Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma

Matejec, Reginald; Schulz, Axel; Harbach, Heinz W.; Uhlich, Holger; Hempelmann, G.; Teschemacher, Hansjoerg

doi:10.1152/japplphysiol.01292.2003

Cited by 12 publications

(4 citation statements)

References 37 publications

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“…Prior surgical studies generally involved increasing the tourniquet pressure to above the mean arterial pressure (MAP) in order to ensure a bloodless field during extremity surgery. [6][7][8][9][10] These results may indicate that blood pressure cuff increase to above the MAP could also falsely increase lactate values in clinical practice; however, this has not been adequately studied.…”

Section: Discussionmentioning

confidence: 98%

“…5 In orthopedic studies utilizing tourniquet for hemostasis, lactate levels have been found to increase; however, these studies also used tourniquet times far in excess of what is applied for a blood draw. [6][7][8][9][10] As a result of these studies as well as due to the theoretical reasoning for tourniquet avoidance, many hospitals have protocols in place indicating that lactate levels must be drawn without a tourniquet. Some manufacturers of lactate assays as well as the Surviving Sepsis Campaign Bundle also recommend drawing lactates without tourniquets.…”

Section: Introductionmentioning

confidence: 99%

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Impact of Phlebotomy Tourniquet Use on Blood Lactate Levels in Acutely Ill Patients

Balakrishnan

Wilson

Taggart

et al. 2016

CJEM

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Objective: Lactate levels are increasingly used to guide resuscitation efforts. Some surgical literature suggests that tourniquet use during phlebotomy falsely elevates results, although studies in healthy volunteers have not demonstrated this. The purpose of this study was to determine in clinical practice whether tourniquet use during the drawing of a lactate results in significantly altered levels compared to the result of a level drawn without a tourniquet. Methods: A prospective cohort study was carried out on emergency department patients whose clinical presentation led a physician to order a lactate level. Written informed consent was obtained from patients or their proxies. Study lactates were obtained using a tourniquet during the draw sequence of other laboratory studies. Lactate levels for clinical use were drawn per hospital protocol with no tourniquet. The time of lactate measurements and patient demographic information were recorded. Lactate levels for each patient were compared with the Wilcoxon RankSum Test. Results: 40 patients were consented and enrolled. The median clinical lactate level was 1.9 (interquartile range 1.5-2.6), and the median study lactate level was 1.9 (interquartile range 1.4-2.7). There was no difference between paired lactate values (p = 0.95). Conclusions: Tourniquet use appears to have no impact on measured lactate levels. Our findings suggest that current practices at many institutions regarding lactate collection are likely too stringent and should be changed.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Impact of Phlebotomy Tourniquet Use on Blood Lactate Levels in Acutely Ill Patients

Balakrishnan

Wilson

Taggart

et al. 2016

CJEM

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“…A fluid-phase two-site immunoprecipitation RIA as described previously was used to determine β-END(1–31) in plasma extracts [13, 23, 24]. In brief, a monoclonal mouse antibody (code 3E7), directed against the N-terminus of β-END (YGGF), and a polyclonal rabbit antiserum (code 11P), directed against the C-terminal fragment of β-END (KKGE) were used.…”

Section: Methodsmentioning

confidence: 99%

Corticotropin-Releasing Hormone Reduces Pressure Pain Sensitivity in Humans without Involvement of β-Endorphin(1–31), but Does Not Reduce Heat Pain Sensitivity

Matejec

Uhlich

Hotz³

et al. 2005

Neuroendocrinology

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In the present study the effects of intravenously administered corticotropin-releasing hormone (CRH) on the release of proopiomelanocortin (POMC) derivatives such as adrenocorticotropic hormone (ACTH), β-lipotropin (β-LPH) and β-endorphin (β-END) as well as direct effects of CRH on pain sensitivity were examined. In 16 healthy volunteers we studied the effects of 100 µg intravenously administered CRH in absence or presence of 12 mg naloxone on heat or pressure pain sensitivity, using a double-blind, cross-over and placebo-controlled design. To evaluate analgesic effects of CRH via release of POMC derivatives, we determined plasma concentrations of β-END-immunoreactive material (IRM), authentic β-END (β-END(1–31)) and β-LPH IRM, in parallel with heat and pressure pain tolerance thresholds before and 15 and 30 min after treatment with CRH (or placebo), and 5 min after naloxone (or placebo) administration which was administered 40 min after CRH (or placebo) injection. CRH increased levels of β-END IRM, β-END(1–31) and β-LPH IRM. As compared to β-END IRM levels measured by a commercial RIA kit, the β-END(1–31) levels determined by a highly specific two-site RIA, proved to be remarkably small. Furthermore, CRH did not induce increases of heat pain tolerance thresholds, but of pressure pain tolerance thresholds, which, however, were not reversible by naloxone. Neither β-END nor β-LPH IRM nor β-END(1–31) levels correlated with heat or pressure pain tolerance thresholds. We conclude that CRH does not modulate heat, but pressure pain; POMC derivatives like β-END IRM, β-END(1–31) or β-LPH do not mediate this effect.

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“…13 -17 Metabolic stressors including ischemia may evoke the release of endogenous opioids from the peripheral tissues to provide protection against sustained ischemia–reperfusion injury in the heart. 40 -43 Patel et al described the putative role of opioids in mediating RIPC-induced cardioprotection in an intact rat model of myocardial infarction. Mesenteric remote preconditioning (15-minute occlusion followed by 10-minute reperfusion)-induced cardioprotective effects were completely abolished in the presence of naloxone (nonspecific opioid antagonist), suggesting that the endogenous release of opioids may mediate mesenteric remote preconditioning-induced cardioprotection.…”

Section: Role Of Opioids In Ripcmentioning

confidence: 99%

Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection

Randhawa

Jaggi

2016

J Cardiovasc Pharmacol Ther

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Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia-reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

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Effects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma

Abstract: fects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma.

Cited by 12 publications

References 37 publications

Impact of Phlebotomy Tourniquet Use on Blood Lactate Levels in Acutely Ill Patients

Impact of Phlebotomy Tourniquet Use on Blood Lactate Levels in Acutely Ill Patients

Corticotropin-Releasing Hormone Reduces Pressure Pain Sensitivity in Humans without Involvement of β-Endorphin(1–31), but Does Not Reduce Heat Pain Sensitivity

Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection

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