Anesthesia and analgesia
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Anesthesia and analgesia · Jan 1993
Comparative StudyOn the mechanisms of potentiation of local anesthetics by bicarbonate buffer: drug structure-activity studies on isolated peripheral nerve.
Impulse inhibition by local anesthetics (LAs) is potentiated by extracellular solutions containing HCO3-. CO2 (BC), relative to the inhibition in BC-free solutions at the same pH. We studied the mechanistic basis of this potentiation by assaying compound action potential amplitudes in desheathed frog sciatic nerves with the sucrose-gap method. ⋯ However, slight differences in the molecular structure of 3 degrees-amine LAs with similar pKa values resulted in significantly different potentiations (e.g., procaine, PF = 3.9; 2-chloroprocaine, PF = 8.7), suggesting that the HCO3- or CO2 molecules interact specifically with the LA molecule or with LA binding sites in the nerve membrane. Spectrophotometric measurements of the free [Ca2+] in Ringer's showed it to be similar (+/- 0.03 mM) for both buffers, obviating changes in extracellular Ca2+ as a mechanism of BC potentiation. The resting potential of the nerve was slightly more negative (approximately -4 mV) in BC-R, so membrane depolarization cannot explain the potentiation.(ABSTRACT TRUNCATED AT 400 WORDS)
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Anesthesia and analgesia · Jan 1993
Comparative StudyRecovery from pancuronium and vecuronium administered simultaneously in the isolated forearm and the effect on recovery following administration after cross-over of drugs.
If recovery of neuromuscular block in the isolated arm is determined by biophase binding, then a significant amount of drug will still be present in the biophase at 50% recovery of twitch response. To test this hypothesis we administered pancuronium at 50% recovery from vecuronium block and vecuronium at 50% recovery from pancuronium block in the isolated forearms of volunteers. ⋯ Prior administration of vecuronium significantly shortened the recovery from subsequent pancuronium when administered at 50% recovery, but not 100% recovery, and pancuronium significantly increased the recovery rate of vecuronium when given at 50% recovery but not 100% recovery. These findings support the concept of biophase binding of nondepolarizing neuromuscular blocking drugs.
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Anesthesia and analgesia · Jan 1993
Comparative StudyWork hours of residents in seven anesthesiology training programs.
Medical educators and credentialing organizations recently have called attention to the long hours that some house staff are required to spend in the hospital during training. To determine the average duration of in-hospital work hours of anesthesiology residents, 148 residents at seven, university-affiliated training programs kept daily logs of their activities for one week. Residents in clinical anesthesia years 1, 2, and 3 spent an average of 66, 65, and 64 hours per week, respectively, in the hospital with a range of 43 to 104 hours per week. ⋯ The largest portion of the in-hospital time was devoted to patient care activities in the operating room. Residents had time for educational activities, conferences, and reading while in the hospital. The overall work hours of the residents in the anesthesiology training programs included in this survey appeared to be within current guidelines.
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Anesthesia and analgesia · Jan 1993
Propofol produces endothelium-independent vasodilation and may act as a Ca2+ channel blocker.
The mechanism of vasodilation induced by propofol was investigated using isolated rat thoracic aortic rings. Aortic rings were precontracted with potassium chloride (KCl) (40 mM) or phenylephrine (PE) (3 x 10(-8) to 3 x 10(-7) M) in the presence and absence of intact endothelium. Propofol produced similar concentration-dependent relaxation in aortic rings with and without endothelium regardless of whether they were precontracted with KCl or PE. ⋯ These effects are similar to those produced by verapamil. Propofol (5 x 10(-5) M) had minimal effect on the intracellular Ca2+ release elicited by PE (10(-5) M). We conclude that vasodilation produced by propofol is not endothelium-dependent but is likely due to blockade of voltage-gated influx of extracellular Ca2+.