The proper concentrations of dextrose and lidocaine in regenerative injection therapy: in vitro study

Background@#Prolotherapy is a proliferation therapy as an alternative medicine. A combination of dextrose solution and lidocaine is usually used in prolotherapy. The concentrations of dextrose and lidocaine used in the clinical field are very high (dextrose 10%-25%, lidocaine 0.075%-1%). Several studies show about 1% dextrose and more than 0.2% lidocaine induced cell death in various cell types. We investigated the effects of low concentrations of dextrose and lidocaine in fibroblasts and suggest the optimal range of concentrations of dextrose and lidocaine in prolotherapy. @*Methods@#Various concentrations of dextrose and lidocaine were treated in NIH-3T3. Viability was examined with trypan blue exclusion assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Migration assay was performed for measuring the motile activity. Extracellular signal-regulated kinase (Erk) activation and protein expression of collagen I and α-smooth muscle actin (α-SMA) were determined with western blot analysis. @*Results@#The cell viability was decreased in concentrations of more than 5% dextrose and 0.1% lidocaine. However, in the concentrations 1% dextrose (D1) and 0.01% lidocaine (L0.01), fibroblasts proliferated mildly. The ability of migration in fibroblast was increased in the D1, L0.01, and D1 + L0.01 groups sequentially. D1 and L0.01 increased Erk activation and the expression of collagen I and α-SMA and D1 + L0.01 further increased. The inhibition of Erk activation suppressed fibroblast proliferation and the synthesis of collagen I. @*Conclusions@#D1, L0.01, and the combination of D1 and L0.01 induced fibroblast proliferation and increased collagen I synthesis via Erk activation.

The proper concentrations of dextrose and lidocaine in regenerative injection therapy: in vitro study

Background@#Prolotherapy is a proliferation therapy as an alternative medicine. A combination of dextrose solution and lidocaine is usually used in prolotherapy. The concentrations of dextrose and lidocaine used in the clinical field are very high (dextrose 10%-25%, lidocaine 0.075%-1%). Several studies show about 1% dextrose and more than 0.2% lidocaine induced cell death in various cell types. We investigated the effects of low concentrations of dextrose and lidocaine in fibroblasts and suggest the optimal range of concentrations of dextrose and lidocaine in prolotherapy. @*Methods@#Various concentrations of dextrose and lidocaine were treated in NIH-3T3. Viability was examined with trypan blue exclusion assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Migration assay was performed for measuring the motile activity. Extracellular signal-regulated kinase (Erk) activation and protein expression of collagen I and α-smooth muscle actin (α-SMA) were determined with western blot analysis. @*Results@#The cell viability was decreased in concentrations of more than 5% dextrose and 0.1% lidocaine. However, in the concentrations 1% dextrose (D1) and 0.01% lidocaine (L0.01), fibroblasts proliferated mildly. The ability of migration in fibroblast was increased in the D1, L0.01, and D1 + L0.01 groups sequentially. D1 and L0.01 increased Erk activation and the expression of collagen I and α-SMA and D1 + L0.01 further increased. The inhibition of Erk activation suppressed fibroblast proliferation and the synthesis of collagen I. @*Conclusions@#D1, L0.01, and the combination of D1 and L0.01 induced fibroblast proliferation and increased collagen I synthesis via Erk activation.

Iatrogenic common carotid artery rupture during neck surgery rescued using covered stent: A case report

Carotid artery rupture during head and neck surgery is a catastrophic, life-threatening emergency. Although recent incidence has declined, it still occurs in many patients. Hemorrhage from the carotid artery is usually massive and uncontrollable. Fast, aggressive treatment to prevent hemodynamic instability is required. Even if patients survive this event, they may experience severe neurological sequelae. A ruptured carotid artery is usually controlled by direct compression and arterial ligation. However, apart from the inherent difficulty of operation, these traditional surgical treatments are associated with high morbidity and mortality. In the past two decades, endovascular management has become a mainstay of carotid rupture treatment. We report a case of successful recovery without any sequelae after cardiovascular collapse due to an unintentional common carotid artery (CCA) rupture during neck surgery. The exposed CCA was treated with a covered stent. In such a case, multidisciplinary cooperation is crucial.

