Predictive Value of Intraoperative Thromboelastometry for the Risk of Perioperative Excessive Blood Loss in Infants and Children Undergoing Congenital Cardiac Surgery: A Retrospective Analysis.

OBJECTIVE: Laboratory hemostatic variables and parameters of rotational thromboelastometry (ROTEM) were evaluated for their ability to predict perioperative excessive blood loss (PEBL) after congenital cardiac surgery. DESIGN: Retrospective and observational. SETTING: Single, large university hospital. PARTICIPANTS: The study comprised 119 children younger than 10 years old undergoing congenital cardiac surgery with cardiopulmonary bypass (CPB). MEASUREMENTS AND MAIN RESULTS: Intraoperative excessive blood loss was defined as estimated blood loss≥50% of estimated blood volume (EBV). Postoperative excessive blood loss was defined as measured postoperative chest tube and Jackson-Pratt drainage≥30% of EBV over 12 hours or≥50% of EBV over 24 hours in the intensive care unit. PEBL was defined as either intraoperative or postoperative excessive blood loss. External temogram (EXTEM) and fibrinogen temogram (FIBTEM) were analyzed before and after CPB with ROTEM and laboratory hemostatic variables. Multivariate logistic regression was performed. Incidence of PEBL was 19.3% (n = 23). Independent risk factors for PEBL were CPB time>120 minutes, post-CPB FIBTEM alpha-angle, clot firmness after 10 minutes<5 mm, post-CPB EXTEM alpha-angle, clot firmness after 10 minutes<30 mm, and post-CPB EXTEM maximal lysis>20%. Laboratory hemostatic variables were not significant in multivariate analysis. The risk prediction model was developed from the results of multivariate analysis. The area under the receiver operating characteristic curve was 0.94 (95% confidence interval: 0.90-0.99). CONCLUSIONS: Post-CPB ROTEM may be useful for predicting both intraoperative and postoperative excessive blood loss in congenital cardiac surgery. This study provided an accurate prediction model for PEBL and supported intraoperative transfusion guidance using post-CPB FIBTEM-A10 and EXTEM-A10.

Intravenous patient-controlled analgesia regimen in postoperative pain management following elective cesarean section: A single-center retrospective evaluation.

Intravenous patient-controlled analgesia (IV PCA; IVA) is the most widely used method for postoperative pain management. An appropriate IVA regimen is required, depending on the expected intensity of pain after surgery. This study expected that a decrease in the second prescription rate of IVA after elective cesarean section (CS) would help establish an appropriate regimen for the initial IVA. We retrospectively reviewed the records of 632 patients who were prescribed IVA after CS. We classified patients into phase 1 (basal rate 15.00 mcg/hours, bolus dose 15.00 mcg, total volume 100 mL) and phase 2 (basal rate 31.25 mcg/hours, bolus dose 31.25 mcg, nefopam 60 mg, paracetamol 3 g, total volume 160 mL) according to the IVA regimen, and patients in phase 2 were classified into the basal 15 group and basal 30 group according to the basal rate of IVA. We compared the rates of second prescription, drug removal, and side effects of IVA between the 2 phases and the 1 group. We analyzed the data of 631 eligible patients. The second prescription rate of IVA in phase 2 was 3.77%, a significant decrease compared to that in phase 1 (27.48%); however, the incidence of complications in phase 2 was 6.92%, a significant increase compared to that in phase 1 (0.96%). Within phase 2, in the basal 30 group, the basal rate was almost double that in the basal 15 group. However, there were no significant differences in the rate of second prescription, removed drug IVA, or adverse events between the basal 15, and 30 groups. In the case of CS, which has a high degree of postoperative pain, it is beneficial to control acute pain by properly setting the regimen of the initial IVA with a basal rate infusion to nullify a second prescription.

Are there effects of lunar cycle on pediatric febrile seizure?: A single-center retrospective study (2005-2018).

