Dae-Lim Jee

The Effect of Pudendal Block on Voiding After Hemorrhoidectomy

PURPOSEUrinary retention in common benign anal surgery is a burden to ambulatory surgery. A pudendal nerve block was used in hemorrhoid surgery to reduce voiding complications.METHODSThe effects of a pudendal nerve block in anal surgery were compared with those of spinal anesthesia. In this prospective study, 163 consecutive patients who underwent elective hemorrhoids surgery by a single surgeon were randomized to receive pudendal nerve block (pudendal group) with 0.5 percent bupivacaine (n = 81) with 1:20,000 epinephrine or spinal anesthesia (spinal group) with 0.5 percentbupivacaine (n = 82).RESULTSThere were no statistically significant differences in the patient demographics, total amount of fluid administered, time to the onset of anesthesia, or intraoperative pain. All patients had a successful block during surgery. However, puborectalis muscle relaxation was not complete in the pudendal group. The time from the injection of the anesthetics to the first sensation of pain was longer in the pudendal group (9.1 vs. 3.1 hours; P < 0.001). Urinary catheterization was required in only 6 patients in the pudendal group compared with 57 patients in the spinal group (P < 0.001). The degree of pain was significantly lower in the pudendal group (2.7 vs. 5.2, Visual Analog Scale; P < 0.001). The amount of analgesics injected was significantly lower in the pudendal group (16/81 vs. 45/82; P < 0.001).CONCLUSIONSA pudendal nerve block with bupivacaine results in fewer postoperative voiding complications and less pain compared with the traditional spinal anesthesia in a hemorrhoidectomy.

Magnesium sulphate attenuates arterial pressure increase during laparoscopic cholecystectomy

BACKGROUND Magnesium is well known to inhibit catecholamine release and attenuate vasopressin-stimulated vasoconstriction. We investigated whether i.v. magnesium sulphate attenuates the haemodynamic stress responses to pneumoperitoneum by changing neurohumoral responses during laparoscopic cholecystectomy. METHODS Thirty-two patients undergoing laparoscopic cholecystectomy were randomly assigned to two groups; a control group was given saline, and a magnesium group received magnesium sulphate 50 mg kg(-1) immediately before pneumoperitoneum. Arterial pressure, heart rate, serum magnesium, plasma renin activity (PRA), and catecholamine, cortisol, and vasopressin levels were measured. RESULTS Systolic and diastolic arterial pressures were greater in the control group (P<0.05) than in the magnesium group at 10, 20, and 30 min post-pneumoperitoneum. Norepinephrine or epinephrine levels [pg ml(-1), mean (SD)] were higher in the control group than in the magnesium group at 5 [211 (37) vs 138 (18)] or 10 min [59 (19) vs 39 (9)] post-pneumoperitoneum, respectively (P<0.05). In the control group, vasopressin levels [pg ml(-1), mean (SD)] were higher compared with the magnesium group at 5 [64 (18) vs 35 (9), P<0.01] and 10 min [65 (18) vs 47 (11), P<0.05] post-pneumoperitoneum. There were no significant differences between the groups in PRA and cortisol levels. CONCLUSIONS I.V. magnesium sulphate before pneumoperitoneum attenuates arterial pressure increases during laparoscopic cholecystectomy. This attenuation is apparently related to reductions in the release of catecholamine, vasopressin, or both.

Magnesium sulphate attenuates tourniquet-induced hypertension and spinal c-fos mRNA expression: a comparison with ketamine.

Magnesium and ketamine are well-known N-methyl-d-aspartic acid receptor antagonists. The aim of this study was to determine whether magnesium, in comparison with ketamine, attenuates tourniquet-induced hypertension and spinal c-fos mRNA expression. Rats were divided into four treatment groups: normal (baseline for c-fos mRNA expression); control (saline injection); magnesium injection; and ketamine injection. Arterial blood pressure and c-fos mRNA expression at 60 min were higher in the control than in the magnesium and ketamine groups. Human patients under sevoflurane–oxygen/nitrous oxide anaesthesia were also assigned to receive similar treatments. In humans, arterial blood pressure was increased in the control group at 50 min and thereafter compared with the magnesium and ketamine groups; the magnesium and ketamine groups did not differ. Magnesium and ketamine are equally effective in attenuating tourniquet-induced hypertension and spinal c-fos mRNA expression, suggesting that this effect may be due to reduced pain transmission.

Propofol attenuates Kupffer cell activation during hypoxia-reoxygenation.