Anti-apoptotic and myocardial protective effects of ethyl pyruvate after regional ischaemia/reperfusion myocardial damage in an in vivo rat model

<p><b>INTRODUCTION</b>The integration of reactive oxygen species is strongly associated with important pathophysiological mechanisms that mediate myocardial ischaemia/reperfusion (I/R) damage. Pyruvate is an efficacious scavenger of reactive oxygen species and a previous study has shown that ethyl pyruvate (EP) has a myocardial protective effect against regional I/R damage in an in vivo rat model. The purpose of this study was to determine whether the myocardial protective effect of EP is associated with anti-apoptosis.</p><p><b>METHODS</b>Rats were allocated to receive EP dissolved in lactated Ringer's solution or lactated Ringer's solution alone, via intraperitoneal infusion one hour before ischaemia. They were exposed to 30 minutes of ischaemia followed by reperfusion of the left coronary artery territory over two hours. Anti-apoptotic effects were checked using several biochemical parameters after two hours of reperfusion. Apoptosis was analysed using measured caspase-3 activity, Western blotting of B-cell lymphoma 2 (Bcl-2) family protein cleaved by caspase-3, and assessment of DNA laddering patterns and the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining test.</p><p><b>RESULTS</b>In ischaemic myocardium, EP increased Bcl-2 expression, but reduced Bcl-2-associated X protein and cleaved caspase-3 expressions. EP reduced the expression of DNA laddering and the number of myocardial I/R-damaged TUNEL-positive cells.</p><p><b>CONCLUSION</b>This study demonstrated that EP has an anti-apoptotic effect after regional I/R damage in an in vivo rat heart model. The myocardial protective effect of EP may be related to its anti-apoptotic effect.</p>

Lipofundin(R) MCT/LCT 20% increase left ventricular systolic pressure in an ex vivo rat heart model via increase of intracellular calcium level / 대한마취과학회지

BACKGROUND: Lipid emulsions have been used to treat various drug toxicities and for total parenteral nutrition therapy. Their usefulness has also been confirmed in patients with local anesthetic-induced cardiac toxicity. The purpose of this study was to measure the hemodynamic and composition effects of lipid emulsions and to elucidate the mechanism associated with changes in intracellular calcium levels in myocardiocytes. METHODS: We measured hemodynamic effects using a digital analysis system after Intralipid(R) and Lipofundin(R) MCT/LCT were infused into hearts hanging in a Langendorff perfusion system. We measured the effects of the lipid emulsions on intracellular calcium levels in H9c2 cells by confocal microscopy. RESULTS: Infusion of Lipofundin(R) MCT/LCT 20% (1 ml/kg) resulted in a significant increase in left ventricular systolic pressure compared to that after infusing modified Krebs-Henseleit solution (1 ml/kg) (P = 0.003, 95% confidence interval [CI], 2.4-12.5). Lipofundin(R) MCT/LCT 20% had a more positive inotropic effect than that of Intralipid(R) 20% (P = 0.009, 95% CI, 1.4-11.6). Both lipid emulsion treatments increased intracellular calcium levels. Lipofundin(R) MCT/LCT (0.01%) increased intracellular calcium level more than that of 0.01% Intralipid(R) (P < 0.05, 95% CI, 0.0-1.9). CONCLUSIONS: These two lipid emulsions had different inotropic effects depending on their triglyceride component. The inotropic effect of lipid emulsions could be related with intracellular calcium level.