BACKGROUND: Several studies have reported an association between seizure and the lunar cycle; however, results are conflicting. Thus, we investigated whether emergency department (ED) visits due to febrile seizure (FS) or FS plus were affected by lunar cycle. METHODS: We reviewed the medical records of patients who were admitted to the ED with a main diagnosis of FS or FS plus from January 1, 2005 to August 31, 2018 (13 years 8 months), a period of 4991 days with 169 lunar cycles. During that period, we collected weather data such as mean temperature, average atmospheric pressure (AP), and humidity according to lunar phase (new moon, first quarter, full moon, and third or last quarter). RESULTS: A total of 1979 patients were identified. We found male predominant with a mean age of 2.62 ±â€¯2.09 years. Acute pharyngotonsillitis was the most common cause of fever, generalized tonic-clonic seizure was the most common type of seizure, and the mean peak body temperature was 38.77 ±â€¯0.81 °C. The lunar cycle did not affect the onset or frequency of FS after adjustment; however, several factors, including season, O3 and NO2 concentrations, and holidays, were associated with FS. CONCLUSION: We did not find an association between lunar cycle and FS or FS plus. However, several factors, including season, O3, NO2, and holidays were associated with FS or FS plus.

Metabolic syndrome is associated with hearing disturbance.

BACKGROUND: Although metabolic syndrome (MetS) has been associated with various diseases, few studies to date have addressed the association between MetS and hearing loss. AIMS/OBJECTIVES: This cross-sectional review of health examination center data sought to determine the association between MetS and hearing disturbance. MATERIAL AND METHODS: This study involved 28,866 subjects. Height, weight, waist circumference, and blood pressure were measured, and basic blood tests and pure-tone audiometry (PTA) were performed. Other factors analyzed included body mass index, hypertension, diabetes mellitus, and hyperlipidemia. RESULTS: Age and gender did not differ between subjects with and without MetS. PTA was slightly higher in subjects with than without MetS, but the difference was not statistically significant (p = .47). The incidence of hearing loss was no higher in subjects who met three of the five diagnostic criteria of MetS than in those who met 0-2 criteria, but was significantly higher in subjects who met four (p = .04) and five (p < .01) criteria. CONCLUSIONS AND SIGNIFICANCE: MetS may be associated with hearing loss, especially in subjects who meet four or five of the diagnostic criteria for MetS.

Expression of C-type lectin receptor mRNA in otitis media with effusion and chronic otitis media with and without cholesteatoma.

BACKGROUND & OBJECTIVES: C-type lectin receptors (CLRs) are a family of pattern recognition receptors (PRPs). The expression of CLRs has been analyzed in other diseases but has not yet been compared in patients with otitis media with effusion (OME), chronic otitis media (COM) and COM with cholesteatoma (Chole OM). This study therefore evaluated the levels of expression of mRNAs encoding Dectin-1, MR1, MR2, DC-SIGN, Syk, Card-9, Bcl-10, Malt-1, Src, DEC-205, Tim-3, Trem-1, and DAP-12 in patients with OME, COM, and Chole OM. METHODS: CLR mRNA levels in patients with OME, COM, and Chole OM were assessed by real-time polymerase chain reaction. The level of expression of each mRNA was compared in patients with and without bacteria, and in patients with conductive hearing loss (CHL) and sensorineural hearing loss (SNHL). RESULTS: The patterns of expression of CLRs differed in patients with OME, COM, and Chole OM. Galectin-1 mRNA level was significantly higher in the COM than in the Chole OM group (p<0.05), and MR1 and Galectin-1 mRNA levels among patients with CHL were significantly higher in those with COM than with Chole OM (p<0.05). Galectin-1 mRNA level among patients with SNHL was also significantly higher in the COM than in the Chole OM group (p<0.05). CONCLUSIONS: The levels of expression of mRNAs encoding the CLRs Dectin-1, MR1, MR2, DC-SIGN, Syk, Card-9, Bcl-10, Malt-1, Src, DEC-205, Tim-3, Trem-1 and DAP-12 differ among patients with OME, COM, and Chole OM.

Association of Metabolic Syndrome With Sudden Sensorineural Hearing Loss.