Objectif Determiner si le propofol diminue ľactivation des cellules de Kupffer (CK), protegeant ainsi les cellules contre une lesion ďhypoxie-reoxygenation par la modulation du calcium intracellulaire ([Ca2+]i).PurposeWe undertook a study to determine whether propofol may attenuate Kupffer cell (KC) activation, thus protecting the cells against hypoxia-reoxygenation injury through the modulation of intracellular calcium ([Ca2+]i).Methods[Ca2+]i, the expression of tumour necrosis factor (TNF)-α mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 μg·mL-1 (Groups P1 and P2, respectively) or without propofol (Group HRC). KCs were isolated and cultured from male Sprague-Dawley rats. KCs were incubated under an atmosphere of hypoxia (95% N2 + 5% CO2) for 60 min with subsequent 120 min reoxygenation (95% air + 5% CO2). [Ca2+]i for the first 12 min after reoxygenation, TNF-α mRNA, and KC viability at the end of reoxygenation in groups P1 and P2 were compared with those of HRC.ResultsThe increase of [Ca2+]i from the baseline was attenuated in P1 (96.6 ± 6.9%) and P2 (96.1 ± 5.4%) compared with HRC (143.8 ± 11.5%), (P < 0.001), with no difference between P1 and P2. The expression of TNF-α mRNA increased only in HRC during hypoxia-reoxygenation. KC viability increased in P1 (97.5 ± 2.6%) and P2 (94.6 ± 2.9%), compared with HRC (89.9 ± 1.4%), (P < 0.005), with no difference between P1 and P2.ConclusionThe results indicate that propofol attenuates KC activation and protects KC from hypoxia-reoxygenation injury at clinically relevant concentrations. This attenuation seems to result from inhibition of [Ca2+]i increase in KC.RésuméObjectifDéterminer si le propofol diminue ľactivation des cellules de Kupffer (CK), protégeant ainsi les cellules contre une lésion ďhypoxie-réoxygénation par la modulation du calcium intracellulaire ([Ca2+]i).MéthodeLe [Ca2+]i, expression du facteur de nécrose tumorale (FNT)-α ARNm, et la viabilité des CK ont été mesurés en réponse à ľhypoxie-réoxygénation suivant le prétraitement avec 0,5 et 5 μg·mL-1 de propofol (Groupes P1 et P2, respectivement) ou sans propofol (Groupe HRC). Des CK de rats Sprague-Dawley ont été isolées et mises en culture. Elles ont été incubées sous une atmosphère ďhypoxie (95 % N2 + 5 % de CO2) pendant 60 min et 120 min supplémentaires de réoxygénation (95 % ďair + 5 % CO2). Le [Ca2+]i pendant les 12 premières minutes après la réoxygénation, le FNT-α ARNm et la viabilité des CK à la fin de la réoxygénation dans les groupes P1 et P2 ont été comparés avec ceux du groupe HRC.RésultatsĽaugmentation du [Ca2+]i, au-dessus des mesures de base, a été réduite dans les groupes P1 (96,6 ± 6,9 %) et P2 (96,1 ± 5,4 %) comparés au groupe HRC (143,8 ± 11,5 %), (P < 0,001), sans différence entre P1 et P2. ľexpression du FNT-α ARNm a augmenté seulement dans le groupe HRC pendant ľhypoxie-réoxygénation. La viabilité des CK a augmenté dans les groupes P1 (97,5 ± 2,6 %) et P2 (94,6 ± 2,9 %), comparés au groupe HRC (89,9 ± 1,4 %), (P < 0,005) sans différence entre P1 et P2.ConclusionLe propofol diminue ľactivation des CK et protège ďune lésion liée à ľhypoxie-réoxygénation des CK selon des concentrations cliniquement significatives. Cette baisse semble résulter de ľinhibition de la hausse de [Ca2+]i dans les CK.

Inhibition of Oxidative Stress in Renal Ischemia-Reperfusion Injury.