Anesthetic management for percutaneous computed tomography-guided radiofrequency ablation of reninoma: a case report / 대한마취과학회지

A reninoma is an uncommon, benign, renin-secreting juxtaglomerular cell tumor that causes secondary hypertension in young patients. This hypertension is treated by tumor resection. Except for increased levels of plasma renin and angiotensin I and II, the other physical and laboratory examinations and electrocardiographs were within normal limits upon admission of a 19-year-old woman with a reninoma. For percutaneous computed tomography-guided radiofrequency ablation, general anesthesia was induced by thiopental sodium and rocuronium bromide and maintained with servoflurane (2-4 vol%) and oxygen. The operation ended uneventfully in hemodynamic stability. However, the patient complained of dizziness while sitting 5 hours after the operation, and hypotension was diagnosed. After aggressive normal saline (1 L) infusion over 30 min, the hypotension was corrected and the patient recovered without any other surgical complications. Here, we report the anesthetic management of a patient who underwent percutaneous computed tomography-guided radiofrequency ablation for reninoma destruction, particularly focusing on postoperative hypotension.

Bupivacaine-induced Vasodilation Is Mediated by Decreased Calcium Sensitization in Isolated Endothelium-denuded Rat Aortas Precontracted with Phenylephrine

BACKGROUND: A toxic dose of bupivacaine produces vasodilation in isolated aortas. The goal of this in vitro study was to investigate the cellular mechanism associated with bupivacaine-induced vasodilation in isolated endotheliumdenuded rat aortas precontracted with phenylephrine. METHODS: Isolated endothelium-denuded rat aortas were suspended for isometric tension recordings. The effects of nifedipine, verapamil, iberiotoxin, 4-aminopyridine, barium chloride, and glibenclamide on bupivacaine concentration-response curves were assessed in endothelium-denuded aortas precontracted with phenylephrine. The effect of phenylephrine and KCl used for precontraction on bupivacaine-induced concentration-response curves was assessed. The effects of verapamil on phenylephrine concentration-response curves were assessed. The effects of bupivacaine on the intracellular calcium concentration ([Ca2+]i) and tension in aortas precontracted with phenylephrine were measured simultaneously with the acetoxymethyl ester of a fura-2-loaded aortic strip. RESULTS: Pretreatment with potassium channel inhibitors had no effect on bupivacaine-induced relaxation in the endothelium-denuded aortas precontracted with phenylephrine, whereas verapamil or nifedipine attenuated bupivacaine-induced relaxation. The magnitude of the bupivacaine-induced relaxation was enhanced in the 100 mM KCl-induced precontracted aortas compared with the phenylephrine-induced precontracted aortas. Verapamil attenuated the phenylephrine-induced contraction. The magnitude of the bupivacaine-induced relaxation was higher than that of the bupivacaine-induced [Ca2+]i decrease in the aortas precontracted with phenylephrine. CONCLUSIONS: Taken together, these results suggest that toxic-dose bupivacaine-induced vasodilation appears to be mediated by decreased calcium sensitization in endothelium-denuded aortas precontracted with phenylephrine. In addition, potassium channel inhibitors had no effect on bupivacaine-induced relaxation. Toxic-dose bupivacaine- induced vasodilation may be partially associated with the inhibitory effect of voltage-operated calcium channels.

Lipid emulsion treatment of systemic toxicity induced by local anesthetics or other drugs

Although intravenous lipid emulsion (LE) is used mainly for parenteral nutrition, recently it has been used to treat patients with cardiopulmonary resuscitation (CPR)-resistant cardiovascular collapse induced by a toxic dose of local anesthetics or other drugs. Intravenous LE resolves symptoms of local anesthetic systemic toxicity, including convulsion, myoclonus, loss of consciousness, cardiac arrest, supraventricular tachycardia, and ventricular fibrillation. The main underlying mechanisms suggested to be responsible for LE-induced reversal of cardiac arrest due to drug toxicity are the lipid sink effect and the metabolic effect. The lipid sink theory posits that LE extracts a lipid-soluble toxic drug from the tissue. When a patient with cardiovascular collapse induced by a local anesthetic or another lipid-soluble drug is unresponsive to supportive treatments, including CPR and vasopressor therapy, LE administration can be considered. The suggested dosing regimen is as follows: 1) an initial intravenous bolus administration of 20% LE (1.5 mL/kg) is followed by a continuous infusion of 20% LE (0.25 mL/kg/min); and 2) when hemodynamic functions are unstable after the initial LE infusion, an intravenous administration of 20% LE (1.5 mL/kg) is repeated and followed by an increased continuous infusion of 20% LE (0.5 mL/kg/min). Further research is warranted regarding other possible mechanisms of LE's effect, the timing of LE administration, and the effect of various fatty acids on the LE-mediated reversal of cardiac arrest. This article reviews case reports and experimental evidence concerning the LE-mediated reversal of intractable cardiac arrest induced by drug toxicity, the underlying mechanism, and the dosing regimen.

