Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1999
Attenuated additional hypocapnic constriction, but not hypercapnic dilation, of spinal pial arterioles during spinal ropivacaine.
Ropivacaine constricts spinal vessels. Because the CO2 response of spinal vessels is similar to that of cerebral vessels, we tested to see if hypocapnia would cause further spinal vasoconstriction during ropivacaine administration. In 12 pentobarbital-anesthetized dogs, spinal pial arteriolar diameter was measured using a closed spinal window preparation. Either ropivacaine solution (0.1%; n = 6) or artificial cerebrospinal fluid (n = 6) was infused continuously into the spinal window. After a period of hypocapnia (Paco2, 20-25 mm Hg) had been induced, inspired CO2 levels were adjusted to produce normocapnia (35-40 mm Hg) followed by hypercapnia (55-60 mm Hg). When the desired Paco2 was reached, measurements were made of the arteriolar diameter and physiological variables. During normocapnia, ropivacaine infusion produced a significant constriction of pial arterioles, whereas artificial cerebrospinal fluid caused no change. Hypocapnia induced a much smaller (almost nonexistent) additional vasoconstriction in the ropivacaine group than in the control group (P < 0.01). The final hypercapnic vasodilation was somewhat greater during ropivacaine (P < 0.05 versus control group). Topical ropivacaine induced no change in hemodynamic variables. We conclude that hypocapnia of the magnitude tested did not cause further constriction in spinal vessels during spinal ropivacaine. ⋯ During topical application of the local anesthetic ropivacaine in dogs, hypocapnia (Paco2, 20-25 mm Hg) induced almost no additional constriction of spinal arterioles, and the hypercapnic vasodilation was maintained. These data suggest that an additional constriction in spinal vessels is unlikely when hypocapnia occurs during spinal ropivacaine.
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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
The systemically administered competitive AMPA receptor antagonist, YM872, has analgesic effects on thermal or formalin-induced pain in rats.
A new competitive alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist, (2,3-dioxo-7-[1H-imidazol-1-yl]-6-nitro-1,2,3,4-tetrahydro-1-quinoxal inyl) acetic acid (YM872) has analgesic effects on acute thermal- and formalin-induced nociception by intrathecal administration. The purpose of this study was to determine the analgesic effects of systemically administered YM872 in both acute thermal- and irritant-induced pain. Sprague-Dawley rats were tested for tail withdrawal response by the tail flick test and for paw flinches by formalin injection after intraperitoneal administration of YM872. The tail flick latency increased dose-dependently with a 50% effective dose value of 156.3 microg. The number of flinches in both first and second phases of the formalin test decreased with increasing the dose of YM872. The 50% effective dose values were 1.0 microg in the first phase and 38.7 microg in the second phase. Transiently, intraperitoneal administration of 1 and 10 mg of YM872 induced motor disturbance and 10 mg induced loss of pinna reflex. We conclude that intraperitoneal administration of YM872 had analgesic effects on both acute thermal- and formalin-induced nociceptions in rats. Transient motor disturbance and loss of pinna reflex occurred only with large doses. ⋯ Intraperitoneally administered YM872, a new alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist, had analgesic effects on thermal- and formalin-induced pain in rats. Larger doses induced transient motor disturbance and loss of pinna reflex mediated in the brain.