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Reperfusion Injury clinical trials

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NCT ID: NCT02850471 Suspended - Reperfusion Injury Clinical Trials

Pulmonary Protection of Transcutaneous Electrical Acupoint Stimulation in Gynecologic Laparoscopic Surgery

Start date: March 2015
Phase: Phase 1/Phase 2
Study type: Interventional

TEAS might protect against postoperative pulmonary such as ischemia-reperfusion injury (IRI) and atelectasis. We tested the hypothesis that transcutaneous electrical acupoint stimulation protects against postoperative pulmonary complications in patients who are receiving mechanical ventilation during general anesthesia for gynecologic laparoscopic surgery.

NCT ID: NCT00846378 Suspended - Clinical trials for Acute Myocardial Infarction

Minimizing Reperfusion Injury in Patients With Acute Myocardial Infarction

PCinAMI
Start date: March 2008
Phase: Phase 1
Study type: Interventional

The size of a heart attack will be decreased by the use of timed balloon inflations to open the blocked blood vessel.

NCT ID: NCT00184938 Suspended - Clinical trials for Ischemia-Reperfusion Injury

Opioid Receptors Influence Ischemia-Reperfusion Injury

Start date: January 2005
Phase: N/A
Study type: Interventional

The most powerful protective mechanism against ischemia-reperfusion injury other than rapid reperfusion is ischemic preconditioning. Ischemic preconditioning is defined as the development of tolerance to ischemia-reperfusion injury by a previous short bout of ischemia resulting in a marked reduction in infarct size. This mechanism can be mimicked by several pharmacological substances such as adenosine and morphine. We, the researchers at Radboud University Nijmegen Medical Centre, have recently developed a method in which we can detect ischemia-reperfusion injury in the human forearm by using Annexin A5 scintigraphy (Rongen et al). With this method we will determine whether opioid receptors are involved in ischemic preconditioning. We expect to find that morphine can mimic ischemic preconditioning and that acute ischemic preconditioning can be blocked with the opioid receptor antagonist naloxon. This study will increase our knowledge about the mechanism of ischemic preconditioning and may also provide leads to exploit this endogenous protective mechanism in a clinical setting.

NCT ID: NCT00184847 Suspended - Clinical trials for Ischemia-Reperfusion Injury

Adenosine Receptors Influence Ischemia-Reperfusion Injury

Start date: March 2005
Phase: N/A
Study type: Interventional

Ischemic preconditioning is defined as the development of tolerance to ischemia-reperfusion injury by a previous short bout of ischemia resulting in a marked reduction in infarct size. This mechanism can be mimicked by several pharmacological substances such as acetylcholine and adenosine. To detect ischemia-reperfusion injury in humans in vivo Kharbanda et al. developed a method in which endothelial dysfunction represents the effects of ischemic preconditioning. This method, however, uses acetylcholine to measure endothelial function before and after forearm ischemia. We, the investigators at Radboud University, hypothesize that the use of acetylcholine in this model reduces ischemia-reperfusion injury. Therefore, we will compare this protocol with a protocol in which endothelial function is only measured after ischemia. We expect an increase in ischemia-reperfusion injury when endothelial function is only measured after the forearm ischemia. After determining the optimal method to measure ischemia-reperfusion injury of the vascular endothelium we will determine the effect of acute and chronic caffeine, an adenosine receptor antagonist, on ischemic preconditioning. With this study we expect to find that adenosine mimics ischemic preconditioning of the vascular endothelium. Moreover, we expect to find that acute caffeine intake reduces ischemia-reperfusion injury whereas chronic caffeine intake does not. This study will increase our knowledge about the mechanism of ischemic preconditioning and may also provide leads to exploit this endogenous protective mechanism in a clinical setting.