Postoperative Acute Cerebral Infarction Occurring after General Anesthesia / 대한구급학회지

The common predisposing risk factors for perioperative stroke include: previous stroke, atrial fibrillation, old age (> 75 years), carotid stenosis, and diabetes mellitus. An endoscopic sinus surgery was performed in a 49-year-old male with chronic paranasal sinusitis and nasal polyps. The vital signs, physical and laboratory examinations, and electrocardiography on admission were within the normal limit. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The operation and anesthesia were uneventful with the exception of transient intraoperative hypotension. The patient recovered fully from the anesthesia (modified Aldrete score: 10) in the recovery room. However, he developed right arm weakness and dysarthria in the general ward 7 hours after the operation. We report a rare case of multifocal acute cerebral infarctions found on the postoperative magnetic resonance imaging in a noncardiac surgical patient.

Lipid emulsion-mediated reversal of toxic-dose aminoamide local anesthetic-induced vasodilation in isolated rat aorta / 대한마취과학회지

BACKGROUND: Intravenous lipid emulsion has been used to treat systemic toxicity of local anesthetics. The goals of this in vitro study were to determine the ability of two lipid emulsions (Intralipid(R) and Lipofundin(R) MCT/LCT) to reverse toxic dose local anesthetic-induced vasodilation in isolated rat aortas. METHODS: Isolated endothelium-denuded aortas were suspended for isometric tension recording. Vasodilation was induced by bupivacaine (3 x 10(-4) M), ropivacaine (10(-3) M), lidocaine (3 x 10(-3) M), or mepivacaine (7 x 10(-3) M) after precontraction with 60 mM KCl. Intralipid(R) and Lipofundin(R) MCT/LCT were then added to generate concentration-response curves. We also assessed vasoconstriction induced by 60 mM KCl, 60 mM KCl with 3 x 10(-4) M bupivacaine, and 60 mM KCl with 3 x 10(-4) M bupivacaine plus 1.39% lipid emulsion (Intralipid(R) or Lipofundin(R) MCT/LCT). RESULTS: The two lipid emulsions reversed vasodilation induced by bupivacaine, ropivacaine, and lidocaine but had no effect on vasodilation induced by mepivacaine. Lipofundin(R) MCT/LCT was more effective than Intralipid(R) in reversing bupivacaine-induced vasodilation. The magnitude of lipid emulsion-mediated reversal of vasodilation induced by high-dose local anesthetics was as follows (from highest to lowest): 3 x 10(-4) M bupivacaine-induced vasodilation, 10(-3) M ropivacaine-induced vasodilation, and 3 x 10(-3) M lidocaine-induced vasodilation. CONCLUSIONS: Lipofundin(R) MCT/LCT-mediated reversal of bupivacaine-induced vasodilation was greater than that of Intralipid(R); however, the two lipid emulsions equally reversed vasodilation induced by ropivacaine and lidocaine. The magnitude of lipid emulsion-mediated reversal of vasodilation appears to be correlated with the lipid solubility of the local anesthetic.

A Patient with Kikuchi's Disease: What Should Pain Clinicians Do?

Kikuchi's disease (KD) is an idiopathic and self-limiting necrotizing lymphadenitis that predominantly occurs in young females. It is common in Asia, and the cervical lymph nodes are commonly involved. Generally, KD has symptoms and signs of lymph node tenderness, fever, and leukocytopenia, but there are no reports on treatment for the associated myofacial pain. We herein report a young female patient who visited a pain clinic and received a trigger point injection 2 weeks before the diagnosis of KD. When young female patients with myofascial pain visit a pain clinic, doctors should be concerned about the possibility of KD, which is rare but can cause severe complications.

