MYOCARDIAL-ISCHEMIA ALTERS IMMUNOREGULATORY CELL TRAFFIC AND FUNCTIONIN THE RAT INDEPENDENT OF EXOGENOUS CATECHOLAMINE ADMINISTRATION

Recent investigation has suggested there is an adrenergically-driven e fflux of beta(2)-receptor rich lymphocyte subsets into the circulation with altered function following either exercise or infusion of exogen ous catecholamines. Myocardial ischemia, like exercise, is associated with generalized sympathoadrenal activation. To determine whether isch emia 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 myocard ial ischemia was induced, led to lymphocytosis, reflected primarily by an increase in T-helper (T-h) cells and, to a lesser degree, in T-sup pressor/cytotoxic (T-s/c) and natural killer (NK) cells; with a tenden cy toward an increased T-h/T-s/c ratio. To the contrary, isoproterenol injection resulted in a relative lymphopenia characterized by diminis hed B and T-h cell numbers, preserved T-s/c and increased NK cell numb ers leading to a significant decrease in the T-h/T-s/c ratio. With res pect to splenic composition, 60 but not 15 min of myocardial ischemia led to diminished T-h and B cell numbers compared to sham operated con trols, whereas isoproterenol appeared to stimulate an efflux of only N K cells. Both ischemia and isoproterenol enhanced basal splenocyte fun ction; however, only ischemia significantly boosted splenocyte respons iveness to the mitogen Concanavalin A. Surgically induced myocardial i schemia leads to alterations in immunoregulatory cell migration and fu nction which are distinct from those found with beta(2)-adrenergic sti mulation via isoproterenol.