Anesthesia and analgesia
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Anesthesia and analgesia · Feb 1998
Randomized Controlled Trial Clinical TrialThe effect of needle gauge and lidocaine pH on pain during intradermal injection.
Local anesthetics can produce pain during skin infiltration. We designed a randomized, prospective trial to determine whether needle gauge and/or solution pH affect pain during the intradermal infiltration of lidocaine. After approval by our institution's human studies review board, 40 healthy adult volunteers gave their consent to participate in this study. All of the volunteers randomly received four intradermal injections. Each volunteer was blinded as to the content of the intradermal injections and to which needle size was used for each injection. Each volunteer randomly received a 0.25-mL intradermal injection of the following four solutions: 1) lidocaine 2% administered through a 25-gauge needle (lido-25); 2) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate, pH 7.26) administered through a 25-gauge needle (lido-bicarb-25); 3) lidocaine 2% administered through a 30-gauge needle (lido-30); and 4) lidocaine 2% mixed with sodium bicarbonate (4 mL of 2% lidocaine plus 1 mL of sodium bicarbonate) administered through a 30-gauge needle (lido-bicarb-30). In each patient, the injection site was in the same region for each of the four injections. The skin wheal was tested for appropriate anesthesia using a 19-gauge needle on the skin wheal. A visual analog pain score was recorded after each intradermal injection. The pain scores were significantly higher in the lido-25 (3.2 +/- 0.2) group than in the lido-30 (2.5 +/- 0.3), lido-bicarb-25 (1.9 +/- 0.2), and lido-bicarb-30 (1.3 +/- 0.2) groups. The lido-bicarb-30 injection was also rated as less painful than the lido-30 injection. We found no differences between the lidobicarb-25 and the lido-bicarb-30 injections. Complete analgesia for the 19-gauge needle pain stimulus was achieved in all patients for each injection. We conclude that, overall, the pain intensity of an intradermal injection of 2% lidocaine is low. The addition of sodium bicarbonate to 2% lidocaine decreases the pain associated with an intradermal skin wheal, and although the use of a 30-gauge needle decreases the pain of injection, the addition of sodium bicarbonate seems to have a greater overall effect than needle size. ⋯ Forty volunteers randomly received four intradermal injections consisting of 2% lidocaine with or without sodium bicarbonate via a 25- or 30-gauge needle. The addition of bicarbonate had a greater overall effect than needle size in decreasing the pain associated with the intradermal injection of lidocaine.
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Anesthesia and analgesia · Feb 1998
The effect of halothane and sevoflurane on fatigue-induced changes in hamster diaphragmatic contractility.
The purpose of this study was to examine the effect of halothane and sevoflurane on fatigue-induced changes in diaphragmatic contractility. Forty-two hamster diaphragm strips were randomly allocated according to anesthetics (no anesthesia control, 1%-3% halothane, 2%-6% sevoflurane) and stimulated directly in an organ bath. Under the influence of the anesthetics, muscle fatigue was induced by repetitive tetanic contraction, and diaphragmatic contractilities (i.e., peak twitch and tetanic tension, twitch contraction time, and half-relaxation time) were measured before and after fatigue. Neither halothane nor sevoflurane changed tension generation before or after fatigue, but each anesthetic significantly enhanced fatigue-induced prolongations of the contraction time and half-relaxation time after fatigue. Specifically, the half-relaxation times after fatigue in the 3% halothane, 4% sevoflurane, and 6% sevoflurane groups (225.6 +/- 37.6, 236.0 +/- 76.5, and 287.3 +/- 55.5 ms, respectively) were more than twice as long as those of the control group (104.7 +/- 19.7 ms, P < 0.05). We conclude that halothane and sevoflurane augment fatigue-induced prolongations of the contraction and relaxation times. Diaphragmatic function may deteriorate when there is a fatiguing task during the clinical administration of halothane or sevoflurane anesthesia. ⋯ This study implicates diaphragmatic fatigue during anesthesia. An in vitro hamster diaphragm muscle preparation was used to study the effect of halothane and sevoflurane on fatigue-induced change in contractility. Our findings suggest that increased load on the diaphragm during volatile anesthesia may lead to impaired diaphragmatic contractility.
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Anesthesia and analgesia · Feb 1998
Catecholamine activation in the vasomotor center on emergence from anesthesia: the effects of alpha2 agonists.