Myocardial protective effect by ulinastatin via an anti-inflammatory response after regional ischemia/reperfusion injury in an in vivo rat heart model / 대한마취과학회지

BACKGROUND: Ulinastatin has anti-inflammatory properties and protects organs from ischemia/reperfusion-induced injury. The aim of this study was to investigate whether ulinastatin provides a protective effect on a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model and to determine whether the anti-inflammatory response is related to its myocardial protective effect. METHODS: Rats were randomized to two groups. One group is received ulinastatin (50,000 U/kg or 100,000 U/kg) diluted in normal saline and the other group is received normal saline, which was administered intraperitoneally 30 min before the ischemic insult. Reperfusion after 30 min of ischemia of the left coronary artery territory was applied. Hemodynamic measurements were recorded serially during 6 h after reperfusion. After the 6 h reperfusion, myocardial infarct size, cardiac enzymes, myeloperoxidase activity, and inflammatory cytokine levels were compared between the ulinastatin treated and untreated groups. RESULTS: Ulinastatin improved cardiac function and reduced infarct size after regional ischemia/reperfusion injury. Ulinastatin significantly attenuated tumor necrosis factor-alpha expression and reduced myeloperoxidase activity. CONCLUSIONS: Ulinastatin showed a myocardial protective effect after regional ischemia/reperfusion injury in an in vivo rat heart model. This protective effect of ulinastatin might be related in part to ulinastatin's ability to inhibit myeloperoxidase activity and decrease expression of tumor necrosis factor-alpha.

Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta / 대한마취과학회지

BACKGROUND: The intravenous administration of indigo carmine has been reported to produce transiently increased blood pressure in patients. The goal of this in vitro study was to examine the effect of indigo carmine on phenylephrine-induced contractions in an isolated rat aorta and to determine the associated cellular mechanism with particular focus on the endothelium-derived vasodilators. METHODS: The concentration-response curves for phenylephrine were generated in the presence or absence of indigo carmine. Phenylephrine concentration-response curves were generated for the endothelium-intact rings pretreated independently with a nitric oxide synthase inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME), a cyclooxygenase inhibitor, indomethacin, and a low-molecular-weight superoxide anion scavenger, tiron, in the presence or absence of indigo carmine. The fluorescence of oxidized dichlorofluorescein was measured in rat aortic vascular smooth muscle cells cultured in the control, indigo carmine alone and tiron plus indigo carmine. RESULTS: Indigo carmine (10(-5) M) increased the phenylephrine-induced maximum contraction in the endothelium-intact rings with or without indomethacin, whereas indigo carmine produced a slight leftward shift in the phenylephrine concentration-response curves in the endothelium-denuded rings and L-NAME-pretreated endothelium-intact rings. In the endothelium-intact rings pretreated with tiron (10(-2) M), indigo carmine did not alter phenylephrine concentration-response curves significantly. Indigo carmine (10(-5) M) increased the fluorescence of oxidized dichlorofluorescein in the vascular smooth muscle cells, whereas tiron abolished the indigo carmine-induced increase in oxidized dichlorofluorescein fluorescence. CONCLUSIONS: Indigo carmine increases the phenylephrine-induced contraction mainly through an endothelium-dependent mechanism involving the inactivation of nitric oxide caused by the increased production of reactive oxygen species.

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy: A case report / 대한마취과학회지

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy.

Ethyl Pyruvate Has Anti-Inflammatory and Delayed Myocardial Protective Effects after Regional Ischemia/Reperfusion Injury

