The effects of hypoxic stress on the fine structure of the flounder heart (Platichthys flesus)

Lennard, Roger; Huddart, H.

doi:10.1016/0300-9629(92)90350-y

Cited by 22 publications

(14 citation statements)

References 33 publications

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“…Such a conclusion would be consistent with the findings of Lennard and Huddart (Lennard and Huddart, 1992) who showed that cardiomyocytes in flounder (Platichthys flesus) subjected to 3weeks of hypoxia (water P O2~5 kPa) showed striking changes in mitochondrial morphology (decreased size, budding and necrosis) and evidence of myofibril degeneration. However, the level of hypoxia in this study (8-9kPa) was not nearly as severe as that used by Lennard and Huddart (Lennard and Huddart, 1992), and several studies have shown that, at least in the trout heart, acute (<30min) exposure to severe anoxia (perfusate P O2 ≤1kPa) does not result in myocardial necrosis or a disruption in myocardial energetic and enzymatic status Overgaard et al, 2004a;Overgaard et al, 2004b). These data thus raise the question of whether myocardial damage and/or necrosis was experienced by our hypoxia-acclimated cod.…”

Section: Maximum Cardiac Function: Normoxiasupporting

confidence: 91%

“…First, it is possible that enhanced glucose uptake and glycolytic capacity were primary factors mediating the enhanced cardiac function of hearts from hypoxiaacclimated cod. Lennard and Huddart (Lennard and Huddart, 1992) report that endogenous glycogen stores are increased in flounder myocytes after 3weeks at a Pw O2 of 5kPa. Several studies have reported the reliance of hypoxic and anoxic teleost cardiac performance on extracellular glucose Bailey P in (kPa) Normoxia-acclimated Hypoxia-acclimated P out (kPa) Fig.5.…”

Section: Maximum Cardiac Function: Hypoxia and Reperfusionmentioning

confidence: 95%

“…For example, stroke volume in fishes is controlled by aneural and neural factors such as cardiac filling/venous pressure, blood oxygen levels and chemistry, myocardial contractility, circulating hormones, and by alterations in cholinergic and adrenergic nervous activity (Kiceniuk and Jones, 1977;Farrell, 1984;Axelsson, 1988;Axelsson and Nilsson, 1986;Satchell, 1991;Farrell, 1991;Zhang et al, 1998;Sandblom and Axelsson, 2005;Sandblom and Axelsson, 2006;Hanson et al, 2006;Hanson and Farrell, 2007). Further, while 3weeks of acclimation to a water oxygen partial pressure (Pw O2 ) of 5kPa (25% air saturation) induced myocardial degeneration and subsequent fibrosis in the flounder (Platichthys flesus) heart (Lennard and Huddart, 1992), Driedzic et al showed that myocardial strips from eelpout (Zoarces vivparous) acclimated to a Pw O2 of 6kPa (~30% air saturation) for 4-6weeks were better able to sustain peak tension development during anoxia in the presence of elevated Ca 2+ levels. In situ heart preparations, first developed for fish by Farrell et al (Farrell et al, 1982), are devoid of any nervous and hormonal input, are extremely robust and tractable, and perform at maximum levels typical of those measured in vivo (Farrell et al, 1985;Farrell et al, 1989;Hanson et al, 2006;Hanson and Farrell, 2007).…”

Section: Introductionmentioning

confidence: 99%

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In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Petersen

Gamperl

2010

Journal of Experimental Biology

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SUMMARYRecent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12weeks at 10°C; PW O2~8 -9kPa) revealed a considerable decrease in the pumping capacity of the heart. To examine whether this diminished cardiac performance was due to the direct effects of chronic moderate hypoxia on the myocardium (as opposed to alterations in neural and/or hormonal control), we measured the resting and maximum in situ function of hearts from normoxia-and hypoxia-acclimated cod:(1) when initially perfused with oxygenated saline; (2) at the end of a 15min exposure to severe hypoxia (P O2~0 .6kPa); and (3) 30min after the hearts had been reperfused with oxygenated saline. Acclimation to hypoxia did not influence resting (basal) in situ cardiac performance during oxygenated or hypoxic conditions. However, it caused a decrease in maximum cardiac output (Q max ) under oxygenated conditions (from 49.5 to 40.3mlmin , yet, the hearts of hypoxiaacclimated fish were better able to sustain this level of Q under hypoxia, and the recovery of Q max (as compared with initial values under oxygenated conditions) was significantly improved (94% vs 83%). These data show that acclimation to hypoxia has a direct effect on cod myocardial function and/or physiology, and suggest that the cod heart shows some adaptations to prolonged hypoxia.

