Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning

Sofia Iris Bibli, Ioanna Andreadou, Constantinos Glynos, Athanasia Chatzianastasiou, Dimitris Toumpanakis, Spyros Zakynthinos, Theodoros Vasilakopoulos, Efstathios K. Iliodromitis, Andreas Papapetropoulos

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Cigarette smoking is one of the risk factors for coronary artery disease. Although conditioning decreases infarct size in hearts from healthy animals, comorbidities may render it ineffective. We investigated the effects of cigarette smoke (CS) exposure on intracellular myocardial signaling, infarct size after ischemia-reperfusion, and the potential interference with ischemic conditioning. Exposure of mice to CS increased blood pressure, caused cardiac hypertrophy, and upregulated the nitric oxide synthatse (NOS)/soluble guanylate cyclase (sGC)/cGMP pathway. To test the effect of CS exposure on the endogenous cardioprotective mechanisms, mice were subjected to regional myocardial ischemia and reperfusion with no further intervention or application of preconditioning (PreC) or postconditioning (PostC). Exposure to CS did not increase the infarction compared with the room air (RA)-exposed group. PreC was beneficial for both CS and RA vs. nonconditioned animals. PostC was effective only in RA animals, while the infarct size-limiting effect was not preserved in the CS group. Differences in oxidative stress markers, Akt, and endothelial NOS phosphorylation and cGMP levels were observed between RA and CS groups subjected to PostC. In conclusion, exposure to CS does not per se increase infarct size. The beneficial effect of ischemic PreC is preserved in mice exposed to CS, as it does not affect the cardioprotective signaling; in contrast, PostC fails to protect CS-exposed mice due to impaired activation of the Akt/eNOS/cGMP axis that occurs in parallel to enhanced oxidative stress.

Original languageEnglish (US)
Pages (from-to)H1321-H1332
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume311
Issue number5
DOIs
StatePublished - Jan 1 2016
Externally publishedYes

Fingerprint

Ischemic Postconditioning
Smoke
Tobacco Products
Air
Nitric Oxide
Oxidative Stress
Ischemic Preconditioning
Myocardial Reperfusion
Cardiomegaly
Infarction
Reperfusion
Myocardial Ischemia
Comorbidity
Coronary Artery Disease
Ischemia

Keywords

  • cGMP
  • Cigarette smoke
  • Conditioning
  • eNOS
  • Infarct size

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning. / Bibli, Sofia Iris; Andreadou, Ioanna; Glynos, Constantinos; Chatzianastasiou, Athanasia; Toumpanakis, Dimitris; Zakynthinos, Spyros; Vasilakopoulos, Theodoros; Iliodromitis, Efstathios K.; Papapetropoulos, Andreas.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 311, No. 5, 01.01.2016, p. H1321-H1332.

Research output: Contribution to journalArticle

Bibli, SI, Andreadou, I, Glynos, C, Chatzianastasiou, A, Toumpanakis, D, Zakynthinos, S, Vasilakopoulos, T, Iliodromitis, EK & Papapetropoulos, A 2016, 'Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning', American Journal of Physiology - Heart and Circulatory Physiology, vol. 311, no. 5, pp. H1321-H1332. https://doi.org/10.1152/ajpheart.00925.2015
Bibli, Sofia Iris ; Andreadou, Ioanna ; Glynos, Constantinos ; Chatzianastasiou, Athanasia ; Toumpanakis, Dimitris ; Zakynthinos, Spyros ; Vasilakopoulos, Theodoros ; Iliodromitis, Efstathios K. ; Papapetropoulos, Andreas. / Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning. In: American Journal of Physiology - Heart and Circulatory Physiology. 2016 ; Vol. 311, No. 5. pp. H1321-H1332.
@article{e07dcfab863643f88d2ca820dffc8927,
title = "Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning",
abstract = "Cigarette smoking is one of the risk factors for coronary artery disease. Although conditioning decreases infarct size in hearts from healthy animals, comorbidities may render it ineffective. We investigated the effects of cigarette smoke (CS) exposure on intracellular myocardial signaling, infarct size after ischemia-reperfusion, and the potential interference with ischemic conditioning. Exposure of mice to CS increased blood pressure, caused cardiac hypertrophy, and upregulated the nitric oxide synthatse (NOS)/soluble guanylate cyclase (sGC)/cGMP pathway. To test the effect of CS exposure on the endogenous cardioprotective mechanisms, mice were subjected to regional myocardial ischemia and reperfusion with no further intervention or application of preconditioning (PreC) or postconditioning (PostC). Exposure to CS did not increase the infarction compared with the room air (RA)-exposed group. PreC was beneficial for both CS and RA vs. nonconditioned animals. PostC was effective only in RA animals, while the infarct size-limiting effect was not preserved in the CS group. Differences in oxidative stress markers, Akt, and endothelial NOS phosphorylation and cGMP levels were observed between RA and CS groups subjected to PostC. In conclusion, exposure to CS does not per se increase infarct size. The beneficial effect of ischemic PreC is preserved in mice exposed to CS, as it does not affect the cardioprotective signaling; in contrast, PostC fails to protect CS-exposed mice due to impaired activation of the Akt/eNOS/cGMP axis that occurs in parallel to enhanced oxidative stress.",
keywords = "cGMP, Cigarette smoke, Conditioning, eNOS, Infarct size",
author = "Bibli, {Sofia Iris} and Ioanna Andreadou and Constantinos Glynos and Athanasia Chatzianastasiou and Dimitris Toumpanakis and Spyros Zakynthinos and Theodoros Vasilakopoulos and Iliodromitis, {Efstathios K.} and Andreas Papapetropoulos",
year = "2016",
month = "1",
day = "1",
doi = "10.1152/ajpheart.00925.2015",
language = "English (US)",
volume = "311",
pages = "H1321--H1332",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Exposure to cigarette smoke abrogates the beneficial effect of ischemic postconditioning