PURPOSE: Ethyl pyruvate has anti-inflammatory properties and protects organs from ischemia/reperfusion (I/R)-induced tissue injury. The aim of this study was to determine whether ethyl pyruvate decreases the inflammatory response after regional I/R injury and whether ethyl pyruvate protects against delayed regional I/R injury in an in vivo rat heart model after a 24 hours reperfusion. MATERIALS AND METHODS: Rats were randomized to receive lactated Ringer's solution or ethyl pyruvate dissolved in Ringer's solution, which was given by intraperitoneal injection 1 hour prior to ischemia. Rats were subjected to 30 min of ischemia followed by reperfusion of the left coronary artery territory. After a 2 hours reperfusion, nuclear factor kappaB, myocardial myeloperoxidase activity, and inflammatory cytokine levels were determined. After the 24 hours reperfusion, the hemodynamic function and myocardial infarct size were evaluated. RESULTS: At 2 hours after I/R injury, ethyl pyruvate attenuated I/R-induced nuclear factor kappaB translocation and reduced myeloperoxidase activity in myocardium. The plasma circulating levels of inflammatory cytokines decreased significantly in the ethyl pyruvate-treated group. At 24 hours after I/R injury, ethyl pyruvate significantly improved cardiac function and reduced infarct size after regional I/R injury. CONCLUSION: Ethyl pyruvate has the ability to inhibit neutrophil activation, inflammatory cytokine release, and nuclear factor kappaB translocation. Ethyl pyruvate is associated with a delayed myocardial protective effect after regional I/R injury in an in vivo rat heart model.

Propofol has delayed myocardial protective effects after a regional ischemia/reperfusion injury in an in vivo rat heart model / 대한마취과학회지

BACKGROUND: It is well known that propofol protects myocardium against myocardial ischemia/reperfusion injury in the rat heart model. The aim of this study was to investigate whether propofol provides a protective effect against a regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion. METHODS: Rats were subjected to 25 min of left coronary artery occlusion followed by 48 h of reperfusion. The sham group received profopol without ischemic injury. The control group received normal saline with ischemia/reperfusion injury. The propofol group received profopol with ischemia/reperfusion injury. The intralipid group received intralipid with ischemia/reperfusion injury. A microcatheter was advanced into the left ventricle and the hemodynamic function was evaluated. The infarct size was determined by triphenyltetrazolium staining. The serum level of cardiac troponin-I (cTn-I) was determined by ELISA (enzyme-linked immunosorbent assay). RESULTS: Propofol demonstrated protective effects on hemodynamic function and infarct size reduction. In the propofol group, the +dP/dt(max) (P = 0.002) was significantly improved compared to the control group. The infarct size was 49.8% of the area at risk in the control group, and was reduced markedly by administration of propofol to 32.6% in the propofol group (P = 0.014). The ischemia/reperfusion-induced serum level of cTn-I was reduced by propofol infusion during the peri-ischemic period (P = 0.0001). CONCLUSIONS: Propofol, which infused at clinically relevant concentration during the peri-ischemic period, has delayed myocardial protective effect after regional myocardial ischemia/reperfusion injury in an in vivo rat heart model after 48 h of reperfusion.

Anesthetic management for the endoscopic sinus surgery of a patient with coexisting severe cervical spine ankylosing spondylitis and unruptured cerebral aneurysm: A case report / 대한마취과학회지

A 61-year-old man was admitted to the emergency room complaining of a severe left exophthalmos caused by frontal and ethmoid sinus mucoceles that were visualized on a brain computerized tomogram. In addition, he had coexisting ankylosing spondylitis with a 20 year duration that resulted in total fixation of the cervical spine and progressive thoracic kyphosis. An unruptured anterior communicating artery aneurysm was found incidentally on the cerebral angiogram. We report that the anesthetic management for endoscopic sinus surgery of a frontal sinus mucocele in a patient with coexisting severe cervical spine ankylosing spondylitis and an unruptured cerebral aneurysm requires a detailed preoperative assessment of the airway, cardiac, pulmonary, and neurologic system. This case highlights the need for careful measures to avoid rupturing the cerebral aneurysm by the increased blood pressure induced by endotracheal intubation and the infiltration of an epinephrine-containing local anesthetic.

