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@#Thymectomy is an important treatment for thymoma and myasthenia gravis. The application of minimally invasive surgery to complete thymectomy and rapid recovery of patients after surgery is a developmental goal in thoracic surgery technology. Surgical robots have many technical advantages and are applied for many years in mediastinal tumor resections, a process that has led to its recognition. We published this consensus with the aim of examining how to ensure surgical safety based on the premise that better use of surgical robots achieving rapid recovery after surgery. We invited multiple experts in thoracic surgery to discuss the safety and technical issues of thymectomy under nonintubated anesthesia, and the consensus was made after several explorations and modifications.
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Objective:To evaluate the improved efficacy of transversus thoracic muscle plane (TTP) block combined with general anesthesia for off-pump coronary artery bypass grafting (OP-CABG).Methods:Sixty American Society of Anesthesiologists physical status Ⅲ or Ⅳ patients of both sexes, aged 55-63 yr, weighing 65-81 kg, scheduled for elective OP-CABG, were divided into 2 groups ( n=30 each) using a random number table method: TTP block combined with general anesthesia group (group TG) and general anesthesia group (group G). Midazolam-propofol-sufentanil-rocuronium was used to induce anesthesia, and sevoflurane-remifentanil-propofol was used to maintain anesthesia.In group TG, ultrasound-guided TTP block was performed at 20 min before anesthesia induction, and 0.375% ropivacaine plus 0.5% lidocaine 20 ml was injected between bilateral intercostal and transverse pectoral muscles.Both groups received patient-controlled intravenous analgesia with sufentanil, oxycodone 0.05 mg/kg was intravenously injected as rescue analgesic, and the postoperative visual analogue scale scores were maintained≤ 4 points.The intraoperative consumption of remifentanil and propofol, consumption of sufentanil within 24 h after operation, and requirement for rescue analgesia were recorded.The postoperative length of stay in intensive care unit, time to first flatus, length of hospitalization, postoperative nausea/vomiting, lung inflammation, pruritus and nerve block-related complications were recorded. Results:Compared with group G, the consumption of intraoperative remifentanil and postoperative sufentanil after operation were significantly reduced, the requirement for postoperative rescue analgesia was decreased, the postanesthesia care unit stay time, length of hospitalization and time to first flatus were shortened, and the incidence of postoperative nausea/vomiting and lung inflammation was decreased in group TG ( P<0.05). No pruritus and nerve block-related complications were found in the two groups. Conclusion:Ultrasound-guided TTP block combined with general anesthesia can provide good perioperative analgesia for the patients undergoing OP-CABG and reduce the amount of opioids used, which is helpful in improving the prognosis.
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Objective:To evaluate the role of monocyte-derived macrophages (Mo-Mφ) in postoperative cognitive dysfunction (POCD) induced by cardiopulmonary bypass (CPB) in rats.Methods:Forty SPF healthy adult Sprague-Dawley rats, weighing 350-400 g, aged 11-12 weeks, were divided into 4 groups ( n = 10 each) using a random number table method: sham operation group (S group), CPB group (C group), CPB plus PBS liposome group (P group), and CPB plus clodronate liposome group (L group). In C, P, and L groups, CPB was performed for 60 min, the equal volume of normal saline, PBS liposomes 4 μl/g and clodronate liposomes 4 μl were injected via the tail vein at 48 and 24 h before CPB, respectively.Blood was collected from the saphenous vein before CPB for determination of the clearance rate of Mo-Mφ by flow cytometry.Cognitive function was assessed using the Morris water maze test at 7 days after CPB.Blood was collected from the abdominal aortic vein, and the levels of serum inflammatory factors (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-α], and interleukin-1beta [IL-1β]) and brain injury markers (S100β protein and neuron-specific enolase [NSE]) were measured by enzyme-linked immunosorbent assay. Results:Compared with group S, the serum IL-1β, IL-6 and TNF-α concentrations were significantly increased, the serum S100β protein and NSE concentrations were increased, the escape latency was prolonged, and the number of crossing the platform was decreased in C, P, and L groups ( P<0.05). Compared with group C, the clearance rate of blood-derived monocytes was significantly decreased, the serum S100β concentrations were increased, the escape latency was prolonged, and the number of crossing the platform was decreased ( P<0.05), and no significant change was found the parameters mentioned above in group P ( P>0.05). Conclusion:Mo-Mφ infiltration is the endogenous protective mechanism of CPB-induced POCD in the rats.
