Lidoflazine

Vanhoutte, Paul M.; Nueten, J. M. Van

doi:10.1111/j.1527-3466.1983.tb00448.x

Cited by 1 publication

(1 citation statement)

References 42 publications

(43 reference statements)

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“…All these observations suggest that in all these situations, the bulk of calcium is not entering the cell through slow channels. This is supported by the fact that the diarylalkylpiperazines, without or with only a very weak affinity for slow calcium channels (3,9,25,26), were highly protective under the various conditions mentioned.…”

Section: Discussionmentioning

confidence: 67%

Effects of lidoflazine and mioflazine against potassium and veratrine induced shape changes in isolated rat cardiac myocytes

et al. 1987

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The protective effects of lidoflazine and mioflazine against shape changes in isolated rat cardiac myocytes induced by depolarizing concentrations of potassium and veratrine have been examined. Myocardial cells, isolated from adult rat hearts and plated in Petri-dishes, yielded a population of nearly 100% rod-shaped calcium-tolerant myocytes. Addition of veratrine or potassium resulted in a calcium-dependent cell shortening and finally rounding up of nearly all cells. Ultrastructurally, the shape changes were accompanied by a complete loss of calcium associated with the sarcolemmal and T-tubular bilayer. Calcium deposits accumulated in the mitochondria, indicating intracellular calcium overload. Pretreatment of the myocytes with lidoflazine or mioflazine (10(-7)-10(-5) M) dose-dependently increased the number of remaining rod-shaped cells after potassium or veratrine addition. Such rod-shaped cells retained a normal pattern of calcium distribution along the sarcolemma and T-tubuli with no evidence of mitochondrial calcium overload. The protective effects of lidoflazine and mioflazine are explained in terms of preserving sarcolemmal integrity, whereby excessive calcium influx and subsequent cytosolic calcium overload could be prevented.

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Section: Discussionmentioning

confidence: 67%