Inhibitory Effect of Fentanyl on Phenylephrine-Induced Contraction of the Rat Aorta

PURPOSE: Fentanyl was reported to inhibit the alpha1-adrenoceptor agonist-induced contraction. The goal of this in vitro study was to identify the alpha1-adrenoceptor subtype primarily involved in the fentanyl-induced attenuation of phenylephrine-induced contraction in isolated endothelium-denuded rat aorta. MATERIALS AND METHODS: Aortic rings were suspended in order to record isometric tension. Concentration-response curves for phenylephrine (10-9 to 10-5 M) were generated in the presence or absence of one of the following drugs: fentanyl (3x10-7, 10-6, 3x10-6 M), 5-methylurapidil (3x10-8, 10-7, 3x10-7 M), chloroethylclonidine (10-5 M) and BMY 7378 (3x10-9, 10-8, 3x10-8 M). Phenylephrine concentration-response curves were generated in the presence or absence of fentanyl in rings pretreated with either 3x10-9 M prazosin, 10-9 M 5-methylurapidil or 3x10-9 M BMY 7378. RESULTS: Fentanyl (10-6, 3x10-6 M) attenuated phenylephrine-induced contraction in the rat aorta. 5-Methylurapidil and BMY 7378 produced a parallel rightward shift in the phenylephrine concentration-response curve. The pA2 values for 5-methylurapidil and BMY 7378 were estimated to be 7.71 +/- 0.15 and 8.99 +/- 0.24, respectively. Fentanyl (10-6 M) attenuated phenylephrine-induced contraction in rings pretreated with 10-9 M 5-methylurapidil, but did not alter the rings when pretreated with 3x10-9 M BMY 7378. Pretreatment of the rings with chloroethylclonidine showed a 72.9 +/- 2.3% reduction in phenylephrine-induced maximal contraction. CONCLUSION: The results suggest that fentanyl attenuates phenylephrine-induced contraction by inhibiting the pathway involved in the alpha1D-adrenoceptor-mediated contraction of the rat aorta.

Dose remifentanil have a myocardial protective effect against a regional ischemia-reperfusion injury in an in vivo rat heart model? / 대한마취과학회지

BACKGROUND: It is known that some opioids protect the myocardial tissue from myocardial ischemia-reperfusion (I/R) injury. The aim of this study was to investigate whether remifentanil, at a clinically relevant concentration that's during the peri-ischemic period, has a protective effect against a regional I/R injury in an in vivo rat heart model. METHODS: Rats were subjected to 25 minutes of coronary artery occlusion and this was followed by 24 hours of reperfusion. A microcatheter was advanced into the left ventricle and the hemodynamic function was evaluated after 24 hours of reperfusion. The infarct size was determined by triphenyltetrazolium staining. The serum level of cardiac troponin-I (cTnI) was determined by ELISA (enzyme-linked immunosorbent assay). RESULTS: Remifentanil administration during the peri-ischemic period didn't show any identifiable protective effects for the hemodynamic function or to reduce the infarct size. In the control group, the peak rate of the ventricular pressure increase (+dP/dt(max)) (P < 0.05) and the peak rate of the intraventricular pressure decline (-dP/dt(max) P < 0.05) were significantly decreased as compared to those values for the sham group. In the remifentanil group, the +dP/dt(max) and -dP/dt(max) were not improved compared to those values of the control group. The infarct size was 45.6% of the area at risk in the control group, and the infarct size was reduced by administration of remifentanil to 43.2% in the remifentanil group. The I/R-induced serum level of cTn-I was not reduced by remifentanil infusion during the peri-ischemic period. CONCLUSIONS: Remifentanil, at a clinically relevant concentration that's infused during the peri-ischemic period, has no myocardial protective effect after regional myocardial I/R injury in an in vivo rat heart model.

Spinal cord stimulation for intractable post-thoracotomy pain syndrome: A case report / 대한마취과학회지

Post-thoracotomy syndrome is a condition characterized by pain that continues for more than 2 months after a thoracotomic procedure. Some patients suffer from devastating chest pain despite receiving multimodal treatment such as analgesics, antidepressants, anticonvulsants and nerve blockers. Spinal cord stimulation has been reported to be a promising relief for the intractable neuropathic pain. A 60-year-old man who had been suffering from post-thoracotomy pain for 20 years showed relief of pain after spinal cord stimulation. Spinal cord stimulation thus seems to be a viable option for patients who do not respond to conventional pain management therapy.