Background:
Sepsis is a common condition known to impair blood flow regulation and microcirculation, which can ultimately lead to organ dysfunction but such contribution of the coronary circulation remains to be clarified. We investigated coronary blood flow regulatory mechanisms, including autoregulation, metabolic regulation, and endothelial vasodilatory response, in an experimental porcine model of early hyperdynamic
sepsis. Methods: Fourteen pigs were randomized to
sham (n = 7) or fecal
peritonitis-induced
sepsis (n = 7) procedures. At baseline, 6 and 12 h after
peritonitis induction, the animals underwent general and coronary hemodynamic evaluation, including determination of autoregulatory breakpoint pressure and
adenosine-induced maximal coronary vasodilation for coronary flow reserve and hyperemic microvascular resistance calculation. Endothelial-derived vasodilatory response was assessed both in vivo and ex vivo using
bradykinin. Coronary arteries were sampled for pathobiological evaluation. Results:
Sepsis resulted in a right shift of the autoregulatory breakpoint pressure, decreased coronary blood flow reserve and increased hyperemic microvascular resistance from the 6th h after
peritonitis induction. In vivo and ex vivo endothelial vasomotor function was preserved.
Sepsis increased coronary arteries expressions of
nitric oxide synthases,
prostaglandin I2 receptor, and
prostaglandin F2α receptor. Conclusion: Autoregulation and metabolic blood flow regulation were both impaired in the coronary circulation during experimental hyperdynamic
sepsis, although endothelial vasodilatory response was preserved.