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Objective To evaluate the development of cerebral anoxia during controlled hypoten-sion with nicardipine or urapidil after carotid endarterectomy in patients. Methods Forty-four patients of either sex, aged 48-64 yr, scheduled for elective carotid endarterectomy under general anesthesia, requi-ring controlled hypotension after operation, were divided into nicardipine group ( group N ) and urapidil group ( group U) using a random number table method, with 22 patients in each group. Nicardipine at 2. 5μg·kg-1 ·min-1 was intravenously infused in group N, and urapidil 2μg·kg-1 ·min-1 was intravenously infused in group U. After systolic blood pressure was decreased to 130-140 mmHg, the consumption of nicardipine was adjusted to 0. 2 - 0. 5 μg·kg-1 ·min-1 and the consumption of urapidil to 1-2μg·kg-1 ·min-1 in group N and group U, respectively, to maintain systolic pressure at 130-140 mmHg. Heart rate ( HR) , cardiac index ( CI) , bispectral index ( BIS) value, regional cerebral oxygen saturation (rSO2) and end-tidal pressure of carbon dioxide (PETCO2) were recorded after entering the operating room ( baseline) , at the beginning of controlled hypotension ( T1 ) , and at 5, 10, 20, 30, 60 and 120 min af-ter systolic blood pressure was decreased to the target hypotension ( T2-7 ) . Development of cerebral anoxia( the relative decrease in rSO2>12％ of the baseline value) was recorded in controlled hypotension period. Results Compared with the value at T1 , the HR at T2,3 and CI at T3-7 were significantly increased ( P<0. 05), and no significant change was found in rSO2, PETCO2 or BIS value at the other time points in group N (P>0. 05), and rSO2 was significantly decreased at T3-7 (P<0. 05), and no significant change was found in HR, CI, PETCO2 or BIS value at the other time points in group U (P>0. 05). Compared with group N, the HR at T2,3, CI at T3-7 and rSO2 at T3-7 were significantly decreased in group U (P<0. 05). The incidence of cerebral anoxia was significantly higher in group U than in group N ( P<0. 05) . Conclu-sion Controlled hypotension with nicardipine is recommended after carotid endarterectomy in order to avoid the development of cerebral anoxia in the patients.
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Objective To evaluate the effect of environmental hypothermia exposure on hemodynamics and oxygen metabolism during general anesthesia in a pig model of hemorrhagic shock.Methods Twelve pathogen-free Bama miniature pigs of both sexes,weighing 20-24 kg,were divided into 2 groups (n=6 each) using a random number table:room temperature group (group RT) and environmental hypothermia group (group EH).The animals inhaled 2％ isoflurane for maintenance of anesthesia.The pigs were placed at room temperature (20-22℃) and at low temperature (-10 ℃) in group RT and group EH,respectively.Hemorrhagic shock was induced by withdrawing blood from the right femoral artery within 20 min (30 ml/kg).Before withdrawing blood (T1),immediately after the end of withdrawing blood (T2),and at 1,2,3,4 and 5 h of shock (T3-7),heart rate,mean arterial pressure,mean pulmonary artery pressure,cardiac index and systemic vascular resistance index were recorded.Blood samples were collected from the right femoral artery and internal jugular vein for blood gas analysis,and lactic acid concentrations,hemoglobin,arterial oxygen partial pressure,arterial oxygen saturation,and mixed venous oxygen saturation were recorded.Oxygen delivery index,oxygen consumption index and O2 extraction rate were calculated.Results Compared with group RT,heart rate at T3-7,cardiac index and oxygen delivery index at T5-7,oxygen consumption index at T1-7,O2 extraction rate at T2-6,and lactic acid concentrations at T5-7 were significantly decreased,and mean arterial pressure at T4,5,mean pulmonary artery pressure at T4-7,systemic vascular resistance index at T3-7,and mixed venous oxygen saturation at T2-6 were increased in group EH (P＜0.05).Conclusion Environmental hypothermia exposure inhibits cardiac compensatory responses,increases the peripheral vascular resistance,and aggravates oxygen dysmetabolism during general anesthesia in a pig model of hemorrhagic shock.