BACKGROUND: Superoxide, nitric oxide (NO), and peroxynitrite are important mediators in the pathogenesis of ischemia-reperfusion (I/R) injury. We tested the renoprotective effects of allopurinol (ALP), a xanthine oxidase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), and 5,10,15,20-tetrakis (N-methyl-4-pyridyl) porphyrinato iron (III) (FeTMPyP) by selective inhibition of superoxide, NO, and peroxynitrite, respectively. METHODS: Male Sprague-Dawley rats were randomly assigned to 5 groups (n = 6 per group). Group 1 was a sham-operated group. Group 2 was the renal I/R group (30-minute ischemia followed by 24-hour reperfusion). Rats in groups 3, 4, and 5 received ALP, L-NAME, or FeTMPyP, respectively, at 5 minutes before the reperfusion. Serum creatinine (Cr), blood urea nitrogen (BUN), renal tissue malondialdehyde, superoxide dismutase, histological changes, apoptosis, and monocyte infiltration were evaluated. In addition, the combined treatment with ALP and L-NAME was compared with FeTMPyP in a second independent experiment. RESULTS: The administration of ALP, L-NAME, and FeTMPyP diminished the increase in Cr (P = .0066 for all) and BUN (P = .0066 for ALP; and P = .013 for L-NAME) induced by I/R injury and decreased the histological damage (P = .0066 for all). In addition, ALP, L-NAME, and FeTMPyP attenuated the oxidative stress response as determined by a decrease in malondialdehyde level (P = .0066 for all), apoptotic renal tubular cells (P = .0066 for all), and monocyte infiltration (P = .0066 for all). The combined treatment of ALP and L-NAME decreased Cr and BUN levels to a greater degree than FeTMPyP (P = .016 for Cr; P = .0079 for BUN). CONCLUSIONS: Superoxide, NO, and peroxynitrite are involved in renal I/R injury. The reduction of peroxynitrite formation, via inhibition of superoxide or NO, or the induction of peroxynitrite decomposition may be beneficial in renal I/R injury.

Le propofol diminue ľactivation des cellules de Kupffer pendant ľhypoxie-réoxygénation

Objectif Determiner si le propofol diminue ľactivation des cellules de Kupffer (CK), protegeant ainsi les cellules contre une lesion ďhypoxie-reoxygenation par la modulation du calcium intracellulaire ([Ca2+]i).PurposeWe undertook a study to determine whether propofol may attenuate Kupffer cell (KC) activation, thus protecting the cells against hypoxia-reoxygenation injury through the modulation of intracellular calcium ([Ca2+]i).Methods[Ca2+]i, the expression of tumour necrosis factor (TNF)-α mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 μg·mL-1 (Groups P1 and P2, respectively) or without propofol (Group HRC). KCs were isolated and cultured from male Sprague-Dawley rats. KCs were incubated under an atmosphere of hypoxia (95% N2 + 5% CO2) for 60 min with subsequent 120 min reoxygenation (95% air + 5% CO2). [Ca2+]i for the first 12 min after reoxygenation, TNF-α mRNA, and KC viability at the end of reoxygenation in groups P1 and P2 were compared with those of HRC.ResultsThe increase of [Ca2+]i from the baseline was attenuated in P1 (96.6 ± 6.9%) and P2 (96.1 ± 5.4%) compared with HRC (143.8 ± 11.5%), (P < 0.001), with no difference between P1 and P2. The expression of TNF-α mRNA increased only in HRC during hypoxia-reoxygenation. KC viability increased in P1 (97.5 ± 2.6%) and P2 (94.6 ± 2.9%), compared with HRC (89.9 ± 1.4%), (P < 0.005), with no difference between P1 and P2.ConclusionThe results indicate that propofol attenuates KC activation and protects KC from hypoxia-reoxygenation injury at clinically relevant concentrations. This attenuation seems to result from inhibition of [Ca2+]i increase in KC.RésuméObjectifDéterminer si le propofol diminue ľactivation des cellules de Kupffer (CK), protégeant ainsi les cellules contre une lésion ďhypoxie-réoxygénation par la modulation du calcium intracellulaire ([Ca2+]i).MéthodeLe [Ca2+]i, expression du facteur de nécrose tumorale (FNT)-α ARNm, et la viabilité des CK ont été mesurés en réponse à ľhypoxie-réoxygénation suivant le prétraitement avec 0,5 et 5 μg·mL-1 de propofol (Groupes P1 et P2, respectivement) ou sans propofol (Groupe HRC). Des CK de rats Sprague-Dawley ont été isolées et mises en culture. Elles ont été incubées sous une atmosphère ďhypoxie (95 % N2 + 5 % de CO2) pendant 60 min et 120 min supplémentaires de réoxygénation (95 % ďair + 5 % CO2). Le [Ca2+]i pendant les 12 premières minutes après la réoxygénation, le FNT-α ARNm et la viabilité des CK à la fin de la réoxygénation dans les groupes P1 et P2 ont été comparés avec ceux du groupe HRC.RésultatsĽaugmentation du [Ca2+]i, au-dessus des mesures de base, a été réduite dans les groupes P1 (96,6 ± 6,9 %) et P2 (96,1 ± 5,4 %) comparés au groupe HRC (143,8 ± 11,5 %), (P < 0,001), sans différence entre P1 et P2. ľexpression du FNT-α ARNm a augmenté seulement dans le groupe HRC pendant ľhypoxie-réoxygénation. La viabilité des CK a augmenté dans les groupes P1 (97,5 ± 2,6 %) et P2 (94,6 ± 2,9 %), comparés au groupe HRC (89,9 ± 1,4 %), (P < 0,005) sans différence entre P1 et P2.ConclusionLe propofol diminue ľactivation des CK et protège ďune lésion liée à ľhypoxie-réoxygénation des CK selon des concentrations cliniquement significatives. Cette baisse semble résulter de ľinhibition de la hausse de [Ca2+]i dans les CK.

