Loss of preconditioning in rabbits with vascular tolerance to nitroglycerin

Szilvássy, Zoltán; Ferdinándy, Péter; Bor, P.; Jakab, I; Szilvássy, Judit; Nagy, I.; Lonovics, J.; Koltai, M.

doi:10.1111/j.1476-5381.1994.tb13180.x

Cited by 28 publications

(22 citation statements)

References 7 publications

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“…Fakete et al [27] also reported the loss of protection by IPostC in isolated rat hearts in which nitrate tolerance was induced by the administration of nitroglycerin 3 days before the ischemic insult. Similar findings were obtained in a rabbit model; in that study, nitrate tolerance abolished the protection afforded by IPreC [28,29]. Together, these results highlight the important role of NO in the intracellular signal transduction mechanism of IPreC and IPostC [30,31].…”

Section: Discussionsupporting

confidence: 86%

Duration of the Reoxygenation Interval Applied before Ischemic Post-conditioning: Fine-Tuning the Protocol for Human Myocardium

Soler-Ferrer¹,

Casós²,

Pérez³

et al. 2017

J Clin Exp Cardiolog

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Ischemic post-conditioning (IPostC) is a cardioprotection strategy applied after prolonged ischemia. In an in vitro model of human myocardium we previously demonstrated that one cycle of 120 s of ischemia is the most protective; however the optimal duration of the reperfusion interval between prolonged ischemia and the application of IPostC have not been determined. To investigate the importance of this reperfusion interval, myocardial muscles from the right atrial appendage of 26 patients were subjected to 90 min of ischemia followed by 120 min of reoxygenation. IPostC was induced by four different reperfusion intervals (30, 60, 120 and 180 s) followed by 120 s of ischemia. Lactate dehydrogenase leakage and caspase 3 activity were measured to assess cell injury and apoptosis, respectively. The results showed that intervals of 120 and 180 s were more protective than those of 30 and 60 s, although protection was obtained in only approximately one-third of the patients. Importantly, the muscles from patients receiving nitric oxide donors as anti-anginal agents were not protected by any of the IPostC protocols used.In conclusion, the present study demonstrates the importance of the duration of the reoxygenation interval before the application of IPostC, with 120 and 180 s conferring the greatest protection. This finding is relevant for the design of future studies on the clinical utility of IPostC and on the investigation of the underlying protective mechanisms.

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Section: Discussionsupporting

confidence: 86%

Duration of the Reoxygenation Interval Applied before Ischemic Post-conditioning: Fine-Tuning the Protocol for Human Myocardium

Soler-Ferrer¹,

Casós²,

Pérez³

et al. 2017

J Clin Exp Cardiolog

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“…We have recently reported that a significant decrease in cardiac NO content assessed by electron spin resonance (ESR) abolished pacing-induced preconditioning in rat heart (Ferdinandy et al 1996). We have also shown that the cardioprotective effect of pacing-induced preconditioning was proportional to the elevation of myocardial cGMP content (Szilvassy et al 1994a), and that the reduced cardiac cGMP content due to experimental nitroglycerin tolerance led to the loss of preconditioning in rabbits (Szilvassy et al 1994b). These data suggest that the NO-cGMP pathway may be involved in the mechanism of pacing-induced preconditioning in rabbits and rats, however, the major source of NO in the heart has not been identified.…”

Section: Introductionmentioning

confidence: 96%

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Ferdinándy

Csont

Csonka

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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100

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“…In this series of studies, changes in whole body insulin sensitivity were assessed by the RIST method in conscious animals, an approach specifically proposed to investigate the effect of food on insulin sensitivity 14 . Development of vascular tolerance to GTN was confirmed on the 7 th day by testing endothelium free carotid artery rings for isometric tension as described previously 5,6 . Rings of 5 mm in length were precontracted with an EC 50 concentration of norepinephrine in addition to a resting tension of 10 mN.…”

