Coronary perfusion pressure, end-tidal CO2 and adrenergic agents in haemodynamic stable rats.

Abstract

Coronary perfusion pressure (CPP) determines myocardial perfusion during low flow. CPP correlates with end-tidal CO2 (PetCO2) during cardiac arrest. Recent studies have demonstrated that after adrenaline, increased CPP was associated with decreased PetCO2. Intravenous infusions (4 min, N = 10) or bolus (10 s, N = 6) of methoxamine (60 micrograms/kg), isoproterenol (10 micrograms/kg), adrenaline and noradrenaline (3 micrograms/kg) were compared with saline placebo (0.2 ml/min) during spontaneous circulation in anaesthetized Sprague-Dawley rats. Infusion and bolus of methoxamine, adrenaline and noradrenaline increased CPP between 39 and 46% above baseline. Isoproterenol decreased CPP by 67%. PetCO2 decreased by 27% after bolus and only 10% after infusion of methoxamine but increased after infusion (7%) and bolus (10%) of isoproterenol and after infusion of adrenaline (11%) and noradrenaline (17%). Equipressor bolus of methoxamine, adrenaline and noradrenaline reduced PetCO2 between 10 and 27%. Bolus application induced more alpha-effects and drug infusion more beta-effects in the pulmonary vasculature. Thus, changes in pulmonary vascular resistance and associated increases in dead space were responsible for differences in PetCO2. Alpha-effects increased CPP, decreased P(et)CO2 and conversely, beta-effects decreased CPP but increased PetCO2 indicating caution when P(et)CO2 is used as non-invasive monitor of perfusion, especially after alpha-adrenergic agents.