Question: Which phenomenon is known as the "calcium paradox" in the isolated perfused heart?

Context:
"Calcium paradox" as a term describes the deleterious effects conferred to a heart perfused with a calcium-free solution followed by repletion, including loss of mechanical activity and sarcomere disruption.
Calcium paradox was found to markedly activate members of the MAPKs (p43-ERK, JNKs, p38-MAPK). 
To our knowledge, this is the first time that the calcium paradox has been shown to induce apoptosis in amphibians, with p38-MAPK and calpain playing significant roles.
The Ca(2+) paradox represents a good model to study Ca(2+) overload injury in ischemic heart diseases. We and others have demonstrated that contracture and calpain are involved in the Ca(2+) paradox-induced injury.
The Ca(2+) paradox was elicited by perfusing isolated rat hearts with Ca(2+)-free KH media for 3 min or 5 min followed by 30 min of Ca(2+) repletion.
These results provide evidence suggesting that contracture is the main cause for contractile dysfunction, while activation of calpain mediates cell death in the Ca(2+) paradox.
The Ca2+ -paradox is an important phenomenon to study cell injury induced by Ca2+ -overload in myocardium. Although intracellular Ca2+ -overload acts as a trigger and modulator of cell death due to apoptosis under various pathophysiological conditions, the presence of apoptosis in hearts subjected to Ca2+ -paradox has not been demonstrated.
Ca2+ -paradox was induced by perfusing the isolated rat heart with Ca2+ -free medium for 5 min followed by reperfusion with Ca2+ -containing medium for 30 min.
This study suggests that cardiac dysfunction due to Ca2+ -paradox may be associated with apoptosis.
Normothermic 3 min lasting perfusion of the isolated rat heart by Krebs--Henseleit solution in which Ca2+ was replaced by EDTA and subsequent perfusion with a Ca2+ containing medium induced structural and metabolic changes demonstrated electron microscopically and histochemically. In contrast to the ischemic reperfusion damage, in calcium paradox, the histochemically studied enzymes alpha-glucan-phosphorylase, lactate dehydrogenase, succinic dehydrogenase, beta-hydroxybutyric dehydrogenase, and ATPases were better preserved in the subendocardial region of the left ventricle.
On the other hand, myocytes in the subepicardial region and in the midmyocardium were markedly damaged and all characteristic signs of calcium paradox were present, including hypercontraction bands with myofilament fusion, extrusion and accumulation of edematous mitochondria with occurrence of electron dense material in mitochondrial cristae, ruptures of the sarcolemma in all its layers, separation of intercalated discs, etc.
Intracellular Ca2+-overload in the myocardium can be induced not only after readmission of Ca2+-containing fluid to rat hearts previously perfused with a Ca2+-free buffer, a phenomenon called "the calcium paradox", but also during administration of a Ca2+-ionophore to cardiac tissue. In rat hearts, the myocardial damage induced by the Ca2+ paradox was more pronounced than that after administration of the Ca2+-ionophore A23187, as indicated by the amount of lactate dehydrogenase released.
When hearts were reperfused with Ca++ after a short period of Ca++-free perfusion, irreversible loss of electrical and mechanical activity was observed. This phenomenon, first described by Zimmerman and Hulsmann, was termed the "calcium paradox". Chizzonite and Zak recently reported that rat hearts exhibited an age-dependent response in a calcium paradox model. 
Injury is sustained by isolated hearts on repletion with calcium after a short period of perfusion with calcium-free medium at 37 degrees. A possible mechanism for the 'calcium paradox' is that exposure to a calcium-fre medium removes extracellular calcium rendering the sarcolemma more permeable to calcium. On calcium repletion, cell injury is triggered by calcium influx.
Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox. A similar paradoxical effect of Ca2+ has also been reported to occur in the kidney
It is concluded that there is no calcium paradox in canine kidney under these conditions and it is suggested that the Ca2+ paradox may be characteristics only of muscle tissue that can undergo Ca2+-dependent contraction.
When isolated rat hearts are perfused with Ca2+-containing medium, after a brief Ca2+-free period, irreversible cell damage occurs (calcium paradox). This phenomenon is concomitant with a rapid consumption of myocardial high-energy phosphate stores, prior to the appearance of these compounds in the effluent perfusion medium. 
Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox.
Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox

Answer: "Calcium paradox" as a term describes the deleterious effects conferred to a heart perfused with a calcium-free solution followed by repletion, including loss of mechanical activity and sarcomere disruption.Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox. A similar paradoxical effect of Ca2+ has also been reported to occur in the kidney
When hearts are reperfused with Ca++ after a short period of Ca++-free perfusion, irreversible loss of electrical and mechanical activity is observed. This phenomenon, first described by Zimmerman and Hulsmann, was termed the "calcium paradox". This phenomenon is concomitant with a rapid consumption of myocardial high-energy phosphate stores. The Ca(2+) paradox represents a good model to study Ca(2+) overload injury in ischemic heart diseases. The Ca(2+) paradox can be elicited by perfusing isolated hearts with Ca(2+)-free media for 3 min or 5 min followed by 30 min of Ca(2+) repletion. A possible mechanism for the 'calcium paradox' is that exposure to a calcium-free medium removes extracellular calcium rendering the sarcolemma more permeable to calcium. On calcium repletion, cell injury is triggered by calcium influx. Cardiac dysfunction due to Ca2+ -paradox may be associated with apoptosis.
Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox. A similar paradoxical effect of Ca2+ has also been reported to occur in the kidney  When isolated rat hearts are perfused with Ca2+-containing medium, after a brief Ca2+-free period, irreversible cell damage occurs (calcium paradox). This phenomenon is concomitant with a rapid consumption of myocardial high-energy phosphate stores, prior to the appearance of these compounds in the effluent perfusion medium.   
Isolated perfusion of the heart with a Ca2+-free perfusate followed by a Ca2+-containing perfusate causes dramatic alterations in the physiology and biochemistry of the tissue, a phenomenon known as the calcium paradox. A similar paradoxical effect of Ca2+ has also been reported to occur in the kidney  When isolated rat hearts are perfused with Ca2+-containing medium, after a brief Ca2+-free period, irreversible cell damage occurs (calcium paradox). This phenomenon is concomitant with a rapid consumption of myocardial high-energy phosphate stores, prior to the appearance of these compounds in the effluent perfusion medium.   When hearts were reperfused with Ca++ after a short period of Ca++-free perfusion, irreversible loss of electrical and mechanical activity was observed. This phenomenon, first described by Zimmerman and Hulsmann, was termed the  calcium paradox . Chizzonite and Zak recently reported that rat hearts exhibited an age-dependent response in a calcium paradox model.