Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits

Qiu, Yumin; Rizvi, Ali A.; Tang, Xian Liang; Manchikalapudi, Srinivas; Takano, Hitoshi; Jadoon, Asad K.; Wu, Wen Jian; Bolli, Roberto

doi:10.1152/ajpheart.1997.273.6.h2931

Cited by 100 publications

(146 citation statements)

References 30 publications

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“…For studies of ischemic preconditioning, initially we used a protocol of six 4-min occlusion/4-min reperfusion cycles [the same protocol we have used in our previous studies in conscious rabbits (20,23,25) and in open-chest mice (9, 10)]. We tested this protocol in four conscious rats and found that all four animals developed ventricular fibrillation upon reperfusion after the first 4-min coronary occlusion.…”

Section: Methodsmentioning

confidence: 99%

Cardioprotection by postconditioning in conscious rats is limited to coronary occlusions <45 min

Tang

Sato

Tiwari

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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tection by postconditioning in conscious rats is limited to coronary occlusions Ͻ45 min. Am J Physiol Heart Circ Physiol 291: H2308-H2317, 2006. First published June 30, 2006 doi:10.1152 doi:10. /ajpheart.00479.2006 Brief episodes of ischemia and reperfusion after a lethal ischemic insult confer cardioprotection, a phenomenon termed "ischemic postconditioning." However, all studies reported to date have been conducted in open-chest animal models. We sought to determine whether postconditioning occurs in conscious animals and whether it protects against severe myocardial injury. Methods: Chronically instrumented rats were assigned to a 30-(Subset 1), 45-(Subset 2), or 60-min (Subset 3) coronary occlusion followed by 24 h of reperfusion. In each subset, rats received no further intervention (control), were preconditioned with 12 cycles of 2-min occlusion/2-min reperfusion immediately (early preconditioning; EPC) or 24 h (late preconditioning; LPC) before myocardial infarction, or were postconditioned with 20 cycles of 10-s occlusion/10-s reperfusion immediately after myocardial infarction (20-10 PostC). Results: With a 30-min occlusion, infarct size (54.4 Ϯ 2.3% of risk region in control-30) was significantly reduced in EPC-30, LPC-30, and 20-10 PostC-30 groups (by 72, 70, and 47%, respectively; all P Ͻ 0.05 vs. control-30). With a 45-min occlusion, infarct size (62.2 Ϯ 2.4% in control-45) was reduced in EPC-45 and LPC-45 groups (by 47 and 41%, respectively; all P Ͻ 0.05 vs. control-45) but not in the 20-10 PostC-45 group [55.4 Ϯ 2.3%, P ϭ not significant (NS) vs. control-45]. With a 60-min occlusion, infarct size (72.7 Ϯ 2.2% in control-60) was reduced in the EPC-60 (by 20%, P Ͻ 0.05) but not in the LPC-60 (63.6 Ϯ 2.5%, P ϭ NS) or in the 20-20 PostC group (71.5 Ϯ 3.4%, P ϭ NS). Conclusions: Both early and late ischemic preconditioning as well as ischemic postconditioning confer protection in conscious rats; however, unlike early preconditioning, postconditioning protects only against coronary occlusions Ͻ45 min. In the conscious rat, the cardioprotection afforded by postconditioning is limited to mild to moderate myocardial injury. myocardium; ischemia; infarct size; preconditioning ISCHEMIC PRECONDITIONING, a powerful endogenous protective phenomenon (17), is manifest in all species tested and is associated with two distinct phases of cardioprotection (early and late) (3,5). In addition, a recent study by Zhao et al. (32) in open-chest dogs has shown that brief episodes of ischemia and reperfusion after a lethal ischemic insult confer cardioprotection, a phenomenon termed ischemic postconditioning. This phenomenon has subsequently been confirmed in vivo in dogs (11), rabbits (1, 4, 13, 30), rats (14, 15, 31), and humans (22) and in vitro in rabbits (7, 29), rats (14, 26), and mice (12, 14), although a study in pigs (21) failed to detect myocardial protection with ischemic postconditioning. The cardioprotection conferred by postconditioning appears to vary greatly with species, experimental settings, and proto...

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Section: Methodsmentioning

confidence: 99%

Cardioprotection by postconditioning in conscious rats is limited to coronary occlusions <45 min

Tang

Sato

Tiwari

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Chronically instrumented New Zealand White male rabbits (2.0ϳ2.5 kg wt; age 3 to 4 mo) were prepared as described previously (5,6,25,26,47,49,50,(63)(64)(65)71). Briefly, rabbits were instrumented under sterile conditions with a balloon occluder around a major branch of the left coronary artery, a 10-MHz pulsed Doppler ultrasonic crystal in the center of the region to be rendered ischemic, and bipolar ECG leads on the chest wall.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…At the conclusion of the study, the occluded/reperfused vascular bed and the infarct were identified by postmortem perfusion of the heart with triphenyl tetrazolium chloride and phthalo blue dye (26,50,63,65). Infarct size was calculated by using computerized planimetry (26,47,50,59,63,65,71).…”

Section: Experimental Protocolsmentioning

confidence: 99%

Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits

Tang

Xuan

Zhu

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Nicorandil has been shown to induce an infarct-limiting effect similar to that induced by the early phase of ischemic preconditioning (PC). The goals of this study were to determine whether nicorandil induces a delayed cardioprotection that is analogous to the late phase of ischemic PC and, if so, whether nicorandil-induced late PC is associated with upregulation of cardioprotective proteins. Chronically instrumented, conscious rabbits received vehicle (intravenous normal saline; control group, n = 10), nicorandil (100 μg/kg bolus + 30 μg·kg–1·min–1 iv for 60 min; nicorandil group, n = 10), or ischemic PC (6 cycles of 4-min coronary occlusion/4-min reperfusion; PC group, n = 8). Twenty-four hours later, rabbits underwent a 30-min coronary occlusion, followed by 3 days of reperfusion. Myocardial infarct size was significantly reduced in rabbits pretreated with nicorandil (27.5 ± 5.3% of the risk region) or with ischemia (30.3 ± 4.2%) versus controls (59.1 ± 4.7%, P < 0.05 vs. both). Furthermore, the expression of cyclooxygenase-2 (COX-2) and Bcl-2 was significantly elevated (+38% and +126%, respectively; P < 0.05) in myocardium of rabbits given nicorandil 24 h earlier versus controls. We conclude that nicorandil induces delayed cardioprotection against myocardial infarction similar to that afforded by the late phase of ischemic PC, possibly by upregulating COX-2 and Bcl-2.

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“…228 In addition, they demonstrated that in the conscious rabbit, the delayed protection against infarction is also triggered by the generation of nitric oxide during the initial preconditioning ischemia. 229 This "second window" of protection against infarction is not, however, seen in the pig model.…”

Section: Second Windowmentioning

confidence: 99%

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

et al. 1998

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Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits

Cited by 100 publications

References 30 publications

Cardioprotection by postconditioning in conscious rats is limited to coronary occlusions <45 min

Cardioprotection by postconditioning in conscious rats is limited to coronary occlusions <45 min

Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits

Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning

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