Importance: Each of the 5 diagnostic criteria or factors of metabolic syndrome-hyperglycemia or type 2 diabetes, hypertension, obesity, elevated triglyceride levels, and decreased high-density lipoprotein cholesterol level-is associated with the pathophysiologic features of sudden sensorineural hearing loss (SSNHL). Little is known, however, about the association of metabolic syndrome, defined as the presence of at least 3 of these factors, with the prognosis of SSNHL. Objective: To evaluate the association of metabolic syndrome with the rate of recovery from SSNHL. Design, Setting, and Participants: This retrospective medical record review of 124 patients treated for SSNHL at a single tertiary university hospital was performed from June 1, 2014, through May 31, 2016. Medical records were reviewed for demographic and clinical characteristics and audiologic variables. Exposure: Sudden sensorineural hearing loss. Main Outcomes and Measures: Correlation among demographic and clinical characteristics, audiologic results, and prognosis. Results: Of the total 124 patients (52 men [41.9%]; 72 women [58.1%]; mean [SD] age, 56.0 [14.6] years), 70 had metabolic syndrome and 54 did not. Rates of type 2 diabetes (36 [51.4%] vs 6 [11.1%]; mean difference [MD], 40.3%; 95% CI, 24.4%-53.1%), hypertension (46 [65.7%] vs 9 [16.7%]; MD, 49.1%; 95% CI, 32.3%-61.7%), and obesity (47 [67.1%] vs 6 [11.1%]; MD%, 56.0; 95% CI, 40.0%-67.5%) and mean (SD) concentrations of triglycerides (192.9 [159.7] vs 133.4 [116.6] mg/dL; MD, 59.4 mg/dL; 95% CI, 53.0-65.9 mg/dL) were significantly higher and mean (SD) concentrations of high-density lipoprotein cholesterol (45.8 [9.4] vs 62.6 [17.7] mg/dL; MD, 16.8 mg/dL; 95% CI, 16.1-17.4 mg/dL) were significantly lower in the group with metabolic syndrome than in the group without metabolic syndrome. Mean (SD) pure-tone audiometry thresholds were similar at baseline in the groups with and without metabolic syndrome (65.0 [24.2] vs 60.8 [24.2] dB; MD, 4.3 dB; 95% CI, 3.2-5.4 dB), but recovery rates after treatment were significantly lower in the group with metabolic syndrome (16 [22.9%] vs 23 [42.6%]; MD, -19.7%; 95% CI, -35.4% to -3.2%). No differences were found in the 5 factors among patients with metabolic syndrome who did and did not recover. Level of hearing loss was higher in patients with than without metabolic syndrome, but the difference was not statistically significant. Audiogram patterns also differed but not significantly. Hearing recovery rates were similar in patients with 3 factors of metabolic syndrome and those with none but differed significantly between patients with 4 or more factors and those without metabolic syndrome (4 [19.0%] vs 27 [50.0%]; MD, -31.0%; 95% CI, -48.1% to -6.4%). Conclusions and Relevance: The rate of recovery from SSNHL was lower among patients with metabolic syndrome than among those without metabolic syndrome, and prognosis was poorer in patients with 4 or more diagnostic factors of the metabolic syndrome.

Comparative Analysis of the Combined Therapeutic Effects of Lipoprostaglandin E1 on Sudden Idiopathic Sensorineural Hearing Loss.

BACKGROUND AND OBJECTIVES: Viral and vascular disorders are considered to be a major cause of idiopathic sudden sensorineural hearing loss (ISSNHL). Lipoprostaglandin E1 (lipo-PGE1) has vasodilating activity and has been used to treat ISSNHL. The purpose of this study was to determine the specific therapeutic effects of lipo-PGE1 and compare them to other treatment modalities for ISSNHL. SUBJECTS AND METHODS: The study group had 1,052 patients diagnosed with ISSNHL. All were treated with steroid, carbogen inhalation, stellate ganglion block (SGB), or PGE1. The CP group (steroid, carbogen inhalation, and PGE1 injection; 288 patients) was treated with lipo-PGE1 and carbogen inhalation, the CS group (steroid, carbogen inhalation, and stellate ganglion block; 232 patients) with steroid, carbogen inhalation, and SGB, the C group (steroid and carbogen inhalation; 284 patients) with steroid and carbogen, and the control group (steroid only; 248 patients) with steroid only. Patients in the groups receiving lipo-PGE1 received a continuous infusion of 10 µL lipo-PGE1. RESULTS: The overall recovery rate after treatment was 52.2%, and recovery rates by group were 67.7% in the CP group, 54.3% in the CS group, 52.1% in the C group, and 32.2% in the control group. Therefore, the therapeutic results in groups treated with lipo-PGE1 were better than results in other groups. The difference was statistically significant. CONCLUSIONS: The study results suggested that the CP group received effective treatment modalities for ISSNHL. The combined therapy of lipo-PGE1 with carbogen inhalation in patients with ISSNHL was more beneficial than other treatment modalities.

