Diltiazem and verapamil reduce the loss of adenine nucleotide metabolites from hypoxic hearts.

@article{Takeo1988DiltiazemAV,
  title={Diltiazem and verapamil reduce the loss of adenine nucleotide metabolites from hypoxic hearts.},
  author={Satoshi Takeo and Kouichi Tanonaka and Y Tazuma and Nao Fukao and C Yoshikawa and Taiki Fukumoto and T P Tanaka},
  journal={Journal of molecular and cellular cardiology},
  year={1988},
  volume={20 5},
  pages={
          443-56
        }
}
The present study was undertaken to elucidate possible mechanisms for a protection of myocardial cells from hypoxia-induced derangements in cardiac function and metabolism by calcium antagonists. For this purpose, rabbit hearts were perfused for 20 min under hypoxic conditions in the presence of 312 ng/ml diltiazem or 125 ng/ml verapamil, and then for 45 min under reoxygenated conditions. Metabolic changes in the myocardium and the perfusate were examined throughout. Hypoxia induced a marked… Expand
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References

SHOWING 1-10 OF 29 REFERENCES
Diltiazem administered before or during myocardial ischemia decreases adenine nucleotide catabolism.
TLDR
The effect of diltiazem on ATP catabolism in rat heart, perfused according to Langendorff, was studied and effectively reduced purine release, when applied five minutes after the induction of ischemia, but higher concentrations were needed. Expand
Calcium antagonists and adenine nucleotide metabolism in rat heart.
TLDR
It is concluded that calcium antagonists may, through intercalation with the sarcolemmal membrane, inhibit efflux of adenosine formed by catabolism of adenine nucleotides in ischaemic myocytes, which might offer therapeutic advantage since the intracellular concentration ofAdenosine would thereby be increased, allowing an increased rate of incorporation ofadenosine into the adenoine triphosphate pool in reoxygenated myocardium. Expand
Possible mechanisms for reoxygenation-induced recovery of myocardial high-energy phosphates after hypoxia.
TLDR
A crucial role is suggested of hypoxia-induced release of adenine nucleotide metabolites in a differential recovery of ATP and creatine phosphate upon reoxygenation in rabbit heart Langendorff preparation. Expand
Cardiac injury in short duration anoxia and modification by diltiazem, a calcium channel blocking agent.
TLDR
It is suggested that diltiazem decreases tissue calcium and protects mitochondria more than other cellular components against calcium overload, and this protection may be responsible for the beneficial action of this drug. Expand
A protective effect of coenzyme Q10 on ischemia and reperfusion of the isolated perfused rat heart.
TLDR
Although pretreatment with CoQ had no effect on the onset and progression of ischemic contracture, it facilitated the recovery of mechanical performance and tissue ATP content in CoQ-pretreated reperfused hearts. Expand
Synergistic effect of nifedipine and propranolol on adenosine (catabolite) release from ischemic rat heart.
TLDR
It is concluded that propranolol has a synergistic effect, adding to the beneficial action of nifedipine on ischemic myocardium. Expand
Correlation between changes in the endogenous energy stores and myocardial function due to hypoxia in the isolated perfused rat heart.
On perfusing the isolated rat heart for 7 min with substrate-free hypoxic medium, the contractile force, rate of change of contractile force, time to peak tension, and heart rate declined whereasExpand
Enzyme release during myocardial anoxia: a study of metabolic protection.
TLDR
The results underline the importance of the need for the rapid introduction of protective agents to the anoxic myocardium and suggest that protection must be initiated before the transition from reversible to irreversible cellular damage. Expand
Myocardial ATP synthesis and mechanical function following oxygen deficiency.
TLDR
Ventricular performance was directly related to tissue ATP concentration in aerobic control, postischemic, and postanoxic hearts and complete resynthesis of CP suggests that cellular energy-producing pathways were functional. Expand
Effect of hypoxia on myocardial high-energy phosphates in the neonatal mammalian heart.
TLDR
The data indicate that the newborn rabbit is capable of maintaining glycolysis and normal levels of myocardial ATP during hypoxia, which ensures normal myocardIAL mechanical function for longer periods than in the adult. Expand
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