Key result
Simulated ischemia with 1 micromol/L norepinephrine decreased critical coupling conductance from 5.9 to 5.0 nS and increased maximum conduction delay from 31 to 54 ms in ventricular myocytes.
Why the study?
Does exposure to an ischemic solution with or without norepinephrine alter critical coupling conductance and conduction delay in isolated guinea pig ventricular myocytes?
Does exposure to an ischemic solution with or without norepinephrine alter critical coupling conductance and conduction delay in isolated guinea pig ventricular myocytes?
Catecholamine release during ischemia in partially uncoupled cells may produce long conduction delays, potentially facilitating reentrant arrhythmias.
Norepinephrine may facilitate reentry via prolonged conduction delay in ischemic uncoupled myocytes; leaves open relevance to clinical arrhythmias.
BACKGROUND: Acute ischemia often occurs in cardiac tissue that has prior injury, resulting in spatially inhomogeneous distributions of membrane properties and intercellular coupling. Changes in action potential conduction with ischemia, which can be associated with release of catecholamines, may be particularly important in tissue that has discontinuous conduction resulting from prior infarction, hypertrophy, or myopathy. METHODS AND RESULTS: Isolated guinea pig ventricular myocytes were electrically coupled by a coupling-clamp circuit to a comprehensive computer model of a guinea pig ventricular myocyte to assess alterations in the critical value of coupling conductance required for action potential conduction from the real cell to the model cell when the real cell was exposed to a solution that included hypoxia, acidosis, and an elevated extracellular potassium concentration to simulate acute ischemia. The "ischemic" solution increased critical coupling conductance from 6.2+/-0.1 to 7.4+/-0.2 nS and decreased the associated maximum conduction delay from 31+/-1 to 23+/-1 ms (mean+/-SEM, n=11). The ischemic solution plus 1 micromol/L norepinephrine decreased critical coupling conductance from 5.9+/-0.2 to 5.0+/-0.1 nS and increased maximum conduction delay from 31+/-2 to 54+/-4 ms (mean+/-SEM, n=8). CONCLUSIONS: The release of catecholamines with ischemia, in a setting of partially uncoupled cells, may play a major role in producing long conduction delays, which may allow reentrant pathways.
No takes yet. Share an insight, caveat, or question.
Wilders et al. (1999) studied Acute ischemia (n=19). Simulated acute ischemia solution (with or without norepinephrine) vs. Baseline was evaluated on Critical value of coupling conductance and maximum conduction delay. Simulated ischemia with 1 micromol/L norepinephrine decreased critical coupling conductance from 5.9 to 5.0 nS and increased maximum conduction delay from 31 to 54 ms in ventricular myocytes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: