Effects of naloxone on myocardial ischemic preconditioning in humans

Tomai, Fabrizio; Crea, Filippo; Gaspardone, Achille; Versaci, Francesco; Ghini, Anna S.; Ferri, Claudio; Desideri, Giovambattista; Chiariello, Luigi; Gioffrè, Pier Agostino

doi:10.1016/s0735-1097(99)00095-9

Cited by 95 publications

(63 citation statements)

References 46 publications

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“…At the end of each balloon inflation, the intensity of anginal pain was assessed using a visual analog scale. 18 Patients were asked to place a mark on a scale of 10 ranging from no pain (0) to the most severe pain ever experienced (10).…”

Section: Assessment Of Chest Painmentioning

confidence: 99%

Nicorandil Enhances Myocardial Tolerance to Ischemia Without Progressive Collateral Recruitment During Coronary Angioplasty.

Sakai

Yamagata

Teragawa

et al. 2002

Circ J

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Section: Assessment Of Chest Painmentioning

confidence: 99%

Nicorandil Enhances Myocardial Tolerance to Ischemia Without Progressive Collateral Recruitment During Coronary Angioplasty.

Sakai

Yamagata

Teragawa

et al. 2002

Circ J

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“…22 Finally, early results suggest that opioid receptors also seem to play a role in preconditioning during coronary angioplasty. In fact, morphine sulfate 27 and naloxone 28 have, respectively, been shown to mimic and prevent the adaptation to ischemia during repeated balloon inflations.…”

Section: Mechanisms Of Ischemic Preconditioningmentioning

confidence: 99%

Ischemic Preconditioning in Humans

et al. 1999

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Abstract-Ischemic preconditioning, a powerful form of endogenous protection against myocardial infarction, has been demonstrated in several animal species and, recently, in isolated human cardiomyocytes. For both logistic and ethical reasons, no clinical study can meet the strict conditions of experimental studies on preconditioning with infarct size as the end-point. Nevertheless, the demonstration of adaptation to ischemia observed during in vitro studies on human atrial trabeculae, in patients in the setting of coronary bypass surgery, and in the setting of coronary angioplasty in the absence of collateral vessel recruitment strongly suggests that ischemic preconditioning occurs in humans. This notion is further supported by the observation that in these human models, the adaptation to ischemia is influenced by drugs acting on K ATP channels and on purinergic and ␣-adrenergic receptors, similar to what is observed in accepted experimental models of ischemic preconditioning. This important form of myocardial endogenous protection may also play a role in the warm-up phenomenon and in mediating the beneficial effects of preinfarction angina. The demonstration of ischemic preconditioning in humans and the identification of some of its mediators suggests that in patients at high risk for myocardial infarction, drugs known to block this endogenous form of protection should be used with caution, whereas drugs known to elicit preconditioning might have a relevant therapeutic role. (Circulation. 1999;100:559-563.)

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“…[4][5][6][7][8][9][10][11][12][13][14] Previous studies have found that intravenous pre-administration of nicorandil attenuates ST-segment elevation 12) and improves lactate metabolism 13) during coronary angioplasty, suggesting that pharmacological preconditioning is induced by nicorandil. Troponin T (TnT) is one of the reliable metabolic markers of myocardial injury.…”

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confidence: 99%

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

et al. 2002

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SUMMARYNicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of nicorandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 µg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (∑ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. ∑ST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05±0.05 vs 0.11±0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil. (Jpn Heart J 2002; 43: 443-453)

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Effects of naloxone on myocardial ischemic preconditioning in humans

Cited by 95 publications

References 46 publications

Nicorandil Enhances Myocardial Tolerance to Ischemia Without Progressive Collateral Recruitment During Coronary Angioplasty.

Nicorandil Enhances Myocardial Tolerance to Ischemia Without Progressive Collateral Recruitment During Coronary Angioplasty.

Ischemic Preconditioning in Humans

Nicorandil-Induced Preconditioning as Evidenced by Troponin T Measurements after Coronary Angioplasty in Patients with Stable Angina Pectoris.

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