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

INTRODUCTION: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

The effects of uterine artery embolization on ovarian reserve.

OBJECTIVE: To evaluate the effects of UAE for symptomatic uterine fibroids on ovarian reserve based on AMH. STUDY DESIGN: This was a retrospective study conducted between March 2011 and October 2014. All women underwent UAE. At baseline and at the 3-month and 12-month follow-up visits, serum anti-Müllerian hormone (AMH), follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol (E2) levels were assessed, and ovarian volume and antral follicle count (AFC) were evaluated in each patient. RESULTS: There were no statistically significant differences in serum E2, LH, or FSH levels or in ovarian volume 3 or 12 months after UAE (P=0.8194, P=0.3976, P=0.4766, and P=0.6822, respectively). However, AMH and AFC were significantly different 3 and 12 months after the procedure (P=0.00, P=0.029 and P=0.00, P=0.00, respectively). AMH levels remained low after 12 months of follow-up compared to the expected AMH levels. A statistically significant recovery of serum AMH at 12 months compared to at 3 months in those <40 years of age (P=0.00), but not in those ≥40 years (P=0.837). CONCLUSIONS: Ovarian reserve appears to be affected by UAE in premenopausal women. However, younger ovaries (according to biological ovarian age) exhibit a greater capacity for recovery after ovarian damage. Therefore, larger studies are needed for more conclusive results.

Increased IL-17 and 22 mRNA expression in pediatric patients with otitis media with effusion.

OBJECTIVES: Middle ear effusion has been reported to be associated with immune responses in patients with otitis media with effusion (OME). Although various cytokines are involved in immunologic responses in patients with OME, no study to date has assessed the involvement of the pro-inflammatory cytokines interleukin (IL)-17 and IL-22. This study analyzed the levels of expression of IL-17 and IL-22 in the middle ear effusion of patients with OME. METHODS: Patients aged <11 years who were diagnosed with chronic OME and underwent ventilation tube insertion from May 2013 to August 2015 were enrolled. Effusion fluid samples were obtained during surgery and levels of IL-17 and IL-22 mRNAs assessed by real-time PCR. IL-17 and IL-22 mRNA levels were compared in patients with effusion fluid positive and negative for bacteria; in patients with and without accompanying diseases, recurrent disease, and re-operation; and relative to fluid characteristics. RESULTS: The study cohort included 70 pediatric patients, 46 boys and 24 girls, of mean age 4.31 ± 2.11 years. The levels of IL-17 and IL-22 mRNA were higher in patients with than without sinusitis, but only IL-22 mRNA levels differed significantly (p < 0.05). The level of IL-17 mRNA was significantly higher in patients who did than did not undergo T&A (p < 0.05). The level of IL-22 expression was significantly higher in mucoid and purulent middle ear fluid samples than in serous fluid samples (p < 0.05). CONCLUSION: IL-17 and IL-22 mRNAs are involved in the pathophysiology of OME and are significantly higher in subjects with than without accompanying diseases.

Potentially modifiable risk factors for acute kidney injury after surgery on the thoracic aorta: a propensity score matched case-control study.

