Myocardial ischemia alters immunoregulatory cell traffic and function in the rat independent of exogenous catecholamine administration

Recent investigation has suggested there is an adrenergically-driven efflux of beta(2)-receptor rich lymphocyte subsets into the circulation with altered function following either exercise or infusion of exogenous catecholamines. Myocardial ischemia, like exercise, is associated with generalized sympathoadrenal activation. To determine whether ischemia influences immunoregulatory cell traffic and function in a manner comparable to beta(2)-adrenergic stimulation via isoproterenol, rats underwent thoracotomy with or without coronary ligation. Another group of rats received either isoproterenol (1 mg/kg) or vehicle (10 mM HCl) intraperitoneally. Thoracotomy, regardless of whether or not myocardial ischemia was induced, led to lymphocytosis, reflected primarily by an increase in T-helper (T-h) cells and, to a lesser degree, in T-suppressor/cytotoxic (T-s/c) and natural killer (NK) cells; with a tendency toward an increased T-h/T-s/c ratio. To the contrary, isoproterenol injection resulted in a relative lymphopenia characterized by diminished B and T-h cell numbers, preserved T-s/c and increased NK cell numbers leading to a significant decrease in the T-h/T-s/c ratio. With respect to splenic composition, 60 but not 15 min of myocardial ischemia led to diminished T-h and B cell numbers compared to sham operated controls, whereas isoproterenol appeared to stimulate an efflux of only NK cells. Both ischemia and isoproterenol enhanced basal splenocyte function; however, only ischemia significantly boosted splenocyte responsiveness to the mitogen Concanavalin A. Surgically induced myocardial ischemia leads to alterations in immunoregulatory cell migration and function which are distinct from those found with beta(2)-adrenergic stimulation via isoproterenol.