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Objective To evaluate the effect of sevoflurane on the expression of aquaporin 8 (AQP8) in the intestinal mucosa in a pig model of hemorrhagic shock.Methods Twenty-four Bama miniature pigs of both sexes, weighing 22-25 kg, were randomly divided into 3 equal groups using a random number table: sham operation group (group S), hemorrhagic shock group (group HS) and sevoflurane group (group PS).The femoral artery and jugular vein were cannulated for blood pressure monitoring, blood-letting, and blood sampling in anesthetized pigs.Hemorrhagic shock was induced by withdrawing blood from the right femoral artery.Hemorrhagic shock was induced after cannulation in group HS.In group PS, 2％ sevoflurane was inhaled for 30 min after the model of hemorrhagic shock was successfully established.Before anesthesia, and at 0.5, 1, 1.5, 2, 3 and 4 h after hemorrhagic shock, blood samples were collected from the jugular vein for determination of serum D-lactic acid and intestinal fatty acid-binding protein (I-FABP) concentrations.The animals were sacrificed at 4 h after hemorrhagic shock, and the intestinal specimens were obtained for microscopic examination and for determination of AQP8 expression in the intestinal mucosa (by enzyme-linked immunosorbent assay).The intestinal water content was calculated.Results Compared with group S, the serum D-lactic acid and I-FABP concentrations, AQP8 expression, and intestinal water content were significantly increased in HS and PS groups (P＜0.05).Compared with group HS, the serum D-lactic acid and I-FABP concentrations, AQP8 expression, and intestinal water content were significantly decreased in group PS (P＜0.05).The pathological changes of intestinal tissues were significantly reduced in group PS as compared with group HS.Conclusion Sevoflurane can decrease the intestinal mucosal edema through inhibiting AQP8 expression, thus reducing hemorrhagic shockinduced damage to the intestinal mucosa in pigs.
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Objective To evaluate the effect of sevoflurane on myocardial injury induced by hemorrhagic shock and resuscitation (HS/R) in pigs.Methods Twenty-four Bama miniature pigs (12 males, 12 females) , weighing 20-25 kg, aged 3-5 months, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S) , HS/R group and sevoflurane group (group Sev).The left and right femoral arteries and right femoral vein were cannulated for blood pressure monitoring, blood-letting, blood sampling and fluid infusion.HS/R was induced by blood-letting maintaining for 1 h, followed by resuscitation with autologous blood reinfusion and infusion of lactated Ringer's solution 2 times the volume of the blood withdrawn.The pigs in group Sev were exposed to 2％ sevoflurane for 30 min before resuscitation.After cannulation, at 30 min after hemorrhagic shock, before resuscitation, and at 30 min, and 1.5, 2.5 and 3.5 h after resuscitation, blood samples were collected from the femoral artery for determination of creatine kinase-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration in serum using an automatic biochemical analyzer.Myocardial specimens were obtained at 3.5 h after resuscitation for detection of tumor necrosis factor-alpha (TNF-ot) and interleukin-6 (IL-6) contents (by ELISA) , and phosphor-signal transducer and activator of transcription 1 (p-STAT1) expression (by Western blot), and for examination of the pathological changes (with light microscope).Results Compared with S group , the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly increased, and the expression of p-STAT1 was up-regulated in HS/R and Sev groups (P＜0.05).Compared with HS/R group, the CK-MB activity and cTnI concentration in serum and contents of TNF-α and IL-6 were significantly decreased, and the expression of p-STAT1 was downregulated (P＜0.05) , and the pathological changes of myocardia were alleviated in Sev group.Conclusion Sevoflurane can alleviate HS/R-induced damage to myocardia of pigs, and inhibited STAT1 activity and attenuated inflammatory responses in the myocardium are involved in the mechanism.