Perioperative risk factors were identified for acute kidney injury (AKI) defined by the RIFLE criteria (RIFLE = risk, injury, failure, loss, end stage) after surgery on the thoracic aorta with cardiopulmonary bypass (CPB) in this case-control study. A retrospective review was completed for 702 patients who underwent surgery on the thoracic aorta with CPB. A total of 183 patients with AKI were matched 1:1 with patients without AKI by a propensity score. Matched variables included age, gender, body-mass index, preoperative creatinine levels, estimated glomerular filtration rate, a history of hypertension, diabetes mellitus, cerebrovascular accident, smoking history, or chronic obstructive pulmonary disease to exclude the influence of patient demographics, preoperative medical status, and baseline renal function. Multivariate logistic regression analysis was used to evaluate for independent risk factors in the matched sample of 366 patients. The incidence of AKI was 28.6% and 5.9% of patients from the entire sample required renal replacement therapy. AKI was associated with a prolonged postoperative hospital stay and a higher one-month and one-year mortality both in the entire and matched sample set. Independent risk factors for AKI were a left ventricular ejection fraction <55%, preoperative hemoglobin level <10 g/dL, albumin <4.0 g/dL, diagnosis of dissection, operation time >7 hours, deep hypothermic circulatory arrest (DHCA) time >30 min, pRBC transfusion >1000 mL, and FFP transfusion >500 mL. Although the incidence of poor glucose control (blood glucose >180 mg/dL) was higher in patients with AKI in matched sample, it was not an independent risk factor.AKI was still associated with a poor clinical outcome in the matched sample. Potentially modifiable risk factors included preoperative anemia and hypoalbuminemia. Efforts to minimize operation time and DHCA time along with transfusion amount may protect patients undergoing aortic surgery against AKI.

Clinical Risk Scoring Models for Prediction of Acute Kidney Injury after Living Donor Liver Transplantation: A Retrospective Observational Study.

Acute kidney injury (AKI) is a frequent complication of liver transplantation and is associated with increased mortality. We identified the incidence and modifiable risk factors for AKI after living-donor liver transplantation (LDLT) and constructed risk scoring models for AKI prediction. We retrospectively reviewed 538 cases of LDLT. Multivariate logistic regression analysis was used to evaluate risk factors for the prediction of AKI as defined by the RIFLE criteria (RIFLE = risk, injury, failure, loss, end stage). Three risk scoring models were developed in the retrospective cohort by including all variables that were significant in univariate analysis, or variables that were significant in multivariate analysis by backward or forward stepwise variable selection. The risk models were validated by way of cross-validation. The incidence of AKI was 27.3% (147/538) and 6.3% (34/538) required postoperative renal replacement therapy. Independent risk factors for AKI by multivariate analysis of forward stepwise variable selection included: body-mass index >27.5 kg/m2 [odds ratio (OR) 2.46, 95% confidence interval (CI) 1.32-4.55], serum albumin <3.5 mg/dl (OR 1.76, 95%CI 1.05-2.94), MELD (model for end-stage liver disease) score >20 (OR 2.01, 95%CI 1.17-3.44), operation time >600 min (OR 1.81, 95%CI 1.07-3.06), warm ischemic time >40 min (OR 2.61, 95%CI 1.55-4.38), postreperfusion syndrome (OR 2.96, 95%CI 1.55-4.38), mean blood glucose during the day of surgery >150 mg/dl (OR 1.66, 95%CI 1.01-2.70), cryoprecipitate > 6 units (OR 4.96, 95%CI 2.84-8.64), blood loss/body weight >60 ml/kg (OR 4.05, 95%CI 2.28-7.21), and calcineurin inhibitor use without combined mycophenolate mofetil (OR 1.87, 95%CI 1.14-3.06). Our risk models performed better than did a previously reported score by Utsumi et al. in our study cohort. Doses of calcineurin inhibitor should be reduced by combined use of mycophenolate mofetil to decrease postoperative AKI. Prospective randomized trials are required to address whether artificial modification of hypoalbuminemia, hyperglycemia and postreperfusion syndrome would decrease postoperative AKI in LDLT.

Systemic blockage of nitric oxide synthase by L-NAME increases left ventricular systolic pressure, which is not augmented further by Intralipid®.

