Clonidine and the sympatico‐adrenal response to coronary artery by‐pass surgery

Abstract

Clonidine was administered intravenously in an attempt to limit sympatico-adrenal activity and thereby reduce the incidence of arterial hypertension associated with coronary artery by-pass graft surgery (CABG). Forty patients scheduled for CABG were assigned to two groups. Twenty patients received clonidine 4 micrograms kg-1 before surgery, 2 micrograms kg-1 after cardiopulmonary by-pass and 1 microgram kg-1 when the skin was sutured. The other 20 patients served as controls. All patients were anesthetized with fentanyl, droperidol, nitrous oxide and alcuronium. During surgery 5 min after sternotomy, mean arterial pressure was 13 mmHg lower (P less than 0.01) in the clonidine group, while after operation the difference between the groups was negligible. Both during and after surgery the plasma catecholamine concentrations were significantly lower in the clonidine group (P less than 0.01). The greatest difference between the groups was seen 90 min after operation, when plasma noradrenaline and plasma adrenaline concentrations in the clonidine group were less than 1/3 of those in the control group (P less than 0.01). As judged by catecholamine concentrations clonidine was effective in attenuating sympatico-adrenal hyperactivity during and after surgery. Postoperative arterial hypertension was not reduced, however, and it is concluded that other factors besides sympatico-adrenal hyperactivity must be important.

RETRACTED: Dexmedetomidine infusion is associated with enhanced renal function after thoracic surgery

“…It is therefore conceivable that because dexmedetomidine attenuates stress-induced increases in circulating norepinephrine, it may maintain renal blood flow and glomerular filtration. Indeed, it is well established that the administration of a-2 adrenergic agonists can inhibit the surgical stress response [15][16][17] and thereby protect the kidney against the detrimental effects of adrenergic-mediated vasoconstriction [18]. There also may be direct vascular effects in the kidney.…”

Post-Bypass Dexmedetomidine Use and Postoperative Acute Kidney Injury in Patients Undergoing Cardiac Surgery with Cardiopulmonary Bypass

“…It is conceivable that dexmedetomidine attenuates surgical stress-induced increases in circulating epinephrine and norepinephrine and maintain renal blood flow and glomerular filtration. Therefore, it can protect the kidney against the adrenergic-mediated vasoconstriction by activation of α-2c receptors in the wall of vascular smooth muscle [8,30,31]. Dexmedetomidine can also exert direct vascular effects in the kidneys by decreasing the sympathetically mediated presynaptic release of norepinephrine in the kidneys, which could promote renal arterial vasodilatation [32].…”

Effect of Dexmedetomidine on Ischemia-Reperfusion Injury in Rat Kidney: A Histopathologic Study

“…However, it was previously reported that dexmedetomidine decreases the sympathetically mediated presynaptic release of norepinephrine in the kidney, attenuates stress-induced increases in circulating norepinephrine, and may maintain renal blood flow and glomerular filtration. [26] Indeed, it is well established that the administration of α 2 -adrenergic agonists can inhibit the surgical stress response [27][28][29] and thereby protect the kidney against the detrimental effects of adrenergicmediated vasoconstriction. [30] Dexmedetomidine could promote renal arterial vasodilatation as well.…”