Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1999
Effect of small-dose dopamine on mesenteric blood flow and renal function in a pig model of cardiopulmonary resuscitation with vasopressin.
Vasopressin (antidiuretic hormone) seems a promising alternative to epinephrine for cardiopulmonary resuscitation (CPR) in cardiac arrest victims, mediating a pronounced blood flow shift toward vital organs. We evaluated the effects of small-dose dopamine on splanchnic blood flow and renal function after successful resuscitation with this potent vasoconstrictor in an established porcine CPR model. After 4 min of cardiac arrest and 3 min of CPR, animals received 0.4 U/kg vasopressin and were continuously infused with either dopamine 4 microg x kg(-1) x min(-1) (n = 6), or saline placebo (n = 6). Defibrillation was performed 5 min after drug administration; all animals were observed for 6 h after return of spontaneous circulation. During the postresuscitation phase, average mean +/- SD superior mesenteric artery blood flow was significantly (P = 0.002) higher in the dopamine group compared with the placebo group (1185+/-130 vs 740+/-235 mL/min), whereas renal blood flow was comparable between groups (255+/-40 vs 250+/-85 mL/min). The median calculated glomerular filtration rate had higher values in the dopamine group (70-120 mL/min) than in the placebo group (40-70 mL/min; P = 0.1 at 0 min and P = 0.08 at 360 min). We conclude that small-dose dopamine administration may be useful in improving superior mesenteric artery blood flow and renal function after successful resuscitation with vasopressin. ⋯ Long-term survival after cardiac arrest may be determined by the ability to ensure adequate organ perfusion during cardiopulmonary resuscitation and in the postresuscitation phase. In this regard, small-dose dopamine improved postresuscitation blood flow to the mesenteric bed when vasopressin was used as an alternative vasopressor in an animal model of cardiac arrest.
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Volatile anesthetics depress diaphragmatic muscle function; however, no data are available regarding the effect of propofol on diaphragmatic contractility. We therefore studied this effect in dogs. Pentobarbital-anesthetized animals were divided into three groups of 10 each. Group I received only maintenance fluid; Group II was infused with a subhypnotic dose of propofol (0.1-mg/kg initial dose plus 1.5-mg x kg(-1) x h(-1) maintenance dose); Group III was infused with an anesthetic dose of propofol (0.1-mg/kg initial dose plus 6.0-mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of propofol in Groups II and III, Pdi at low-frequency (20-Hz) stimulation decreased from the baseline values (P < 0.05), whereas Pdi at high-frequency (100-Hz) stimulation did not change. Compared with Group I, Pdi at 20-Hz stimulation decreased during propofol administration in Groups II and III (P < 0.05). The decrease in Pdi was more in Group III than in Group II (P < 0.05). We conclude that propofol is associated with a dose-related inhibitory effect on diaphragmatic contractility in dogs. ⋯ Propofol is an effective IV anesthetic for the induction and maintenance of anesthesia. Subhypnotic and anesthetic doses of propofol decrease diaphragmatic contractility in dogs.
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Anesthesia and analgesia · Dec 1999
Comparative StudyHyperalgesia caused by nerve transection: long-lasting block prevents early hyperalgesia in the receptive field of the surviving nerve.
The aim of our study was to test the hypothesis that a long-lasting N-butyl tetracaine nerve block (>2 wk) would be much more effective in the prevention of hyperalgesia caused by nerve transection than the short-lasting lidocaine block. The study was performed with the use of the saphenous nerve section model in rats. The saphenous nerve was exposed and injected with saline, lidocaine (37 mM), or N-butyl tetracaine (37 mM). Ten minutes later, the nerve was transected in some of the rats. The development of mechanical hyperalgesia (pressure threshold) of the hindpaw was assessed during a 5-wk period. In rats with saphenous nerve transection without nerve block (saline injection), 3 h after the transection, the pressure threshold decreased by approximately 30% (from 175+/-11 g to 122+/-23 g, P < 0.0001); the threshold increased somewhat the next day, then it remained stable for 2 wk, with a slow process of recovery afterward. N-butyl tetracaine block without nerve transection caused a slow-developing decrease in the pressure threshold with the first statistically significant change at the sixth day. The comparison of the preventive effects of lidocaine and N-butyl tetracaine blocks on early hyperalgesia caused by nerve transection demonstrated that both lidocaine and N-butyl tetracaine prevented hyperalgesia 3 h after the transection. However, the protective effect of lidocaine disappeared the next day. In contrast, N-butyl tetracaine prevented early hyperalgesia for almost a week. The slow-developing late hyperalgesia caused by long-lasting nerve block makes it impossible to study the protective effect of such a block on late hyperalgesia caused by axotomy. As far as early hyperalgesia is concerned, the preventive effect of the N-butyl tetracaine was much longer than that of lidocaine and continued for approximately 1 wk. ⋯ A long-lasting nerve block can prevent early hyperalgesia caused by nerve transection.
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Anesthesia and analgesia · Dec 1999
Comment Letter Comparative StudyThe difference between actual and calculated osmolality of IU solutions should not be overlooked.