The rostral ventrolateral medulla (RVLM) controls the vascular system and may contribute to postoperative hypertension. It comprises adrenergic cardiovascular neurons, a site for action of alpha2-adrenergic agonists. Because alpha2 agonists minimize perioperative circulatory activation, we asked the following question: do alpha2 agonists, such as clonidine and mivazerol, blunt the catecholamine activation observed in the RVLM on emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetics. With in vivo electrochemistry, a catechol signal was recorded in the RVLM during 150 min of stable halothane anesthesia (saline-halothane group); for 120 min after halothane discontinuation (saline-emergence group); after emergence and administration of the reference alpha2 agonist, clonidine 7 microg/kg or 21 microg/kg I.V. (50% or 90% effective dose [ED50 or ED90], respectively); and after emergence and administration of a new alpha2 agonist, mivazerol 20 microg/kg or 150 microg/kg I.V. (ED50 or ED90). Under halothane, dose-response curves for the RVLM catecholamine signal were constructed for mivazerol and an alpha2 antagonist, idazoxan (ED50 2.3 mg/kg I.V.). Stable halothane anesthesia (n = 5) led to no change in mean arterial pressure (MAP), heart rate (HR), or catechol signal (CAOC). During emergence from anesthesia, the MAP, HR, and CAOC increased (n = 5). Clonidine led to a near total suppression of the RVLM catecholamine activation noticed on emergence from anesthesia (n = 5). Hypertension was partially blunted with clonidine 7 microg/kg (n = 5). Tachycardia was partially blunted with mivazerol 20 microg/kg (n = 5). Pretreatment with idazoxan suppressed all the effects of mivazerol (n = 5). ⋯ On emergence from anesthesia, alpha2 agonists modify the activity of adrenergic cardiovascular neurons located within the vasomotor center, as assessed by in vivo electrochemistry. We provide a rationale for the use of alpha2 agonists on emergence from anesthesia in coronary/hypertensive patients.
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Anesthesia and analgesia · Feb 1998
Propofol and thiopental in a 1:1 volume mixture is chemically stable.
Propofol and thiopental have been used clinically in combination for induction of anesthesia. Studies suggest that this mixture has synergistic activity, recovery characteristics similar to propofol alone, and bactericidal effects on multiple organisms. It may therefore be both clinically useful and cost-effective. In this study, we examined the chemical stability of this mixture. We used high-performance liquid chromatography to quantify the concentration of both propofol and thiopental in a given sample. This technique allows the detection of loss in total drug mass and of the appearance of breakdown products resulting from drug interaction. Ten samples of a 1:1 mixture by volume were prepared and assayed at Time 0 and Days 1, 3, and 7. Half the samples were incubated at 23 degrees C and the rest were stored at 4 degrees C. Other mixtures were assayed before and after filtration at Time 0 and Days 1 and 7 after storage at 23 degrees C. The assay was able to measure accurately the quantity of drug present in the samples. There was no significant decrease in the quantities of either propofol or thiopental in the mixture over the 7-day period. We conclude that the 1:1 volume mixture of propofol and thiopental is chemically stable for 1 wk at room temperature. ⋯ A mixture of propofol and thiopental has been used to induce anesthesia. We investigated the chemical stability of this mixture using high-performance liquid chromatography and found it to be stable for at least 24 h.
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Anesthesia and analgesia · Feb 1998
The effects of the alpha2-adrenergic agonist, dexmedetomidine, in the spinal nerve ligation model of neuropathic pain in rats.
Peripheral nerve injury may lead to neuropathic pain. Alpha2-adrenergic agonists acting in the descending inhibitory tracts of the spinal cord are effective in acute nociceptive, inflammatory, and, possibly, neuropathic pain. We studied the prevention and treatment of neuropathy with the selective alpha2-adrenergic agonist dexmedetomidine in male Sprague-Dawley rats with unilateral peripheral mononeuropathy resulting from tight ligation of the L5 and L6 spinal nerves. Rats with ligation injury developed mechanical and cold allodynia, but not heat hyperalgesia. Dexmedetomidine (120 microg/kg subcutaneously [S.C.] 30 min before the injury) did not attenuate mechanical or cold allodynia. Dexmedetomidine infusions (60 microg/d for 7 days after the injury, or 30 microg/d for 7 days started 14 days after the injury) did not attenuate mechanical or cold allodynia in the ipsilateral paw, but they increased mechanical allodynia during the latter treatment in the paw contralateral to the injury. Atipamezole (1 mg/kg S.C.) induced mechanical and cold allodynia in rats that had not developed allodynia in 14 days after the injury. In conclusion, although alpha2-adrenergic mechanisms are recognized as important in the development of neuropathic pain-like symptoms in this animal model, we found no favorable effect from systemic treatment with dexmedetomidine at tolerable doses. ⋯ We studied the prevention and treatment of nerve injury-induced pain with the alpha2-adrenergic agonist dexmedetomidine in an animal model. At tolerable doses, systemic dexmedetomidine neither prevented nor attenuated neuropathic pain behavior.