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R Kolesar

Publications and source records attributed to R Kolesar.

4 recordsLinked to original sources

Oral clonidine reduces postoperative PCA morphine requirements.

PURPOSE: The purpose of this study was to evaluate the effect of perioperative oral clonidine on postoperative analgesia and PCA morphine requirements in adult patients after major orthopaedic knee surgery. METHODS: In this prospective, double blind, placebo-controlled study 44 patients undergoing either total knee replacement or hemiarthroplasty of the knee were randomly assigned to receive oral placebo or clonidine (5 micrograms . kg-1) 1.5 hr before surgery, and at 12 hr, and 24 hr after the initial dose. Five patients were subsequently withdrawn from study. No other preoperative drugs were given. Preoperative sedation score was recorded. A standardized general anaesthetic was administered to all patients. Postoperative blood pressure, heart rate, PCA morphine use, visual analogue score (VAS) for pain, sedation, nausea, and pruritus were recorded for 36 hr postoperatively. RESULTS: The cumulative PCA morphine used was 37% lower after clonidine 57.3 +/- 26.8 mg (mean +/- SD) compared with placebo 91 +/- 31.6 mg (P = 0.031). There was no difference in pain or sedation scores postoperatively but patients who received clonidine were more sedated preoperatively (P < 0.001) and had a lower mean arterial blood pressure throughout the period of study by 10 to 26 mmHg (P < 0.0001). Clonidine reduced the incidence of postoperative nausea (25% vs 74%) (P < 0.01) and vomiting compared with placebo (10% vs 53%) (P < 0.01) and required less antiemetic (dimenhydrinate 37.5 +/- 20.9 mg vs 82.1 +/- 49.4 mg) but not statistically significant (P = 0.065). CONCLUSIONS: Oral clonidine is a useful component to postoperative balanced analgesia as it decreases PCA morphine requirements and decreases the incidence of nausea and vomiting.

Administration, Oral

Intracoronary propofol does not decrease myocardial contractile function in the dog.

The intravenous administration of propofol is associated with a considerable decrease in arterial blood pressure. The present study was undertaken to test the hypothesis that myocardial function is not affected by propofol and therefore does not contribute to the hypotensive effect of this anaesthetic agent. Propofol was administered in anaesthetized, open-chest dogs by direct arterial infusion into the left anterior descending coronary artery (LAD). Mean arterial blood pressure, heart rate, left ventricular pressure, dP/dt, regional lactate and oxygen extraction, as well as coronary blood flow were measured. Diastolic function was determined by calculation of the time constant of isovolumetric relaxation from the left ventricular pressure measurement and dP/dt. Contractility was evaluated by measuring regional systolic shortening in an area of the myocardium supplied by the LAD. This was compared with systolic shortening in the distribution of the circumflex (CIRC) artery and with the effects obtained with the intracoronary administration of thiopentone. Intracoronary infusions of propofol and thiopentone did not produce any change in systemic arterial blood pressure, heart rate, or left ventricular end diastolic pressure. Propofol, at a concentration of 5 or 10 micrograms.ml-1 did not decrease systolic shortening in the area perfused by the LAD while thiopentone (40 micrograms.ml-1) reduced systolic shortening by 33% (P < or = 0.05). Neither drug had an effect on systolic shortening in the CIRC area, LAD blood flow or diastolic function. The results of this study suggest that propofol does not have an effect on myocardial contractility. The hypotension associated with the intravascular administration of propofol is more likely due to either a direct vascular or a central effect.

Animals