Section: Methodsmentioning

confidence: 99%

“…Subsequently, it has also been shown that hemodynamic nitrate tolerance blocks several endogenous adaptive mechanisms underpinned by nitric oxide (NO) release such as the antiischemic effect of myocardial preconditioning 5,6 , the non-adrenergic, non-cholinergic relaxation of gastrointestinal sphincters 7 and yields a state of insulin resistance 1 . The latter was suspected to somehow relate to the meal-induced insulin sensitization phenomenon first described by Sadri & Lautt 8 , since it was widely accepted that the phenomenon was the most effective NO-dependent endogenous insulin sensitizing mechanism.…”

Section: Introductionmentioning

confidence: 99%

Block by Nitrate Tolerance of Meal-Induced Insulin Sensitization in Conscious Rabbits

Bajza¹,

Németh²,

Peitl³

et al. 2011

Journal of Cardiovascular Pharmacology

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Aims: Hemodynamic nitrate tolerance has been shown to result in an insulin resistant state.We studied whether nitrate tolerance induced by a 7-day continuous exposure to transdermal nitroglycerin influenced the meal-induced insulin sensitization phenomenon in rabbits.Methods: Changes in insulin sensitivity in response to feeding in conscious rabbits were determined by rapid insulin sensitivity test, in both nitrate tolerant and non-tolerant animals.In a separate series of experiments with anaesthetized rabbits with or without nitrate tolerance, the hyperinsulinaemic euglycaemic glucose clamping methods was used to study the effect of intraportal infusion of cholecystokinin (CCK) on whole body insulin sensitivity. Results:Rabbits with normal feeding exhibited a 46 ± 6 % increase in insulin sensitivity as compared to their matching fasting control. A 7-day period of treatment with patches releasing 0.07 mg nitroglycerin per hour yielded nitrate tolerance and a state of insulin resistance and no increase in insulin sensitivity in response to food. Intraportal infusion of CCK8 (0.3-3.0 μg/kg over 20 min) resulted in a dose-dependent increase in insulin sensitivity in normal but not in nitrate tolerant fasted anaesthetized animals. Conclusions:Nitrate tolerance blocks both the meal-induced insulin sensitization phenomenon and the insulin sensitizing effect of intraportal cholecystokinin. We studied whether nitrate tolerance induced by a 7-day continuous exposure to transdermal nitroglycerin influenced the meal-induced insulin sensitization phenomenon in rabbits.Methods: Changes in insulin sensitivity in response to feeding in conscious rabbits were determined by rapid insulin sensitivity test, in both nitrate tolerant and non-tolerant animals.In a separate series of experiments with anaesthetized rabbits with or without nitrate tolerance, the hyperinsulinaemic euglycaemic glucose clamping methods was used to study the effect of intraportal infusion of cholecystokinin (CCK) on whole body insulin sensitivity. Results:Rabbits with normal feeding exhibited a 46 ± 6 % increase in insulin sensitivity as compared to their matching fasting control. A 7-day period of treatment with patches releasing 0.07 mg nitroglycerin per hour yielded nitrate tolerance and a state of insulin resistance and no increase in insulin sensitivity in response to food. Intraportal infusion of CCK8 (0.3-3.0 μg/kg over 20 min) resulted in a dose-dependent increase in insulin sensitivity in normal but not in nitrate tolerant fasted anaesthetized animals. Conclusions:Nitrate tolerance blocks both the meal-induced insulin sensitization phenomenon and the insulin sensitizing effect of intraportal cholecystokinin.

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Loss of preconditioning in rabbits with vascular tolerance to nitroglycerin

Cited by 28 publications

References 7 publications

Duration of the Reoxygenation Interval Applied before Ischemic Post-conditioning: Fine-Tuning the Protocol for Human Myocardium

Duration of the Reoxygenation Interval Applied before Ischemic Post-conditioning: Fine-Tuning the Protocol for Human Myocardium

Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: role of nitric oxide and CGRP?

Block by Nitrate Tolerance of Meal-Induced Insulin Sensitization in Conscious Rabbits

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