“Preconditioning at a Distance” in the Isolated Rabbit Heart

Dickson, Eric W.; Porcaro, William A.; Fenton, Richard A.; Heard, Stephen O.; Reindhardt, Christopher P.; Renzi, Francis P.; Przyklenk, Karin

doi:10.1111/j.1553-2712.2000.tb02228.x

Cited by 35 publications

(15 citation statements)

References 27 publications

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“…This study uses a model first pioneered by the Przyklenk laboratory [17], and has been used in several subsequent publications by different groups [11, 43]. Although it is described in the literature as more similar to remote ischaemic preconditioning, in fact it likely reflects the humoral aspect to classical preconditioning.…”

Section: Studymentioning

confidence: 99%

Intrinsic cardiac ganglia and acetylcholine are important in the mechanism of ischaemic preconditioning

et al. 2017

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This study aimed to investigate the role of the intrinsic cardiac nervous system in the mechanism of classical myocardial ischaemic preconditioning (IPC). Isolated perfused rat hearts were subjected to 35-min regional ischaemia and 60-min reperfusion. IPC was induced as three cycles of 5-min global ischaemia–reperfusion, and provided significant reduction in infarct size (IS/AAR = 14 ± 2% vs control IS/AAR = 48 ± 3%, p < 0.05). Treatment with the ganglionic antagonist, hexamethonium (50 μM), blocked IPC protection (IS/AAR = 37 ± 7%, p < 0.05 vs IPC). Moreover, the muscarinic antagonist, atropine (100 nM), also abrogated IPC-mediated protection (IS/AAR = 40 ± 3%, p < 0.05 vs IPC). This indicates that intrinsic cardiac ganglia remain intact in the Langendorff preparation and are important in the mechanism of IPC. In a second group of experiments, coronary effluent collected following IPC, from ex vivo perfused rat hearts, provided significant cardioprotection when perfused through a naïve isolated rat heart prior to induction of regional ischaemia–reperfusion injury (IRI) (IS/ARR = 19 ± 2, p < 0.05 vs control effluent). This protection was also abrogated by treating the naïve heart with hexamethonium, indicating the humoral trigger of IPC induces protection via an intrinsic neuronal mechanism (IS/AAR = 46 ± 5%, p < 0.05 vs IPC effluent). In addition, a large release in ACh was observed in coronary effluent was observed following IPC (IPCeff = 0.36 ± 0.03 μM vs C eff = 0.04 ± 0.04 μM, n = 4, p < 0.001). Interestingly, however, IPC effluent was not able to significantly protect isolated cardiomyocytes from simulated ischaemia–reperfusion injury (cell death = 45 ± 6%, p = 0.09 vs control effluent). In conclusion, IPC involves activation of the intrinsic cardiac nervous system, leading to release of ACh in the ventricles and induction of protection via activation of muscarinic receptors.

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Section: Studymentioning

confidence: 99%

Intrinsic cardiac ganglia and acetylcholine are important in the mechanism of ischaemic preconditioning

et al. 2017

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“…2000). In many mammalian tissues, this complex phenomenon has been documented to occur even ‘at a distance’ (Dickson et al. 2000), indicating that, under stress, cellular procedures may be accomplished through integrated intracellular/extracellular defence mechanisms.…”

Section: Introductionmentioning

confidence: 99%

The heat shock response is dependent on the external environment and on rapid ionic balancing by pharmacological agents in Saccharomyces cerevisiae

2004

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I . V O V O U , A . D E L I T H E O S A N D E . T I L I G A D A . 2004.Aims: To investigate whether non-preconditioned yeast cells survive under heat shock, when placed in growth medium originated from protected cells and to provide insights into the ionic contribution in the response. Methods and Results: The heat shock response was investigated by determining cell viability following exposure of yeast cells to 53°C for 30 min, either in the absence or presence of drugs. Preconditioning was performed by incubating the cultures at 37°C for 2 h. Under heat shock, non-preconditioned cell survival was significantly enhanced by the presence of the cell-free supernatant of resistant cultures. Addition of omeprazole or tetraethylammonium ions during the heat shock resulted in similar increases. Neither amiodarone nor mepivacaine showed any analogous effect. Omeprazole enhanced survival when added before the heat shock, while amiodarone exhibited a cytocidic action. Conclusions: Rapid balancing of ions may contribute to cell survival during heat shock, while survival under mild stress could probably be co-ordinated by additional events. Significance and Impact of the Study: Evidence is provided for the implication of the external environment and ionic homeostasis in the survival of yeast cells under unfavourable environmental conditions. This knowledge may be of importance in controlling both fermentation and therapeutic approaches.

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“…17 Later on, the same team would conduct a study of remote cardioprotective action of IPre in vitro. 18 IPre was performed with three 5-minute cycles of ischemia and reperfusion of the isolated rabbit heart, and coronary effluent was collected. This effluent was passed through acceptor hearts (without IPre), which significantly increased their mechanical function following a transient ischemic insult.…”

Section: Humoral Factorsmentioning

confidence: 99%

A Review of Humoral Factors in Remote Preconditioning of the Heart

Tsibulnikov

Маслов

Gorbunov

et al. 2019

J Cardiovasc Pharmacol Ther

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A humoral mechanism of cardioprotection by remote ischemic preconditioning (RIP) has been clearly demonstrated in various models of ischemia–reperfusion including upper and lower extremities, liver, and the mesenteric and renal arteries. A wide range of humoral factors for RIP have been proposed including hydrophobic peptides, opioid peptides, adenosine, prostanoids, endovanilloids, endocannabinoids, calcitonin gene-related peptide, leukotrienes, noradrenaline, adrenomedullin, erythropoietin, apolipoprotein, A-I glucagon-like peptide-1, interleukin 10, stromal cell-derived factor 1, and microRNAs. Virtually, all of the components of ischemic preconditioning’s signaling pathway such as nitric oxide synthase, protein kinase C, redox signaling, PI3-kinase/Akt, glycogen synthase kinase β, ERK1/2, mitoKATP channels, Connexin 43, and STAT were all found to play a role. The signaling pattern also depends on which remote vascular bed was subjected to ischemia and on the time between applying the rip and myocardial ischemia occurs. Because there is convincing evidence for many seemingly diverse humoral components in RIP, the most likely explanation is that the overall mechanism is complex like that seen in ischemic preconditioning where multiple components are both in series and in parallel and interact with each other. Inhibition of any single component in the right circumstance may block the resulting protective effect, and selectively activating that component may trigger the protection. Identifying the humoral factors responsible for RIP might be useful in developing drugs that confer RIP’s protection in a more comfortable and reliable manner.

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“Preconditioning at a Distance” in the Isolated Rabbit Heart

Cited by 35 publications

References 27 publications

Intrinsic cardiac ganglia and acetylcholine are important in the mechanism of ischaemic preconditioning

Intrinsic cardiac ganglia and acetylcholine are important in the mechanism of ischaemic preconditioning

The heat shock response is dependent on the external environment and on rapid ionic balancing by pharmacological agents in Saccharomyces cerevisiae

A Review of Humoral Factors in Remote Preconditioning of the Heart

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