Acute ischaemic preconditioning and chronic hypoxia independently increase myocardial tolerance to ischaemia

Tajima, Masahiro; Katayose, Dai; Bessho, Motoaki; Isoyama, Shogen

doi:10.1093/cvr/28.3.312

Cited by 83 publications

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“…However, studies on adult mammalian hearts do not support this conclusion. Both Tajima et al, (1994) and Neckár et al (2002) demonstrated that although hearts from chronically hypoxic adult rats had increased resistance to ischaemia-related damage, preconditioning conferred an increased amount of protection. Taken together, these results suggest that the relationship between inherent hypoxia tolerance and the ability to be preconditioned in lower vertebrates and neonatal/immature mammals is similar, but that these two groups differ as compared with adult mammals.…”

Section: Discussionmentioning

confidence: 99%

“…Further, Baker et al (1999) showed that hearts from 7-10-day-old rabbits that were reared in a hypoxic environment (12% oxygen) developed a degree of myocardial ischaemia-tolerance (60% recovery of contractile function following 40·min of ischaemia), and no longer experienced increased functional recovery in response to preconditioning. In contrast, both Tajima et al (1994) and Neckár et al (2002) demonstrated that although hearts from chronically hypoxic adult rats had increased resistance to ischaemia-related damage, preconditioning conferred an additional amount of protection. These results question whether long-term and short-term mechanisms of ischaemic protection in the mammalian heart share the same signal transduction pathways and end-effectors, and whether the relationship between inherent hypoxia/ischaemia tolerance and preconditioning is fundamentally different between life stages.…”

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confidence: 90%

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Hypoxia tolerance and preconditioning are not additive in the trout(Oncorhynchus mykiss) heart

Gamperl

Faust

Dougher

et al. 2004

Journal of Experimental Biology

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Research has shown that the trout heart is normally hypoxia-sensitive, and that it can be preconditioned. However, we have identified a group of rainbow trout Oncorhynchus mykiss that shows a surprising degree of myocardial hypoxia tolerance. In this study, we used in situ hearts from these fish as a comparative model to examine whether the cardioprotective effects afforded by hypoxic adaptation and preconditioning are additive. In situ trout hearts were exposed to severe hypoxia (perfusate P O∑ 5-10·mmHg) in the absence and presence of a transient hypoxic pre-exposure (preconditioning). The four groups studied were: (1) control (no hypoxia); (2) 5·min of severe hypoxia; (3) 30·min of severe hypoxia; and (4) 5·min of severe hypoxia (hypoxic preconditioning) followed 20·min later by 30·min of severe hypoxia. 30·min of severe hypoxia significantly decreased maximum cardiac output and stroke volume by 15-30%. However, hypoxic preconditioning failed to confer any protection against post-hypoxic myocardial dysfunction. This work shows that the protection afforded by inherent myocardial hypoxia tolerance and preconditioning are not additive in this population of trout, and strongly suggests that the relationship between hypoxic adaptation and preconditioning in fishes resembles that of the neonatal/immature, not adult, mammalian heart. Further, our results (1) indicate that stretch (volume loading) and chronic exposure to low levels of adrenaline (15·nmol·l -1 ) do not confer any protection against hypoxia-related myocardial dysfunction in this population, and (2) validate the use of the in situ trout heart as a comparative model for studying aspects of myocardial hypoxia tolerance and preconditioning in vertebrates.

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Section: Discussionmentioning

confidence: 99%

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confidence: 90%

Hypoxia tolerance and preconditioning are not additive in the trout(Oncorhynchus mykiss) heart

Gamperl

Faust

Dougher

et al. 2004

Journal of Experimental Biology

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“…For example, ischaemic preconditioning failed to improve contractile function following 40·min of global ischemia in hypoxia-tolerant neonatal rat hearts (1 or 4 days post partum), only slightly (by 7%) improved contractile function in relatively hypoxia-sensitive rat hearts tested 7 days post partum (Ostadalova et al, 1998), and Baker et al (1999) showed that hearts from 7-10 day old rats that were reared in a hypoxic environment (12% oxygen) no longer experienced increased functional recovery in response to preconditioning. In contrast, both Tajima et al (1994) and Nechár et al (2002) demonstrated that although hearts from chronically hypoxic adult rats had increased resistance to ischaemia-related damage, preconditioning conferred an additional amount of protection. Thus, to examine whether hearts from hypoxiatolerant trout can be preconditioned, we recently conducted in Fig.·4.…”

Section: Hypoxic Acclimationmentioning

confidence: 94%

Cardiac plasticity in fishes: environmental influences and intraspecific differences

