Anesthetic management of conjoined twins undergoing one-stage surgical separation: A single center experience.

OBJECTIVE: To summarize our experience in the anesthetic management of conjoined twins undergoing one-stage surgical separation. METHODOLOGY: Medical records of conjoined twins admitted to our hospital for treatment and considered for surgical separation from 1996 to present were retrospectively reviewed. Four cases of conjoined twins underwent one-stage surgical separation under general anesthesia. Preoperative evaluation was performed to determine the extent of anatomical conjunction and associated anomalies. Anesthesia was simultaneously induced in all conjoined twins. The intubation procedure was successfully performed with the head slightly rotated to each baby's side, followed by the administration of vecuronium. Anesthetic agents were administered according to the estimated weight of each baby. One case of conjoined twins underwent surgical separation with cardiopulmonary bypass due to shared hearts. Results : All conjoined twins were successfully separated. No significant respiratory or cardiac events occurred during surgery except for one twin, which died after separation because of complicated congenital heart disease. Conclusions : Accurate preoperative evaluation, respiratory and circulatory management, and close cooperation of the multidisciplinary team are important aspects of anesthetic management of conjoined twins surgery.

Isoflurane reduces the synthesis of surfactant-related protein a of alveolar type II cells injured by H2O2.

The influence of isoflurane (Iso) on the synthesis of surfactant-related protein A (SP-A) of alveolar type II (AT II) cells in primary culture and after injury by H2O2 was investigated. AT II cells were isolated and purified from adult Sprague-Dawley rats and used for experiments after 32 h in primary culture. The cell cultures were randomized to six groups (n = 8 in each group): control group (no treatment), 0.28 mM Iso group, 2.8 mM Iso group, 75 microM H2O2 group, 75 microM H2O2 + 0.28 mM Iso group, and 75 microM H2O2 + 2.8 mM Iso group. Each group was continuously incubated for 3 h after administration of Iso and/or H2O2. The intracellular SP-A and the SP-A of the culture medium were measured with an enzyme-linked immunosorbent assay (ELISA). Iso significantly decreased the intracellular SP-A content and that of the culture medium, and aggravated the decrease of SP-A content induced by H2O2. These findings suggest that Iso itself may decrease SP-A synthesis of AT II cells in vitro, and aggravate the damage to AT II cells under peroxidation conditions.

Comparative proteomics analysis of differentially expressed phosphoproteins in adult rat ventricular myocytes subjected to diazoxide preconditioning.

Mitochondrial ATP sensitive potassium channels (mitoK(ATP) channels) are involved in the cardioprotection afforded by ischemic preconditioning (IPC) and diazoxide, a selective mitoK(ATP) channel opener. The activation of some kinases, including phoshoprotein kinase (PKC)-epsilon and mitogen-activating protein kinases (MAPK), is involved in signal conduction of preconditioning downstream from mitoK(ATP) channel opening. Diazoxide can open mitoK(ATP) channels and activate PKC-epsilon, which will phosphorylate some substrate proteins. These proteins that exhibit altered post-translational modification via phosphorylation due to diazoxide pretreatment may be the target molecules and play an important role in cellular protection after mitoK(ATP) channel opening. To analyze and identify the phosphoproteins associated with diazoxide preconditioning, phosphoprotein enrichment and comparative two-dimensional gel electrophoresis (2D-GE) were used. Cultured adult rat ventricular myocytes were pretreated in the presence and absence of 100 micronol/1l diazoxide for 10 min and enriched phosphoproteins from control myocytes and those pretreated with 100 micromol/l diazoxide were separated by 2D-GE and stained with a silver staining kit. Phosphoproteins of interest were further identified by matrix-assisted laser desorption ionization tandem mass spectrometry (MALDI-TOF MS). Eight protein spots with different abundance were found, of which six differentially expressed proteins were identified by MALDI-TOF MS. They included 94 kDa glucose-regulated protein, calpactin I heavy chain, chaperonin containing TCP-1 zeta subunit, hypothetical protein XP_346548, ferritin light chain and ferritin light chain 2. These findings provide new clues to understanding the mechanism of ischemic preconditioning in cardiomyocytes downstream from mitoK(ATP) channel opening.

Effect of terbutaline on alveolar liquid clearance after oleic acid-induced lung injury in rats.