Intravenous lipid emulsions (LEs) are effective in the treatment of toxicity associated with various drugs such as local anesthetics and other lipid soluble agents. The goals of this study were to examine the effect of LE on left ventricular hemodynamic variables and systemic blood pressure in an in vivo rat model, and to determine the associated cellular mechanism with a particular focus on nitric oxide. Two LEs (Intralipid(®) 20% and Lipofundin(®) MCT/LCT 20%) or normal saline were administered intravenously in an in vivo rat model following induction of anesthesia by intramuscular injection of tiletamine/zolazepam and xylazine. Left ventricular systolic pressure (LVSP), blood pressure, heart rate, maximum rate of intraventricular pressure increase, and maximum rate of intraventricular pressure decrease were measured before and after intravenous administration of various doses of LEs or normal saline to an in vivo rat with or without pretreatment with the non-specific nitric oxide synthase inhibitor N(ω)-nitro-L-arginine-methyl ester (L-NAME). Administration of Intralipid(®) (3 and 10 ml/kg) increased LVSP and decreased heart rate. Pretreatment with L-NAME (10 mg/kg) increased LSVP and decreased heart rate, whereas subsequent treatment with Intralipid(®) did not significantly alter LVSP. Intralipid(®) (10 ml/kg) increased mean blood pressure and decreased heart rate. The increase in LVSP induced by Lipofundin(®) MCT/LCT was greater than that induced by Intralipid(®). Intralipid(®) (1%) did not significantly alter nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-denuded rat aorta. Taken together, systemic blockage of nitric oxide synthase by L-NAME increases LVSP, which is not augmented further by intralipid(®).

Effect of a target-controlled infusion of remifentanil in combination with desflurane during the "maintenance" phase of general anesthesia.

BACKGROUND: The goal of this study was to determine the optimal target-controlled concentration of remifentanil combined with desflurane, by using a more widely and decreasing end-tidal concentration of desflurane. METHODS: Ninety ASA I patients, who underwent general anesthesia for elective orthopedic or extremity surgeries, were registered and randomly allocated to receive either a target-controlled concentration of 1 ng/ml (group R1), 2 ng/ml (group R2) remifentanil, or desflurane only without remifentanil infusion (group D). Mean arterial pressure (MAP) and heart rate (HR) were recorded at 5-min intervals from after a 10-15 min period of surgical incision to before a 10-min period prior to the end of an operation. End-tidal concentration of desflurane was increased or decreased in proportion to the changes in MAP and HR. If the value of bispectral index (BIS) was from 60-62 for more than 2 min or systolic blood pressure would fall below 90 mmHg, the patient was excluded from the study to prevent a risk of "explicit awareness" and shock. RESULTS: The end-tidal desflurane concentration was lower in the group receiving 1 ng/ml (5.2 ± 0.5 vol%; P < 0.001) and 2 ng/ml remifenanil (4.4 ± 0.5 vol%; P < 0.001) compared to patients in group D (7.9 ± 0.5 vol%). CONCLUSIONS: We recommend the use of 2 ng/ml or less remifentanil combined with desflurane for decreasing concentrations of desflurane without significant side effects, during the "maintenance" phase, and not during the induction phase of general anesthesia.

Dexmedetomidine-induced contraction of isolated rat aorta is dependent on extracellular calcium concentration.