Gamperl

Farrell

2004

Journal of Experimental Biology

229

176

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With over 20·000 species of teleost fish, considerable interspecific diversity in cardiac anatomy and physiology is expected. This is the outcome of evolutionary adaptation to different habits, modes of life and activity levels. For example, athletic species have a more powerful heart than sedentary species, and fish such as hagfish, carp and eel normally show a much higher degree of myocardial hypoxia tolerance than species such as salmonids (Farrell, 1991;Farrell and Jones, 1992). Plasticity in cardiac form and function has also been demonstrated during ontogeny, and the cardiovascular flexibility exhibited during embryonic and larval development, is nicely reviewed by Pelster (2003). What is less well appreciated, however, is the high degree of intraspecific cardiac plasticity displayed by post-larval fishes. Accordingly, this review explores what is known about intraspecific cardiac plasticity among juvenile and adult fishes. This intraspecific plasticity, like that exhibited during development, may well reflect individual variability on which natural selection could act.In this review, we focus primarily on temperature effects, which are relatively well studied, and on the effects of other environmental and biological factors that modify cardiac anatomy and physiology, including food deprivation, sexual maturation, exercise training and rearing under aquaculture conditions. Further, we summarize recent work on cardiac preconditioning and myocardial hypoxia tolerance in fishes, and discuss the potential implications of this work.Preconditioning is a short-term form of cardiac plasticity that has the potential to protect the heart from insults that might normally lead to cardiac damage, dysfunction or death. Preconditioning has been the focus of several thousand mammalian studies (e.g. see review by Yellon and Downey, 2003), and so the handful of recent studies in fish, which already point to important intraspecific differences, may find application outside the piscine world. Similarly, researchers who wish to stimulate cardiac growth to replace damaged myocardial tissue in mammals, may be heartened to discover that fish cardiac tissue, unlike the mammalian heart, does not lose its ability for hyperplastic growth with age. In fact, we suspect that the high degree of intraspecific plasticity that we Fish cardiac physiology and anatomy show a multiplicity of intraspecific modifications when exposed to prolonged changes in environmentally relevant parameters such as temperature, hypoxia and food availability, and when meeting the increased demands associated with training/increased activity and sexual maturation. Further, there is evidence that rearing fish under intensive aquaculture conditions significantly alters some, but not all, aspects of cardiac anatomy and physiology. This review focuses on the responses of cardiac physiology and anatomy to these challenges, highlighting where applicable, the importance of hyperplastic (i.e. the production of new cells) vs hypertrophic (the enlargement of existing cells...

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“…In an isolated adult rat heart model, chronic hypoxia improved postischemic systolic function and protected against prolonged periods of ischemia (27). Although similarities of the phenomena of hypoxic and ischemic preconditioning have been found in protecting the myocardium, the additive cardioprotective effects of hypoxic and ischemic preconditioning suggest different mechanisms of protection (27).…”

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confidence: 99%

Responses of chronically hypoxic rat hearts to ischemia: K_ATP channel blockade does not abolish increased RV tolerance to ischemia

Forkel¹,

Chen²,

Wandinger³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia. Am J Physiol Heart Circ Physiol 286: H545-H551, 2004. First published October 9, 2003 10.1152/ajpheart.00022.2003.-Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O2) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1␣ and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 Ϯ 6% and 67 Ϯ 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 Ϯ 2% of baseline in Hypo vs. 67 Ϯ 3% in Norm (P Ͻ 0.05). Improved postischemic right ventricular function in Hypo (93 Ϯ 2% and 96 Ϯ 2% of baseline) was observed with 95% O 2 or 21% O2 in the perfusate, and it was not attenuated by glibenclamide (5 and 10 mol/l) (86 Ϯ 4% and 106 Ϯ 6% recovery). HIF-1␣ mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K ϩ channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts. chronic hypoxia; glibenclamide; hypoxia-inducible factor-1␣; endothelial nitric oxide synthase ISCHEMIC PRECONDITIONING protects myocardium against subsequent ischemia-reperfusion injury (19). Protection is evident by limitation of infarct size (19,22), better recovery of myocardial contractile function in some models (8), preservation of high-energy phosphate levels (13), and attenuation of arrhythmias (23). ATP-sensitive K ϩ (K ATP ) channels are crucially involved in the protection of ischemic preconditioning (10).Chronic hypoxic preconditioning also increases the tolerance of the myocardium to ischemia. In an isolated adult rat heart model, chronic hypoxia improved postischemic systolic function and protected against prolonged periods of ischemia (27). Although similarities of the phenomena of hypoxic and ischemic preconditioning have been found in protecting the myocardium, the additive cardioprotective effects of hypoxic and ischemic preconditioning suggest different mechanisms of protection (27). Baker et al. (3,4) reported that the increased tolerance to ischemia in isolated crystalloid-perfused immature rabbit hearts exposed to chronic hypoxia is associated with an activation of the K ATP channels. The beneficial effects of chronic hypoxic preconditioning on left and right ventricular (RV) developed pressure were abolished by the K ATP channel antagonist glibenclamide. The K ATP channel agonist bimakalim enhanced postischemic left ventricular (LV) function in normoxic heart...

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Acute ischaemic preconditioning and chronic hypoxia independently increase myocardial tolerance to ischaemia

Cited by 83 publications

References 0 publications

Hypoxia tolerance and preconditioning are not additive in the trout(Oncorhynchus mykiss) heart

Hypoxia tolerance and preconditioning are not additive in the trout(Oncorhynchus mykiss) heart

Cardiac plasticity in fishes: environmental influences and intraspecific differences

Responses of chronically hypoxic rat hearts to ischemia: K_ATP channel blockade does not abolish increased RV tolerance to ischemia

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