Cardiac Preconditioning, Remodeling and Regeneration

2017 ◽  
pp. 185-233 ◽  
Author(s):  
Todd E. Gillis ◽  
Elizabeth F. Johnston
Keyword(s):  
Cardiac Preconditioning

Exosomes in Cardiac Preconditioning with Isoflurane and Hypoxia

2015 ◽  
Vol 63 (S 01) ◽  
Author(s):  
S. Kraemer ◽  
C. Beckers ◽  
C. Stoppe ◽  
A. Goetzenich ◽  
R. Autschbach
Keyword(s):  
Cardiac Preconditioning

Anesthetic Effects on Mitochondrial ATP-sensitive K Channel

2001 ◽  
Vol 95 (6) ◽  
pp. 1435-1440 ◽  
Author(s):  
Shinji Kohro ◽  
Quinn H. Hogan ◽  
Yuri Nakae ◽  
Michiaki Yamakage ◽  
Zeljko J. Bosnjak
Keyword(s):  
Fluorescence Microscopy ◽  
Volatile Anesthetics ◽  
Cardioprotective Effect ◽  
K Channel ◽  
Myocardial Cells ◽  
Intravenous Anesthetics ◽  
Inhalational Anesthetics ◽  
Cardioprotective Effects ◽  
Cardiac Preconditioning ◽  
Dose Dependent

Background Volatile anesthetics show an ischemic preconditioning-like cardioprotective effect, whereas intravenous anesthetics have cardioprotective effects for ischemic-reperfusion injury. Although recent evidence suggests that mitochondrial adenosine triphosphate-regulated potassium (mitoK(ATP)) channels are important in cardiac preconditioning, the effect of anesthetics on mitoK(ATP) is unexplored. Therefore, the authors tested the hypothesis that anesthetics act on the mitoK(ATP) channel and mitochondrial flavoprotein oxidation. Methods Myocardial cells were isolated from adult guinea pigs. Endogenous mitochondrial flavoprotein fluorescence, an indicator of mitochondrial flavoprotein oxidation, was monitored with fluorescence microscopy while myocytes were exposed individually for 15 min to isoflurane, sevoflurane, propofol, and pentobarbital. The authors further investigated the effect of 5-hydroxydeanoate, a specific mitoK(ATP) channel antagonist, on isoflurane- and sevoflurane-induced flavoprotein oxidation. Additionally, the effects of propofol and pentobarbital on isoflurane-induced flavoprotein oxidation were measured. Results Isoflurane and sevoflurane induced dose-dependent increases in flavoprotein oxidation (isoflurane: R2 = 0.71, n = 50; sevoflurane: R2 = 0.86, n = 20). The fluorescence increase produced by both isoflurane and sevoflurane was eliminated by 5-hydroxydeanoate. Although propofol and pentobarbital showed no significant effects on flavoprotein oxidation, they both dose-dependently inhibited isoflurane-induced flavoprotein oxidation. Conclusions Inhalational anesthetics induce flavoprotein oxidation through opening of the mitoK(ATP) channel. This may be an important mechanism contributing to anesthetic-induced preconditioning. Cardioprotective effects of intravenous anesthetics may not be dependent on flavoprotein oxidation, but the administration of propofol or pentobarbital may potentially inhibit the cardioprotective effect of inhalational anesthetics.

scholarly journals Bradykinin mediates cardiac preconditioning at a distance

2000 ◽  
Vol 278 (5) ◽  
pp. H1571-H1576 ◽  
Author(s):  
Regien G. Schoemaker ◽  
Caroline L. van Heijningen
Keyword(s):  
Sensory Nerve ◽  
Artery Occlusion ◽  
Area At Risk ◽  
Risk Area ◽  
Arterial Infusion ◽  
Remote Preconditioning ◽  
Male Wistar Rats ◽  
Hoe 140 ◽  
Cardiac Preconditioning

Preconditioning the heart by brief coronary (CAO) or mesenteric artery occlusion (MAO) can protect against damage during subsequent prolonged CAO and reperfusion. The role of bradykinin (BK) in remote cardiac preconditioning by MAO is investigated by antagonizing the BK B2 receptor [Hoechst 140 (HOE-140)] or simulating local BK release by mesenteric intra-arterial infusion. Anesthetized male Wistar rats ( n = 6–8) were treated with HOE-140 or saline before starting the preconditioning protocol, CAO, MAO, or non-preconditioned control. Infarct size related to risk area [ratio of infarct area to area at risk (IA/AR)] was determined after 3 h of reperfusion following a 60-min CAO. IA/AR was 62 ± 5% in controls and not affected by HOE-140 (58 ± 6%). CAO as well as MAO significantly protected the heart (IA/AR, 37 ± 3 and 35 ± 5%), which was prevented by HOE-140 (IA/AR, 71 ± 6 and 65 ± 7%, respectively). Brief intramesenteric BK infusion mimicked MAO (IA/AR, 26 ± 3%). Pretreatment with hexamethonium could abolish this protection (IA/AR, 67 ± 4%). These data indicate an important role for BK in remote preconditioning by MAO. Results support the hypothesis that remote preconditioning acts through sensory nerve stimulation in the ischemic organ.

