Anesthesia and analgesia
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Anesthesia and analgesia · Aug 1998
Modifications of the inotropic responses to alpha- and beta-adrenoceptor stimulation by propofol in rat myocardium.
Propofol induces cardiovascular depression but without significant effect on intrinsic myocardial contractility in many species. However, its interactions with adrenoceptor stimulation are unknown. We studied the effects of propofol (1 and 10 microg/mL) and its solvent on the inotropic response induced by phenylephrine (10(-8)-10(-4) M) or isoproterenol (10(-8)-10(-4) M) in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, calcium 0.5 mM, stimulation frequency 12 pulses/min). We also studied the lusitropic effects in isotonic and isometric conditions. In control groups, phenylephrine (127% +/- 3% of baseline; P < 0.05) and isoproterenol (169% +/- 11% of baseline; P < 0.05) induced a positive inotropic effect. Propofol (10 microg/mL) completely abolished the positive inotropic effect of phenylephrine (100% +/- 3% of baseline; P = not significant). In contrast, at the lowest concentration (1 microg/mL), propofol did not modify the positive inotropic effect of phenylephrine. Propofol did not modify the inotropic effect of isoproterenol. Propofol (10 microg/mL) enhanced the positive lusitropic effect of isoproterenol under low-load (P < 0.05) but not under high-load conditions. ⋯ A high concentration of propofol abolished the positive inotropic effect of alpha- but not beta-adrenoceptor stimulation and enhanced the positive lusitropic effect of beta-adrenoceptor stimulation.
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Anesthesia and analgesia · Aug 1998
Is there a bilateral block of the thoracic sympathetic chain after unilateral intrapleural analgesia?
This study was designed to ascertain, by telethermography and clinical observation, the effect of injecting anesthetic solutions into the intrapleural space on thoracic sympathetic chains and splanchnic nerves. We studied 15 patients with neoplastic (n = 8) or benign (n = 7) pain, divided into three groups of 5 patients each. The first group received 20 mL of bupivacaine 0.25% in the intrapleural space, the second received 20 mL of bupivacaine 0.5%, and the third received 20 mL of isotonic sodium chloride solution. Each patient was examined telethermographically 30, 60, 90, and 120 min after the blockade. Visceral pain intensity was measured in eight patients using a visual analog scale. Patients receiving bupivacaine had a uniform bilateral increase of cutaneous temperature (+2 degrees C). In those with diffuse visceral pain, the mean value of the pain score decreased from 82 +/- 10 mm at the time of injection to 16 +/- 5 at 120 min. We conclude that intrapleural bupivacaine 0.25% and 0.5% results in bilateral blockade of the thoracic sympathetic chain and also of the splanchnic nerves, which pass in front of the spinal column between the two thoracic sympathetic chains. Our data indicate that intrapleural analgesia can be used in the treatment of not only unilateral visceral and somatic pain, but also diffuse abdominal visceral pain. The bilateral increase of the cutaneous temperature of the trunk (measured telethermographically) and the reduction of the diffuse visceral pain suggest a bilateral block of the sympathetic chain and of the splanchnic nerves. ⋯ We subjected 10 patients to monolateral intrapleural analgesia. Five other patients served as controls. The bilateral increase of the cutaneous temperature of the trunk (measured telethermographically) and the reduction of the diffuse visceral pain suggest a bilateral block of the sympathetic chain and of the splanchnic nerves. Our data indicate that intrapleural analgesia can be used in the treatment of not only unilateral visceral and somatic pain, but also diffuse abdominal visceral pain.
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Anesthesia and analgesia · Aug 1998
Involvement of nitric oxide in peripheral antinociception mediated by kappa- and delta-opioid receptors.
Nitric oxide (NO) has been reported to enhance the analgesic effect of the peripherally administered mu-opioid receptor agonists, but the role of NO on the analgesic effect of the peripherally administered kappa and delta opioid receptor agonists is still unclear. We examined the effects of peripherally applied kappa- and delta-opioid receptor agonists and of their interactions with the NO-releasing drug, FK409, on the behavioral response to intraplantar injection of formalin in rats (the formalin test). The formalin injection results in a biphasic appearance of agitation behavior, consisting of the early (Phase 1; 0-9 min) and late (Phase 2; 10-60 min) responses. The active enantiomer of kappa-opioid receptor agonist, (-)U50,488H, dose-dependently suppressed the agitation response in both phases of the formalin test when applied peripherally. A peripheral delta-opioid receptor agonist, [D-Pen(2,5)] enkephalin (DPDPE), suppressed only Phase 2 of the formalin test. Local application of FK409 after the administration of a subthreshold dose of each opioid resulted in a dose-dependent decrease in the Phase 1, but not Phase 2, response to the formalin test for both agonists. Interactions between peripheral opioids and FK409 were reversed with both naloxone and carboxy-PTIO (NO scavenger). Systemic injections of either a kappa- or delta-agonist had no interaction with peripherally applied FK409. Peripheral FK409 alone did not have any significant effect on the formalin test. These data indicate that the antinociceptive effects of peripherally applied kappa- and delta-opioid agonists on the formalin test are potentiated by the local action of NO. ⋯ The analgesic effects of peripherally applied kappa- and delta-opioid receptor agonists during inflammation induced by formalin injection in the rat are, at least partly, mediated by the NO-cGMP pathway.