Tissue protection by adrenergic blockade in the calcium paradox?

  title={Tissue protection by adrenergic blockade in the calcium paradox?},
  author={Audun N. {\O}ksendal and Per Jynge},
  journal={Basic Research in Cardiology},
SummaryIn a graded model of the calcium paradox phenomenon (minimal and total) the presence of the β-blocker propranolol (5·10−6M) in the perfusion media (10 min prior to, during and 5 min following calcium-free perfusion) has no effect upon tissue injury. Propranolol pretreatment (three days prior to the experiments) significantly reduced the myocardial enzyme release during calcium repletion in the minimal calcium paradox. The presence of the α1 prazosin (1·10−7M) in the perfusion media (10… 


Myocardial protection by micromolar manganese in the calcium paradox and additive effects of verapamil
It is concluded from the study that 50 μmol of manganese, although effective in tissue protection, cannot substitute totally for the loss of calcium during calcium-free perfusion and thatManganese may substitute for the micromolar calcium needed for tissue protection by verapamil.
Protection by verapamil in the calcium paradox: dependence on micromolar calcium.
It is concluded that tissue protection by verapamil in the calcium paradox requires the presence in the myocardium of both verap amil and trace amounts of calcium before the onset of calcium repletion, and is therefore limited to minimal injury types.
Myocardial cAMP and calcium levels in the calcium paradox
It is concluded that calcium-free coronary perfusion induces a complex series of events favouring excessive calcium entry, only one of which may be related to a change in cAMP.
Effects of diltiazem on the calcium paradox in isolated rat hearts.
Diltiazem appears to exert its protective effect against the mild calcium paradox phenomenon by regulating the ionic environment of myocardial cells during the calcium-free period.
Calcium, Sodium, and the Calcium Paradox
It is proposed that the gain in calcium that occurs during calcium repletion after a period of calcium-free perfusion can be divided into at least two phases (early and late), and that the early phase contains a verapamil/nifedipine-sensitive component and a verAPamil / nifedIPine-insensitive component, the latter probably involving sodium-calcium exchange.