Involvement of P2Y receptors in pyridoxal-5′-phosphate-induced cardiac preconditioning

2009 ◽  
Vol 23 (3) ◽  
pp. 279-292 ◽  
Author(s):  
Hervé Millart ◽  
Loubna Alouane ◽  
Floriane Oszust ◽  
Stephane Chevallier ◽  
Arnaud Robinet
Keyword(s):  
P2y Receptors ◽  
Cardiac Preconditioning

Deferoxamine induces prolonged cardiac preconditioning via accumulation of oxygen radicals

2005 ◽  
Vol 38 (1) ◽  
pp. 117-124 ◽  
Author(s):  
Andreas Dendorfer ◽  
Marc Heidbreder ◽  
Thomas Hellwig-Bürgel ◽  
Olaf Jöhren ◽  
Fatimunnisa Qadri ◽  
...  
Keyword(s):  
Oxygen Radicals ◽  
Cardiac Preconditioning

scholarly journals Cardiac preconditioning with 4-h, 17°C ischemia reduces [Ca2+]i load and damage in part via KATP channel opening

2002 ◽  
Vol 282 (6) ◽  
pp. H1961-H1969 ◽  
Author(s):  
Qun Chen ◽  
Amadou K. S. Camara ◽  
Jianzhong An ◽  
Matthias L. Riess ◽  
Enis Novalija ◽  
...  
Keyword(s):  
Infarct Size ◽  
Potential Role ◽  
K Channel ◽  
Moderate Hypothermia ◽  
Channel Opening ◽  
Cardioprotective Effects ◽  
Hypothermic Storage ◽  
Cardiac Preconditioning

Brief ischemia before normothermic ischemia protects hearts against reperfusion injury (ischemic preconditioning, IPC), but it is unclear whether it protects against long-term moderate hypothermic ischemia. We explored in isolated guinea pig hearts 1) the influence of two 2-min periods of normothermic ischemia before 4 h, 17°C hypothermic ischemia on cardiac cytosolic [Ca2+], mechanical and metabolic function, and infarct size, and 2) the potential role of KATP channels in eliciting cardioprotection. We found that IPC before 4 h moderate hypothermia improved myocardial perfusion, contractility, and relaxation during normothermic reperfusion. Protection was associated with markedly reduced diastolic [Ca2+] loading throughout both hypothermic storage and reperfusion. Global infarct size was markedly reduced from 36 ± 2 (SE)% to 15 ± 1% with IPC. Bracketing ischemic pulses with 200 μM 5-hydroxydecanoic acid or 10 μM glibenclamide increased infarct size to 28 ± 3% and 26 ± 4%, respectively. These results suggest that brief ischemia before long-term hypothermic storage adds to the cardioprotective effects of hypothermia and that this is associated with decreased cytosolic [Ca2+] loading and enhanced ATP-sensitive K channel opening.

NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection

2003 ◽  
Vol 284 (6) ◽  
pp. H2053-H2060 ◽  
Author(s):  
Karine Laude ◽  
Julie Favre ◽  
Christian Thuillez ◽  
Vincent Richard
Keyword(s):  
Ischemia Reperfusion ◽  
No Synthase ◽  
Cardiac Ischemia ◽  
Sham Surgery ◽  
Nos Inhibitor ◽  
Coronary Endothelial Cells ◽  
Cardiac Preconditioning ◽  
Coronary Endothelium ◽  
Inos Inhibition

Preconditioning with brief periods of ischemia-reperfusion (I/R) induces a delayed protection of coronary endothelial cells against reperfusion injury. We assessed the possible role of nitric oxide (NO) produced during prolonged I/R as a mediator of this endothelial protection. Anesthetized rats were subjected to 20-min cardiac ischemia/60-min reperfusion, 24 h after sham surgery or cardiac preconditioning (1 × 2-min ischemia/5-min reperfusion and 2 × 5-min ischemia/5-min reperfusion). The nonselective NO synthase (NOS) inhibitor l-NAME, the selective inhibitors of neuronal (7-nitroindazole) or inducible (1400W) NOS, or the peroxynitrite scavenger seleno-l-methionine were administered 10 min before prolonged ischemia. Preconditioning prevented the reperfusion-induced impairment of coronary endothelium-dependent relaxations to acetylcholine (maximal relaxation: sham 77 ± 3; I/R 44 ± 6; PC 74 ± 5%). This protective effect was abolished by l-NAME (41 ± 7%), whereas 7-NI, 1400W or seleno-l-methionine had no effect. The abolition of preconditioning by l-NAME, but not by selective nNOS or iNOS inhibition, suggests that NO produced by eNOS is a mediator of delayed endothelial preconditioning.

Differential Effects of Anesthetics on Mitochondrial KATPChannel Activity and Cardiomyocyte Protection

2002 ◽  
Vol 97 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Michael Zaugg ◽  
Eliana Lucchinetti ◽  
Donat R. Spahn ◽  
Thomas Pasch ◽  
Carlos Garcia ◽  
...  
Keyword(s):  
Clinical Medicine ◽  
Specific Protein ◽  
Blue Staining ◽  
Cellular Model ◽  
Channel Activity ◽  
Cell Protection ◽  
Channel Opening ◽  
Protein Kinase C Inhibitor ◽  
Cardiac Preconditioning ◽  
Alpha Chloralose

Background Mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine. Methods Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoK(ATP) channel activity, in response to the direct and highly selective mitoK(ATP) channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoK(ATP) channels with respect to myocyte viability. Results Diazoxide-induced mitoK(ATP) channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of alpha-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoK(ATP) channel activity. The significance of these modulatory effects of the anesthetics on mitoK(ATP) channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection. Conclusions These results suggest distinctive actions of individual anesthetics on mitoK(ATP) channels and provide evidence that the choice of background anesthesia may play a role in cardiac protection in both experimental and clinical medicine.

Sign in / Sign up

Export Citation Format

Share Document