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- Author or Editor: S. C. Olsen x
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SUMMARY
Furosemide, which commonly is used as a prophylactic treatment for exercise-induced pulmonary hemorrhage in horses, may mediate hemodynamic changes during exercise by altering prostaglandin metabolism. To determine if furosemide's hemodynamic effects during exercise in horses could be reversed, cyclooxygenase inhibitors were administered with furosemide. Four treatments were administered 4 hours prior to treadmill exercise at 9 and 13 m/s. They included a control treatment (10 ml of 0.9% NaCl solution, iv), furosemide (1 mg/kg of body weight, iv) administered alone, and furosemide in combination with phenylbutazone (4 mg/kg, iv, q 12 h for 2 days) or with flunixin meglumine (1.1 mg/kg, iv, on the day of experiment). Five horses were randomly assigned to complete all treatments. Physiologic variables at rest prior to exercise were not influenced by treatments. Furosemide, administered alone, reduced mean right atrial pressure and mean pulmonary artery pressure during exercise. The combinations of furosemide and flunixin meglumine or furosemide and phenylbutazone, at both levels of exercise intensity, returned mean right atrial pressure and mean pulmonary artery pressure to the value of the control treatment. During rest and exercise, plasma lactate concentration, pcv, heart rate, mean carotid artery pressure, oxygen consumption, carbon dioxide elimination, and cardiac output were not altered by any of the treatments. At 5 minutes after exercise, the administration of furosemide, alone or with phenylbutazone, reduced mean right atrial pressure. Other measured variables were not significantly influenced by treatments during recovery from exercise. These results suggested that cyclooxygenase inhibition partially reverses the decrease in mean right atrial pressure or pulmonary artery pressure induced by furosemide during exercise. Furosemide may mediate some of its physiologic activities in exercising horses through the cyclooxygenase pathway.
Summary
Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered iv to 6 horses. Carotid arterial pressure (cap), pulmonary arterial pressure (pap), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (rap) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in rap, cap, pap, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced rap and pap during exercise in dose-dependent manner, but did not influence heart rate. Mean cap was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only rap was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence pcv or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in pcv and hemoglobin concentration were small in comparison with changes in rap and pap, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.
Summary
The lipoxygenase metabolites of arachidonic acid have an important role in lymphocyte activation. We used a specific 5-lipoxygenase inhibitor, A-63162, to examine the role of 5-lipoxygenase (5-lo) in equine blood mononuclear cell (bmc) proliferation and leukotriene B4 (ltb 4) synthesis after stimulation with mitogen (phytohemagglutinin, pha) or calcium ionophore (A23187). The A-63162 inhibited pha-induced equine bmc proliferation and, at the same concentration, also inhibited A23187-induced ltb 4 synthesis. The presence of exogenous interleukin 2 (il-2) or the cyclooxygenase inhibitor indomethacin, failed to reverse the immunosuppression caused by A-63162. Further, we found that A-63162, at the concentration that inhibited bmc proliferation and ltb 4 synthesis, had no effect on bmc viability. The addition of the specific protein kinase C inhibitor, H-7, did not inhibit A23187-induced ltb 4 synthesis. Results indicate that 5-lipoxygenase metabolites may have an important role in equine lymphocyte activation and that protein kinase C has no role in regulating ltb 4 production after A23187 stimulation.