BACKGROUND: Dexmedetomidine is a highly selective α(2)-adrenoceptor agonist that is widely used for sedation and analgesia during the perioperative period. Intravenous administration of dexmedetomidine induces transient hypertension due to vasoconstriction via the activation of the α(2)-adrenoceptor on vascular smooth muscle. The goal of this in vitro study is to investigate the calcium-dependent mechanism underlying dexmedetomidine-induced contraction of isolated endothelium-denuded rat aorta. METHODS: Isolated endothelium-denuded rat thoracic aortic rings were suspended for isometric tension recording. Cumulative dexmedetomidine concentration-response curves were generated in the presence or absence of the following inhibitors: α(2)-adrenoceptor inhibitor rauwolscine; voltage-operated calcium channel blocker verapamil (5 × 10(-7), 10(-6) and 5 × 10(-5) M); purported inositol 1,4,5-trisphosphate receptor blocker 2-aminoethoxydiphenylborate (5 × 10(-6), 10(-5) and 5 × 10(-5) M); phospholipase C inhibitor U-73122 (10(-6) and 3 × 10(-6) M); and store-operated calcium channel inhibitor gadolinium chloride hexahydrate (Gd(3+); 5 × 10(-6) M). Dexmedetomidine concentration-response curves were also generated in low calcium concentrations (1 mM) and calcium-free Krebs solution. RESULTS: Rauwolscine, verapamil, and 2-aminoethoxydiphenylborate attenuated dexmedetomidine-induced contraction in a concentration-dependent manner. Low calcium concentrations attenuated dexmedetomidine-induced contraction, and calcium-free Krebs solution nearly abolished dexmedetomidine-induced contraction. However, U-73122 and Gd(3+) had no effect on dexmedetomidine-induced contraction. CONCLUSIONS: Taken together, these results suggest that dexmedetomidine-induced contraction is primarily dependent on extracellular calcium concentrations that contribute to calcium influx via voltage-operated calcium channels of isolated rat aortic smooth muscle. Dexmedetomidine-induced contraction is mediated by α(2)-adrenoceptor stimulation. Dexmedetomidine-induced contraction appears to be partially mediated by calcium release from the sarcoplasmic reticulum.

Protein kinases participate in the contraction in response to levobupivacaine in the rat aorta.

Levobupivacaine is a long-acting amide local anesthetic that intrinsically produces vasoconstriction both in vivo and in vitro. Levobupivacaine increases intracellular calcium concentrations ([Ca(2+)](i)) in vascular smooth muscle cells. The goals of this in vitro study were to investigate whether levobupivacaine-induced contraction is associated with increased Ca(2+) sensitivity and to identify the protein kinases involved in mediating contraction in response to levobupivacaine in isolated rat aortic smooth muscle. The effect of levobupivacaine and potassium chloride (KCl) on the [Ca(2+)](i) and tension was measured simultaneously with acetoxymethyl ester of fura-2-loaded aortic strips. Cumulative levobupivacaine concentration-response curves were generated in the presence or absence of the following antagonists: GF 109203X; Y-27632; genistein; SP600125; PD 98059; and SB 203580. Levobupivacaine-induced protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and c-Jun NH(2)-terminal kinase (JNK) phosphorylation and Rho-kinase (ROCK-2) membrane translocation were detected in rat aortic vascular smooth muscle cells using Western blotting. The slope of the [Ca(2+)](i)-tension curve for levobupivacaine was higher than that for KCl. Y-27632, GF 109203X, and SP600125 attenuated levobupivacaine-induced contraction in a concentration-dependent manner. Genistein, PD 98059, and SB 203580 attenuated levobupivacaine-induced contraction. Pretreatment with GF 109203X and Y-27632 inhibited levobupivacaine-induced PKC phosphorylation and Rho-kinase (ROCK-2) membrane translocation, respectively. Pretreatment with SP600125 or PD 98059 attenuated the levobupivacaine-induced phosphorylation of JNK and ERK, respectively. These results indicate that levobupivacaine-induced contraction involving an increase in myofilament Ca(2+) sensitivity involves the primary activation of Rho-kinase-, PKC-, and JNK-mediated pathways of rat aortic smooth muscle.

Respiratory failure due to myotonic dystrophy combined with peripartum cardiomyopathy: A case report.

Myotonic dystrophy is an autosomal-dominant inherited neuromuscular disorder that's characterized by slowly progressive muscular dystrophy, muscle weakness and myotonia. The clinical features may vary from just cataracts to involvement of multiple organ systems such as various muscles, the heart, lung and intestine. Its most common complication is postoperative respiratory failure. We encountered a patient who developed sudden unexpected peripartum cardiomyopathy (PPCM) and respiratory failure due to presumed myotonic dystrophy after cesarean section. We report here on our clinical experience with this malady and we include a brief review of the medical literature on myotonic dystrophy.