Intravenous clonidine does not promote hypoxemia or platelet aggregation in man

This study was designed to evaluate hypoxemia and platelet aggregation in man following intravenous administration of clonidine. With Institutional approval and following informed consent, 20 patients (ASA I-II) without spontaneous or drug-induced coagulation disorder undergoing elective total hip replacement were studied. They were randomly divided into two groups. Group A (n = 10) received an IV loading dose of 4 micrograms/kg of clonidine in 30 minutes followed by an infusion of 1 microgram/kg/h till the end of the procedure. Group B (n = 10) received saline. Platelet aggregation was assessed before infusion and at the end of both the loading dose and the infusion. PaO2 was measured before anesthesia (FIO2 = 0.21), before femoral cementation (FIO2 = 0.40), 2 min. after prosthesis implantation (FIO2 = 1), before the end of the procedure (FIO2 = 0.40) and in the recovery room (spontaneous breathing with FIO2 = 0.21). Plasma clonidine levels were assessed at the end of both the loading dose and the infusion. At any time considered, no statistical differences were noted between the groups for platelet aggregation and PaO2. We conclude that intravenous clonidine does not clinically promote platelet aggregation nor hypoxemia in man.