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Section: Maximum Cardiac Function: Normoxiasupporting

confidence: 91%

Section: Maximum Cardiac Function: Hypoxia and Reperfusionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

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In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Petersen

Gamperl

2010

Journal of Experimental Biology

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“…However, whether this reduced pumping capacity is due myocardial stunning (Bolli and Marban, 1999), myocardial necrosis (e.g. Lennard and Huddart, 1992) or remodelling of the myocardium that resulted in a smaller ventricular lumen and outflow tract (Marques et al, 2008) has not been resolved. Hypoxia-acclimated cod were able to increase ƒ H during the hypoxic swim to levels measured during normoxia (Fig.2, Table3).…”

Section: Kgmentioning

confidence: 99%

“…locomotion, digestion) and for appropriate responses to environmental changes (Farrell, 2002;Claireaux et al, 2005;Gollock et al, 2006;Clark and Seymour, 2006;Steinhausen et al, 2008), and an understanding of how chronic hypoxia affects both swimming performance and cardiovascular function could reveal important information about whether fish will survive, and how well they adapt to, hypoxic environments. At present, studies on the effects of chronic (weeks of) hypoxia have been conducted on a limited number of teleost species, and focused on a range of aspects such as food intake (Chabot and Dutil, 1999;Pichavant et al, 2000;Pichavant et al, 2001;Zhou et al, 2001), reproduction (Wu et al, 2003), oxygen carrying capacity (Greaney et al, 1980;Taylor and Miller, 2001;Pichavant et al, 2003), cardiomyocyte physiology (Lennard and Huddart, 1992;Paajanen and Vornanen, 2003) and circulating catecholamine levels (Butler et al, 1979;Montpetit and Perry, 1998). However, to our knowledge only two studies (Kutty, 1968;Bushnell et al, 1984) have investigated how chronic hypoxia affects fish swimming performance and metabolism, and only one study (Burleson et al, 2002) has examined the effect of chronic hypoxia on fish in vivo cardiovascular function.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute and chronic hypoxia on the swimming performance, metabolic capacity and cardiac function of Atlantic cod (Gadus morhua)

Petersen

Gamperl

2010

Journal of Experimental Biology

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SUMMARYLow water oxygen content (hypoxia) is a common feature of many freshwater and marine environments. However, we have a poor understanding of the degree to which diminished cardiac function contributes to the reduction in fish swimming performance concomitant with acute exposure to hypoxia, or how fish cardiorespiratory physiology is altered by, or adapts to, chronic hypoxia. Thus, we acclimated adult Atlantic cod (Gadus morhua) to either ~8-9kPa O 2 (40-45% air saturation) or ~21kPaO 2 (100% air saturation; normoxia) for 6-12weeks at 10°C, and subsequently measured metabolic variables [routine oxygen consumption (M O2 ), maximum M O2 , metabolic scope] and cardiac function (cardiac output, Q; heart rate, f H ; and stroke volume, V S ) in these fish during critical swimming speed (U crit ) tests performed at both levels of water oxygenation. Although surgery (flow probe implantation) reduced the U crit of normoxia-acclimated cod by 14% (from 1.74 to 1.50BLs -1 ) under normoxic conditions, exposure to acute hypoxia lowered the U crit of both groups (surgery and non-surgery) by ~30% (to 1.23 and 1.02BLs -1 , respectively). This reduction in swimming performance was associated with large decreases in maximum M O2 and metabolic scope (≥50%), and maximum f H and Q (by 16 and 22%), but not V S . Long-term acclimation to hypoxia resulted in a significant elevation in normoxic metabolic rate as compared with normoxia-acclimated fish (by 27%), but did not influence normoxic or hypoxic values for U crit , maximum M O2 or metabolic scope. This was surprising given that resting and maximum values for Q were significantly lower in hypoxia-acclimated cod at both levels of oxygenation, because of lower values for V S . However, hypoxia-acclimated cod were able to consume more oxygen for a given cardiac output. These results provide important insights into how fish cardiorespiratory physiology is impacted by short-term and prolonged exposure to hypoxia, and further highlight the tremendous capacity of the fish cardiorespiratory system to deal with environmental challenges.

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Quantitative electron microscopic study of the hypoxic fetal sheep heart

et al. 1999

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In order to determine the effects of chronic, high-altitude hypoxia on the ovine fetal heart, we exposed pregnant ewes to 3,820 m beginning at 30 days gestation. We previously showed that following Ϸ110 days of hypoxia the fetal heart showed significant reduction in cardiac output (76% of control) and contractility, and elevated levels of citrate synthase and lactate dehydrogenase. To investigate ultrastructural influences on these observed physiologic changes at altitude, we hypothesized that the volume densities of myofibrils and mitochondria, and glycogen content would be reduced in the ovine fetal heart and that this may contribute to contraction and cardiac output deficits in hypoxia. Mitochondria and myofibril volume density were determined by standard point-counting techniques and glycogen content was determined by biochemical analysis. The glycogen content from the hypoxic right ventricle (4.8 Ϯ 0.3%) was significantly lower than in control right ventricle (6.8 Ϯ 0.5%) and both left ventricles (hypoxia, 7.2 Ϯ 0.5; control, 7.8 Ϯ 0.4%). Total mitochondrial volume density was also significantly reduced following hypoxia (15.5 Ϯ 0.7%) compared to controls (16.9 Ϯ 0.4%). As is common in the ovine fetal heart, the myofibril volume density of the right ventricle from both groups was significantly higher than the left ventricle (RV, 58.6 Ϯ 1.6; LV 54.3 Ϯ 0.9%). However, it was not different between control and high altitude. In support of our hypothesis, we may speculate that deficits in the quantity of myocyte glycogen and mitochondria contribute to the observed reduction in cardiac output and contractility, despite the upregulation of citrate synthase and lactate dehydrogenase. In contrast, myofibril volume density was unchanged.

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The effects of hypoxic stress on the fine structure of the flounder heart (Platichthys flesus)

Cited by 22 publications

References 33 publications

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Effect of acute and chronic hypoxia on the swimming performance, metabolic capacity and cardiac function of Atlantic cod (Gadus morhua)

Quantitative electron microscopic study of the hypoxic fetal sheep heart

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