardial Infarct in Rats by Alteration of Nitric Oxide Synthase Signaling

Zhang¹,

Ma²,

Wang³

et al. 2012

Shock

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The aim of the current study was to determine whether hypercholesterolemia affects the delayed sevoflurane preconditioning against myocardial ischemia-reperfusion (IR) injury and, if so, the underlying mechanism. Male Sprague-Dawley rats fed 2% cholesterol-enriched chow for 8 weeks were subjected to sevoflurane preconditioning (2.4% vol/vol, 1 h) 24 h before myocardial ischemia was induced by occluding the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min. The hemodynamic parameters left ventricular developed pressure, left ventricular end-diastolic pressure, and maximal rise/fall rate of left ventricular pressure were continuously monitored, and myocardial infarct size was determined at the end of reperfusion. The protein expression of myocardial nitric oxide synthase (NOS), Bcl-2, and Bad was assessed before ischemia. We found that the left ventricular hemodynamic parameters during the whole IR procedure and the myocardial infarct size did not significantly differ between the normocholesterolemic and hypercholesterolemic control groups. The hemodynamic parameters were all markedly improved during the reperfusion period, and the myocardial infarct size was significantly reduced by delayed sevoflurane preconditioning in normocholesterolemic rats, but all of these improvements were reversed by N-(3-(aminomethyl)benzyl) acetamidine (1400W, 1 mg/kg; i.v., 10 min before ischemia), a selective inducible NOS (iNOS) inhibitor, and 5-hydroxy decanoate sodium (5 mg/kg, i.v., 10 min before ischemia), a mitochondrial ATP-dependent K⁺ channel blocker. Such cardiac improvement induced by delayed sevoflurane preconditioning did not occur in hypercholesterolemic rats and was not exacerbated by 1400W or 5-hydroxy decanoate sodium. The expression of myocardial iNOS was markedly enhanced by delayed sevoflurane preconditioning in normocholesterolemic, but not in hypercholesterolemic rats. The expression of endothelial NOS and Bad did not differ among all groups. The expression of myocardial phosphorylated endothelial NOS, Bcl-2, and phosphorylated Bad in normocholesterolemic rats was not affected by delayed sevoflurane preconditioning but was decreased in the hypercholesterolemic control group, and this was not reversed by sevoflurane, compared with the normocholesterolemic control group. Taken together, these results indicate that sevoflurane preconditioning exerts delayed cardioprotection against IR injury in normocholesterolemic rats, which is blocked by hypercholesterolemia potentially via interference with the iNOS/mitochondrial ATP-dependent K⁺ channel pathway.

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Role of Anesthetic Agents on Cardiac and Immune Systems

Cited by 6 publications

References 136 publications

HIV-1 Infection of Female Genital Tract Tissue for Use in Prevention Studies

HIV-1 Infection of Female Genital Tract Tissue for Use in Prevention Studies

Propofol Inhibits Superoxide Production, Elastase Release, and Chemotaxis in Formyl Peptide–Activated Human Neutrophils by Blocking Formyl Peptide Receptor 1

Hypercholesterolemia Abrogates Sevoflurane-Induced Delayed Preconditioning Against Myocardial Infarct in Rats by Alteration of Nitric Oxide Synthase Signaling

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