OBJECTIVE: To investigate whether terbutaline affects alveolar liquid clearance after oleic acid-induced lung injury in rats. METHODS: Forty healthy Wistar rats (weighing 250-280 g) were randomly divided into five groups (n=8 in each group): the normal control group (control group), oleic acid injury group (injury group), terbutaline-treated group (terbutaline group), terbutaline plus amiloride-treated group (terbutaline+amiloride group) and terbutaline plus ouabain-treated group (terbutaline+ouabain group). Acute lung injury model was induced by intravenous oleic acid (0.25 ml/kg body weight). 24 hours later, 1.5 microCi (125) I-labeled 5% albumin solution (5 ml/kg body weight) was dripped into the lungs through trachea. The alveolar liquid clearance rate, extravascular lung water content, and arterial blood gas were measured 1 hour thereafter. RESULTS: At 24 hours after infusion of oleic acid, the rats developed pulmonary edema and severe hypoxemia, with the alveolar liquid clearance rate decreased by 49.2% and the extravascular lung water content elevated by 47.9%. Compared with the rats in the injury group, terbutaline (10(-4) mol/L) significantly increased the alveolar liquid clearance rate, decreased the extravascular lung water content and improved hypoxemia. The effect of terbutaline was partly blocked by amiloride and ouabain, which were inhibitors of sodium transport. Terbutaline increased the alveolar liquid clearance rate by 63.7%, and amiloride and ouabain reduced the alveolar liquid clearance rate by 54.7% and 56.8%, respectively. CONCLUSIONS: Terbutaline can accelerate alveolar liquid clearance through increasing sodium transport to attenuate pulmonary edema, thus improving gas exchange, which may have therapeutical effect on pulmonary edema after acute lung injury.

Changes in liquid clearance of alveolar epithelium after oleic acid-induced acute lung injury in rats.

OBJECTIVE: Impaired active fluid transport of alveolar epithelium may involve in the pathogenesis and resolution of alveolar edema. The objective of this study was to explore the changes in alveolar epithelial liquid clearance during lung edema following acute lung injury induced by oleic acid. METHODS: Forty-eight Wistar rats were randomly divided into six groups, i.e., injured, amiloride, ouabain, amiloride plus ouabain and terbutaline groups. Twenty-four hours after the induction of acute lung injury by intravenous oleic acid (0.25 ml/kg), 5% albumin solution with 1.5 microCi (125)I-labeled albumin (5 ml/kg) was delivered into both lungs via trachea. Alveolar liquid clearance (ALC), extravascular lung water (EVLW) content and arterial blood gases were measured one hour thereafter. RESULTS: At 24 h after the infusion of oleic acid, the rats developed pulmonary edema and severe hypoxemia, with EVLW increased by 47.9% and ALC decreased by 49.2%. Addition of either 2x10(-3) M amiloride or 5x10(-4) M ouabain to the instillation further reduced ALC and increased EVLW. ALC increased by approximately 63.7% and EVLW decreased by 46.9% with improved hypoxemia in the Terbutaline (10(-4) M) group, compared those in injured rats. A significant negative correlation was found between the increment of EVLW and the reduction of ALC. CONCLUSIONS: Active fluid transport of alveolar epithelium might play a role in the pathogenesis of lung edema in acute lung injury.

[Body temperature changes during 7 d -6 degrees head-down bed rest].

Objective. To investigate body temperature changes in man during 7-day -6 degrees head-down bed rest (BR). Method. Body temperatures were measured in the morning (6:00), afternoon (16:00) and evening (20:00) during 7 d BR in 18 healthy males (18-22 years old). Result. Rectal temperature (Tre) in the morning gradually decreased as time (d) of BR increased: after the 4th day of BR (BR4d), Tre significantly reduced compared with the supine control (SC, 36.50 +/- 0.03 degrees C) before BR, and it consistently declined to 36.38 +/- 0.04 degrees C on BR7d; But Tre significantly increased in the afternoon after BR5d and in the evening after BR1d, with the final increments of 0.12 +/- 0.05 degrees C and 0.25 +/- 0.03 degrees C respectively on BR7d. Mean body temperature (Tsk) in the morning was significantly higher from BR2d than its SC, with a final net increase (delta Tsk) of 0.38 +/- 0.14 degrees C on BR7d. And Tsk significantly increased in the afternoon and evening from BR4d, BR2d respectively. Skin temperature on the forehead (Tforehead) elevated in the morning during BR. While in the afternoon and evening, Tforehead were significantly higher from BR7d and BR6d than their SC. Conclusion. Both the difference in time of recording at a BR day and the time (d) of BR have significant influence on Tre, Tsk , and Tforehead (P<0.01). These data suggest that body temperature rhythm, body fluid loss and headward distribution, hypokinesis etc. induced by BR have an impact on human thermal regulation during BR.

Amitriptyline upregulates EAAT1 and EAAT2 in neuropathic pain rats.

