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The major membrane currents responsible for sinoatrial and idioventricular rhythm-generation were studied in isolated rat heart preparations, perfused in Langendorff mode. The rates of whole isolated hearts beating with sinoatrial rhythm decreased with cesium and ivabradine, both blockers of the funny current, and were not affected by nickel, at a dose which blocks T-type calcium current. The sinoatrial rhythm was completely abolished by reduction or removal of sodium from the perfusate (interventions that inhibit calcium-extrusive mode of the sodium/calcium exchanger), or by nifedipine, an L-type calcium channel blocker. Idioventricular rhythm, however, was arrested only by reduction of sodium in the perfusate. Ivabradine reduced the idioventricular rate, nickel did not cause any change, while nifedipine in some cases increased it. The inferences made based on these observations are that INCX and ICaL are obligatory rhythm-generating currents in the sinoatrial node, while INCX is the only obligatory mechanism for an idioventricular rhythm. The funny current is not an obligatory requirement for sinoatrial as well as idioventricular rhythm-generation. However, it enhances the frequency of LCRs. Our results in the isolated whole heart are in corroboration with results from isolated cells.

ObjectiveCell based therapy optimization is constantly underway since regeneration of genuine hyaline cartilage is under par. Although single source derivation of chondrocytes and chondroprogenitors is advantageous, lack of a characteristic differentiating marker obscures clear identification of either cell type which is essential to create a biological profile and is also required to assess cell type superiority for cartilage repair. This study was the first attempt where characterization was performed on the two cell populations derived from the same human articular cartilage samples.DesignCells obtained from normal/osteoarthritic knee joints were expanded in culture (up to passage 10). Characterization studies was performed using flow cytometry, gene expression was studied using RT-PCR, growth kinetics and tri-lineage differentiation was also studied to construct a better biological profile of chondroprogenitors as well as chondrocytes.Results and conclusionsOur results suggest that sorting based on CD34(-), CD166(+) and CD146(+), instead of isolation using fibronectin adhesion assay (based on CD49e+/CD29+), would yield a population of cells primarily composed of chondroprogenitors which when derived from normal as opposed to osteoarthritic cartilage, could provide translatable results in terms of enhanced chondrogenesis and reduced hypertrophy; both indispensable for the field of cartilage regeneration.