Conversion of supraventricular arrhythmia to normal rhythm by propofol and remifentanil: three cases report.

We experienced conversion of supraventricular arrhythmia to normal sinus rhythm in three patients during general anesthesia using propofol and remifentanil. This may be related to direct inhibition of the cardiac conduction system or activation of the parasympathetic system. The literature review suggests that propofol and remifentanil have antiarrhythmic potential, reverting supraventricular arrhythmia during anesthesia.

The comparison of feasibility and safety on fiberoptic guided intubation under conscious sedation with remifentanil and propofol.

Background Oropharyngeal manipulation is problematic when patients have a gag reflex. Sedation can suppress gag reflex, but can cause serious airway problems. We compared remifentanil (Group R) and propofol (Group P) in terms of cooperation and loss of gag reflex, while drugs were administered incrementally using target controlled infusion (TCI). Methods Fifty seven patients who required awake fiberoptic intubation were randomized to Group R or Group P. After measurement of baseline gag trigger point index (GTPI), TCI was set to effect-site concentration (Ce) of 1 ng/ml (Group R) or 1 µg/ml (Group P), then titrated by 0.5 increment until GTPI score reached 0. The incidence of drop-out and decreased cooperation, Ramsay sedation scale (RSS) and Ce at loss of GR, and complications were assessed. Results Seven patients were dropped out in Group P due to deep sedation and disobedient behavior, but none in Group R (P = 0.015). Gag reflex suppressed as RSS increased in both groups (P < 0.001), however, the incidence of elimination of gag reflex clustered at RSS 2 in Group R (P < 0.001), whereas it was evenly distributed in Group P (P = 0.20). The incidence of patients who were spontaneously roused (gag reflex elimination at RSS 1 and 2) were higher in Group R than in Group P (P = 0.002). Conclusions Deep sedation and impaired cooperation were observed only in Group P and spontaneously roused patients were higher in Group R, suggesting that remifentanil is more suitable for cooperative elimination of GR.

Jaw-thrust induces sympathetic responses during induction of general anesthesia

Background Jaw-thrust is a noxious stimulus that might induce sympathetic responses. The purpose of this study, was to evaluate the effects of jaw-thrust on sympathetic responses. Methods We investigated seventy three patients. Patients who received general anesthesia were randomly divided into a control group (maintenance of combined airway maneuver with head tilt, open mouth by mouthpiece, and chin-lift, n = 30) and jaw-thrust group (maintenance of head tilt, open mouth and jaw-thrust, n = 30). In the jaw-thrust group, four minutes of endoscopy-guided force to the mandible to get the best laryngeal view were applied. For the control group, the combined airway maneuver was maintained during the same period. Arterial blood pressure (AP) and heart rate (HR) were recorded at predetermined time points (1 min before anesthesia induction, 2 min after fiberoptic bronchoscopy placement, and thereafter 1 min-interval during each airway maneuver) during jaw-thrust and chin-lift maneuver. The force amplitude applied for best laryngeal view during jaw-thrust was also measured. Results Peak systolic and diastolic AP increased 39.0 ± 17.6 and 39.9 ± 22.8 mmHg from the baseline (P < 0.001) in the jaw-thrust group. HR was also 32.5 ± 19.4 beats/min from the baseline (P < 0.001) in the jaw-thrust group. These remained high at all time points, compared with the control group (P < 0.01). The force magnitude applied for jaw-thrust was not correlated to the AP and HR changes (P > 0.05). Conclusions Performing the jaw-thrust maneuver induces significant sympathetic responses, irrespective of the force magnitude.

Misplaced central venous catheter in the jugular venous arch exposed during dissection before sternotomy

Subclavian vein catheterization rarely results in misplacement of the central venous catheter (CVC) into the jugular venous arch (JVA). We present a case of misplacement of the CVC into the JVA during cardiac surgery.