Excitatory amino acid transporters (EAATs) appear to participate in the pathogenesis of neuropathic pain. The present study was performed to evaluate the effects of the tricyclic antidepressant amitriptyline on the expressions of EAATs in neuropathic pain rats. Using spared nerve injured (SNI) male Sprague Dawley rats, we found that SNI induced an initial EAATs upregulation on postoperative day 1 within the ipsilateral spinal cord dorsal horn, followed by a downregulation on postoperative days 3 and 5. Intraperitoneal administration of amitriptyline reversed the downregulation of EAATs in SNI rats on postoperative days 3-5 and attenuated the mechanical allodynia. We further demonstrated that administration of amitriptyline alone induced an upregulation of EAATs in sham-operated rat but do not produce an antinociceptive effect. These results indicate that amitriptyline could increase the expression of EAATs which may be one of its mechanisms in the treatment of neuropathic pain.

Vagus nerve stimulation may be used in the therapy of myocarditis.

Although a large number of different causes have been identified as leading to myocarditis, inflammation plays a pivotal role in its pathological process. No specific methods are available in the therapy of myocarditis except symptomatic treatment. Vagus nerve stimulation has been found to lower the heart rate and recover the normal heart rhythm which may relieve the cardiac symptoms in myocarditis. Furthermore, the acetylcholine that secreted by vagus nerve stimulation was found to inhibit the production of such inflammatory cytokines as tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta). Based on the above, we hypothesized that vagus nerve stimulation can be used in the therapy of myocarditis and lead to relief of symptoms and inhibition of inflammatory process which may kill two birds with one stone.

[Effect of orexin-A on recovery from ketamine anesthesia in aged rats].

OBJECTIVE: To observe the effect of orexin-A on the recovery and cognitive function of aged rats after ketamine anesthesia. METHODS: Fifty-five aged rats were divided randomly into control group, model control group, 1 nmol/L Orexin-A group, and 4 nmol/L Orexin-A group. In the latter 3 groups, the rats received an intraperitoneal injection of ketamine at 100 mg/kg, and normal saline was injected in the control group. Ten minutes after the injections, the rats received intraventricular injections of artificial cerebrospinal fluid (control and model control group) or of 10 microl 1 or 4 nmol/L Orexin-A as indicated. The behavioral changes of the rats were assessed by the duration of loss of righting reflex (LORR). Electroencephalogram (EEG) recordings were used to evaluate the changes in rat brain activity by comparison of the percent of sigma wave in EEG before and after the intraventricular injections. Morris water maze was used to test the learning and spatial localization abilities of the rats. RESULTS: Ketamine resulted in obvious impairment of learning and memory abilities of the aged rats. Orexin-A at 4 nmol/L induced significant decrease in the duration of LORR and marked reduction of sigma activities in anesthetic rats (P<0.05), and obviously improved the learning and spatial localization abilities of the rats after anesthesia (P<0.05). CONCLUSION: Orexin-A can promote the recovery and improve the cognitive function of aged rats after ketamine anesthesia.

[Changes in the polymorphonuclear leukocyte infiltration, hemorrhage and plasma exudation in the pulmonary tissue in rats with smoke inhalation injury].

OBJECTIVE: To investigate the different velocity of polymorphonuclear neutrophil (PMN) infiltration, erythrocyte diapedesis and plasma exudation into the pulmonary tissue of the rats inflicted with smoke inhalation injury, so as to explore the different mechanisms of their existence in rat pulmonary tissue after inhalation injury. METHODS: The rat smoke inhalation injury model was employed in the study. Wistar rats were inflicted with smoke inhalation injury, and then sacrificed at 1, 3, 6, 12 and 24 post injury hours (PIH). 131I-BSA, 99mTc-PMN or 99mTc-erythrocytes (RBC) were injected into rat pulmonary tissue 1 hour before sacrifice. Isotonic saline was infused into blood vessel to wash out circulation blood. Then the pulmonary tissue samples were harvested for gamma-value counting and then weighed. The infiltration of 131I-BSA, 99mTc-PMN or 99mTc-RBC in pulmonary tissue per gram and per minute was calculated, and MPO content was measured by phosphate T-tolidine method. RESULTS: The amount of RBC diapedesis in rat lung tissue peaked at 1 PIH, decreased thereafter and approached to normal level at 24 PIH. The amount of PMN infiltration increased at 3 PIH, slightly decreased at 6 PIH but still higher than that in normal tissue, and increased again at 24 PIH. The pulmonary tissue content of MPO gradually increased from 1 PIH to 24 PIH. The pulmonary tissue content of 131I-BSA began to increase at 1 PIH and peaked at 6 PIH, and remained higher than that in normal tissue till 24 PIH. CONCLUSION: Even though there was remarkable postburn increase in the erythrocyte diapedesis, neutrophil infiltration and albumin exudation with different peak time points (1, 3 and 6 PIH, respectively), Inflammation seemed not to be the premise of erythrocyte diapedesis, while the secondary inflammatory reaction might be the main cause of pulmonary edema.