Calcium, strontium, and barium movements during ischemia and reperfusion in rabbit ventricle. Implications for myocardial preservation.

Shine, Kenneth I.; Douglas, Annie M.; Ricchiuti, N. V.

doi:10.1161/01.res.43.5.712

Cited by 89 publications

(10 citation statements)

References 11 publications

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“…Although Ba 2ϩ and Sr 2ϩ are permeable through many types of voltage-gated and receptoroperated cation channels, Ba 2ϩ is a poor substrate for sarco-(endo)plasmic reticulum Ca 2ϩ -ATPase (SERCA) and plasma membrane Ca 2ϩ -ATPase (PMCA) pumps (8,21,24,28) and in general has much lower affinity for Ca 2ϩ -binding proteins of the EF-hand and C2 type than does Ca 2ϩ (9). The results of the present study show that the kinetics and the magnitude of each step in the cell death cascade were similar when Ca 2ϩ was isosmotically replaced by Sr 2ϩ , with only a slight delay in the average time to cell lysis.…”

Section: Discussionmentioning

confidence: 99%

Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity

Wisnoskey¹,

Estacion²,

Schilling³

2004

American Journal of Physiology-Cell Physiology

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Section: Discussionmentioning

confidence: 99%

Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity

Wisnoskey¹,

Estacion²,

Schilling³

2004

American Journal of Physiology-Cell Physiology

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“…Most of the experiments in which Ca ++ entry has been shown to occur early in ischemia have employed hearts or portions of heart perfused in vitro under conditions of anoxia or with episodes of low or absent flow (ischemia) (Shine et al, 1978;Nayler et al, 1979;Bourdillon and Poole-Wilson, 1981).…”

Section: The Mitochondrion In the Inset Was The Only Damaged Mitochmentioning

confidence: 99%

“…The reperfused tissue becomes edematous and gains both K + and Na + . However, although Ca ++ overload has been proposed as a potential cause of cell death or cellular dysfunction in ischemia (Shen and Jennings, 1972;Jennings et al, 1975;Farber and El-Mofty, 1975;Shine et al, 1978;Nayler et al, 1979;Bourdillon and Poole-Wilson, 1981;Farber, 1982;Jennings, 1984), an increase in myocardial caldum was not detected after any of the periods of reperfusiori studied. Alterations in ultrastructure induced by ischemia essentially disappeared after 20, but not after 3 minutes of reperfusion.…”

mentioning

confidence: 92%

Effect of reperfusion late in the phase of reversible ischemic injury. Changes in cell volume, electrolytes, metabolites, and ultrastructure.

Jennings¹,

Schaper²,

Hill³

et al. 1985

Circulation Research

341

142

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The acute effects of reperfusion on myocardium reversibly damaged by 15 minutes of severe ischemia in vivo, were studied. Changes in the adenine nucleotide pool, cell volume regulation, myocardial calcium, and ultrastructure were studied at the end of 15 minutes of ischemia and after 0.5, 3.0, and 20 minutes of reflow. Before reperfusion, adenosine triphosphate and the adenylate pool decreased by 63% and 44% of control, respectively, and the adenylate charge was reduced to 0.65. After 3 minutes of reperfusion, the adenylate charge was restored to control by the rephosphorylation of adenosine mono- and diphosphate, but adenosine triphosphate was still reduced by 45%. Mild tissue edema was detected after 0.5 minute of reflow and persisted throughout 20 minutes of reperfusion. The increased tissue water was accompanied by a slight increase in sodium and a marked increase in tissue potassium. Although massive calcium accumulation develops when irreversibly injured tissue is reperfused, no calcium overload was detected during early reperfusion of reversibly injured myocytes. Reperfusion for 3 minutes exaggerated the mitochondrial swelling induced by 15 minutes of ischemia but after 20 minutes of reperfusion, myocardial ultrastructure was essentially normal except for rare swollen, or disrupted, mitochondria. Thus, the cellular abnormalities associated with brief periods of ischemia persist for variable periods of time after reperfusion of reversibly injured myocytes. First: although adenine nucleotide repletion occurs very slowly, the adenylate charge was restored after 3 minutes, indicating rapid resumption of mitochondrial adenosine triphosphate production. Second: calcium overload was not detected, but myocardial edema and increased potassium persisted throughout the 20 minutes of reperfusion. Third: the ultrastructural consequences of ischemia were nearly reversed after 20 minutes of reperfusion.

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“…Oxidative stress is known to occur and to play a relevant pathophysiological role in several diseases, including ischemia-reperfusion [162,163]. Consistent with these observation, a decrease in extracellular Ca 2+ concentration can reduce ischemic injury [145][146][147]. Manipulation of extracellular Ca 2+ may modify the extent of cellular injury even if applied only at the time of reperfusion, suggesting that cytosolic Ca 2+ overload is one of the mechanisms of reperfusion injury [148,149].…”

Section: Reactive Oxygen Species (Ros)mentioning

confidence: 85%

Biochemical Basis of Ischemic Heart Injury and of Cardioprotective Interventions

Zucchi

Ghelardoni²,

Evangelista³

2007

CMC

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Cardioprotective interventions are defined as interventions able to increase myocardial resistance to ischemia. The authors approach the issue of cardioprotection on the basis of the present knowledge about the biochemical mechanisms responsible for the injury produced by myocardial ischemia or ischemia-reperfusion. Reversible and irreversible injury are distinguished. The former is largely accounted for by the direct consequences of reduced ATP synthesis, which causes decreased ATP phosphorylation potential, acidosis and phosphate accumulation. The biochemical mechanisms leading to irreversible injury include osmotic overload, production of toxic lipid metabolites, cytosolic calcium overload, and generation of reactive oxygen species, which lead to membrane disruption, mitochondrial dysfunction and possibly to the activation of apoptotic pathways. The major effect of the classical cardioprotective agents (nitrates, beta adrenergic antagonists, calcium channel blockers) consists in affecting ATP demand/supply ratio in such a way as to delay the decrease in ATP phosphorylation potential. Other drugs have been introduced, which allegedly interfere directly with the mechanisms responsible for irreversible ischemic injury. These include 3-ketoacyl-CoA tiolase inhibitors, modulators of intracellular calcium channels, ionic exchanger inhibitors, free radical scavengers, caspase inhibitors, purinergic agonists, K(+)(ATP) channel openers, and modulators of mitochondrial permeability transition. The results obtained with these substances in experimental models and in the clinical setting are discussed. Special attention is devoted to angiotensin converting enzyme inhibitors, whose direct cardioprotective properties has recently been demonstrated.

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Calcium, strontium, and barium movements during ischemia and reperfusion in rabbit ventricle. Implications for myocardial preservation.

Cited by 89 publications

References 11 publications

Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity

Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity

Effect of reperfusion late in the phase of reversible ischemic injury. Changes in cell volume, electrolytes, metabolites, and ultrastructure.

Biochemical Basis of Ischemic Heart Injury and of Cardioprotective Interventions

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