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Objective To evaluate the effect of dexmedetomidine on lung injury induced by renal ischemia/reperfusion (l/R) in rats.Methods Healthy male Sprague-Dawley rats,aged 4-5 months,weighing 250-300 g,were randomized into 4 groups (n =10 each) using a random number table:sham operation group (group S); group I/R; dexmedetomidine pretreatment group (group D1) and dexmedetomidine postconditioning group (group D2).Renal I/R was induced by right nephrectomy and occlusion of the left kidney for 45 min followed by reperfusion in animals anesthetized with intraperitoneal chloral hydrate.In group D1,dexmedetomidine was infused intravenously starting from 30 min before ischemia until beginning of ischemia.In group D2,starting from onset of reperfusion until 30 min of reperfusion,dexmedetomidine was infused intravenously for 10 min at a rate of 1 μg· kg-1 · h-1,and then infused for 20 min at 0.5 μg· kg-1 · h 1.Blood samples were collected at 6 h of reperfusion to determine serum creatinine,blood urea nitrogen,interleukin-1β (IL-1β),IL-6 and tumor necrosis factor-α (TNF-α) concentrations,and IL-1β,IL-6 and TNF-α concentrations in broncho-alveolar lavage fluid (BALF).Lungs were removed for microscopic examination and for determination of wet/dry lung weight ratio.Results Compared with group S,wet/dry lung weight ratio,serum creatinine and blood urea nitrogen concentrations,and IL-1β,TNF-α and IL-6 concentrations in serum and BALF were significantly increased in the other three groups (P ＜ 0.05).The parameters mentioned above were significantly lower in D1 and D2 groups than in I/R group (P ＜ 0.05).Microscopic examination showed that the pathological changes were significantly attenuated in D1 and D2 groups as compared with I/R group.Conclusion Both dexmedetomidine pretreatment and postconditioning can attenuate lung injury induced by renal I/R and inhibition of inflammatory responses is involved in the mechanism.
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Objective To investigate the effect of different concentrations of propofol on tracheal smooth muscle (TSM) isolated from guinea pigs with induced asthma and the underlying mechanism. Methods Forty-eight guinea pigs of either sex weighing 150-200 g were randomly divided into 2 groups : normal group ( n = 20) and asthma group ( n = 28). Asthma was induced with ovoglobulin. The animals were sacrificed by a blow to the head without anesthesia. Trachea was immediately removed and cut into tracheal rings (3-5 mm in length) . 5-7 tracheal rings were prepared from each animal and suspended in organ bath filled with oxygenated (95% O2 , 5% CO2 ) KHB and stretched to an optimal resting tension which was measured by using a force-displacement transducer with a pen recorder. The two groups were further divided into six subgroups : control subgroup, 10 % intralipid subgroup and 4 propofol subgroups (10, 30, 100, 300?mol?L-1). The effect of different concentrations of propofol and their interaction with acetylcholine ( Ach ) and ryanodine on contraction of TSM were measured. Results (1) Effect of propofol on resting tension of TSM : in normal group propofol had no effect on TSM resting tension, while in asthma group propofol reduced TSM resting tension in a dose-dependent manner. 10% intralipid contracted TSM slightly and insignificantly as compared with control subgroup. (2) Effect of propofol on TSM contraction induced by Ach : propofol inhibited TSM contraction induced by Ach in a dose-dependent manner in both normal and asthma group. (3) Effect of propofol preconditioning on TSM contraction induced by Ach : pretreatment with propofol 100 and 300?mol?L-1 significantly inhibited TSM contraction induced by Ach in both normal and asthma group as compared with control subgroup. Pretreatment with even propofol 30?mol?L-1 was effective in asthma group. (4) There was no significant difference in propofol-inhibition of TSM contraction induced by Ach with or without ryanodine. Conclusion Pretreatment with clinical doses of propofol can significantly inhibit TSM contraction induced by Ach in guinea pigs with asthma and ryanodine receptor-mediated smooth muscle intracellular Ca2+ release is not involved.