AN INTEGRATED HEART-ON-A-CHIP NAM RESOLVES DISTINCT CLINICAL PHENOTYPES OF MYOCARDIAL ISCHEMIA-REPERFUSION INJURY

In neonatal rat ventricular myocytes on a heart-on-a-chip, ischemia followed by reperfusion shows distinct functional and biochemical injury patterns despite unchanged sarcomeric structure, including increased troponin release.

• Why it matters: Cardioprotective strategies often fail because patient-relevant ischemia-reperfusion injury involves structural, biochemical, and contractile dysfunction in the same tissue, yet typical evaluations collapse these into single readouts.
• What they did: The authors built a NAM heart-on-a-chip by culturing NRVMs on muscular thin films and applied normoxia, 2 hours ischemia, and ischemia plus 2 hours reperfusion, then measured immunofluorescent sarcomeric architecture, LIVE/DEAD injury, cardiac troponin I release, and contractile stress plus spontaneous beat frequency on the same films.
• The result: Ischemia reduced z-line density, viability, troponin, and all contractile stress components while beat frequency stayed unchanged; reperfusion further increased cell death and troponin, preserved structure, partially recovered systolic stress, worsened diastolic stress, and increased beat frequency with variability.

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