AU - Bibli, Sofia Iris

AU - Andreadou, Ioanna

AU - Glynos, Constantinos

AU - Chatzianastasiou, Athanasia

AU - Toumpanakis, Dimitris

AU - Zakynthinos, Spyros

AU - Vasilakopoulos, Theodoros

AU - Iliodromitis, Efstathios K.

AU - Papapetropoulos, Andreas

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Cigarette smoking is one of the risk factors for coronary artery disease. Although conditioning decreases infarct size in hearts from healthy animals, comorbidities may render it ineffective. We investigated the effects of cigarette smoke (CS) exposure on intracellular myocardial signaling, infarct size after ischemia-reperfusion, and the potential interference with ischemic conditioning. Exposure of mice to CS increased blood pressure, caused cardiac hypertrophy, and upregulated the nitric oxide synthatse (NOS)/soluble guanylate cyclase (sGC)/cGMP pathway. To test the effect of CS exposure on the endogenous cardioprotective mechanisms, mice were subjected to regional myocardial ischemia and reperfusion with no further intervention or application of preconditioning (PreC) or postconditioning (PostC). Exposure to CS did not increase the infarction compared with the room air (RA)-exposed group. PreC was beneficial for both CS and RA vs. nonconditioned animals. PostC was effective only in RA animals, while the infarct size-limiting effect was not preserved in the CS group. Differences in oxidative stress markers, Akt, and endothelial NOS phosphorylation and cGMP levels were observed between RA and CS groups subjected to PostC. In conclusion, exposure to CS does not per se increase infarct size. The beneficial effect of ischemic PreC is preserved in mice exposed to CS, as it does not affect the cardioprotective signaling; in contrast, PostC fails to protect CS-exposed mice due to impaired activation of the Akt/eNOS/cGMP axis that occurs in parallel to enhanced oxidative stress.

AB - Cigarette smoking is one of the risk factors for coronary artery disease. Although conditioning decreases infarct size in hearts from healthy animals, comorbidities may render it ineffective. We investigated the effects of cigarette smoke (CS) exposure on intracellular myocardial signaling, infarct size after ischemia-reperfusion, and the potential interference with ischemic conditioning. Exposure of mice to CS increased blood pressure, caused cardiac hypertrophy, and upregulated the nitric oxide synthatse (NOS)/soluble guanylate cyclase (sGC)/cGMP pathway. To test the effect of CS exposure on the endogenous cardioprotective mechanisms, mice were subjected to regional myocardial ischemia and reperfusion with no further intervention or application of preconditioning (PreC) or postconditioning (PostC). Exposure to CS did not increase the infarction compared with the room air (RA)-exposed group. PreC was beneficial for both CS and RA vs. nonconditioned animals. PostC was effective only in RA animals, while the infarct size-limiting effect was not preserved in the CS group. Differences in oxidative stress markers, Akt, and endothelial NOS phosphorylation and cGMP levels were observed between RA and CS groups subjected to PostC. In conclusion, exposure to CS does not per se increase infarct size. The beneficial effect of ischemic PreC is preserved in mice exposed to CS, as it does not affect the cardioprotective signaling; in contrast, PostC fails to protect CS-exposed mice due to impaired activation of the Akt/eNOS/cGMP axis that occurs in parallel to enhanced oxidative stress.

KW - cGMP

KW - Cigarette smoke

KW - Conditioning

KW - eNOS

KW - Infarct size

UR - http://www.scopus.com/inward/record.url?scp=84994663337&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84994663337&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.00925.2015

DO - 10.1152/ajpheart.00925.2015

M3 - Article

C2 - 27694220

AN - SCOPUS:84994663337

VL - 311

SP - H1321-H1332

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 5

ER -