Dexmedetomidine aggravates hypotension following mesenteric traction during total gastrectomy: a randomized controlled trial.

BACKGROUND: Mesenteric traction syndrome (MTS), which is characterized by arterial hypotension and tachycardia following mesenteric traction (MT), frequently occurs during abdominal surgery. Dexmedetomidine, commonly used in general anesthesia during major surgery, has a sympatholytic effect and attenuates the compensatory response to hypotension. OBJECTIVE: Assess the effect of dexmedetomidine on hypotension following mesenteric traction. DESIGN: Prospective, randomized, controlled clinical trial. SETTING: Department of Anesthesiology, Zhenjiang First People's Hospital in China. PATIENTS AND METHODS: Patients were randomly divided into three groups. Dexmedetomidine, 0.5 or 1.0 µg/kg, was intravenously administered over 15 minutes before skin incision followed by a maintenance rate of 0.5 µg/kg/h in groups D1 and D2, respectively; saline was administered in group C. MAIN OUTCOME MEASURE(S): The duration of hypotension, heart rate and plasma norepinephrine level in patients with MTS were recorded within 60 minutes following MT. SAMPLE SIZE: 75 patients. RESULTS: The duration of hypotension in the MTS patients in group D1 and D2 was significantly longer than that in groups C (D1 vs. C, P<.05; D2 vs. C, P<.01). Significantly more phenylephrine was required to treat hypotension in group D1 and D2 than was required for patients in group C (P<.05). The increase in heart rate during the first 15 minutes of MT in group D2 was significantly attenuated compared to that in group C (P<.0083). The increases in norepinephrine levels during the first 15 minutes of MT in group C were significantly higher than those in groups D1 and D2 (P<.0167). CONCLUSION: Adjunctive dexmedetomidine in general anesthesia aggravates hypotension during MTS in open total gastrectomy. LIMITATIONS: Postoperative complications were not evaluated. CONFLICT OF INTEREST: None.

Effect of dexmedetomidine on blood coagulation in patients undergoing radical gastrectomy under general anesthesia: A prospective, randomized controlled clinical trial.

BACKGROUND: Dexmedetomidine can inhibit the perioperative stress response, which plays an important role in postoperative hypercoagulability. This study aimed to investigate whether dexmedetomidine could attenuate the activation of postoperative coagulation. METHODS: Patients undergoing open radical gastrectomy under total intravenous anesthesia were randomly allocated to the control group (group Con) and the dexmedetomidine group (group Dex). Dexmedetomidine was intravenously infused at 0.5 µg/kg over 10 minutes before anesthesia induction and then infused at a rate of 0.5 µg/kg/h until peritoneal closure in group Dex, whereas saline was administered in group Con. Blood samples were collected for thrombelastograph (TEG) analysis [reaction time (R time), clot formation time (K time), and clot formation rate (α angle)] and laboratory coagulation testing before dexmedetomidine administration and at the end of surgery. RESULTS: Coagulation was activated after radical gastrectomy, as indicated by TEG analysis and the increased concentrations of plasma fibrin (fibrinogen) degradation product (FDP) and thrombin-antithrombin complex (TAT). The R and K times were significantly prolonged and α angle was significantly decreased in group Dex compared with that in group Con at the end of surgery (P < .05). The concentrations of plasma TAT and FDP in group Dex were significantly lower than those in group Con at the end of surgery (P < .05 or .01). CONCLUSION: Adjunctive dexmedetomidine with general anesthesia attenuates the activation of coagulation following radical gastrectomy.

Connexin 43 Mediates CXCL12 Production from Spinal Dorsal Horn to Maintain Bone Cancer Pain in Rats.

Tumor metastasis to bone can subsequently lead to bone cancer pain (BCP). Currently, BCP is difficult to conquer due to a poor understanding of the potential mechanisms. Several studies have indicated that astrocyte-specific connexin 43 (Cx43) was involved in the neuropathic pain, and Cx43 induced the release of chemokine CXCL12 in bone marrow stromal cells. However, whether spinal Cx43 mediates the production of CXCL12 to participate in the maintenance of BCP is still unknown. Here we showed that Walker 256 tumor cells inoculation into the tibia induced a significant mechanical allodynia, which was accompanied by upregulation of spinal p-Cx43 and CXCL12 expression levels from day 6 to day 18 after inoculation. Spinal Cx43 was mainly expressed in astrocytes, and intrathecal (43)Gap26 (a selective Cx43 blocker) markedly attenuated mechanical allodynia as well as reduced p-Cx43 and CXCL12 expression at day 18 after inoculation. Pre-intrathecal administration of CXCL12 almost abolished the attenuated mechanical allodynia by (43)Gap26. Furthermore, intrathecal injection of anti-CXCL12 neutralizing antibody could ameliorate mechanical allodynia with concomitant inhibition of upregulation of CXCL12 expression, but not influence on p-Cx43 expression. Our results indicate that Cx43 mediates CXCL12 production from spinal dorsal horn in astrocytes to maintain bone cancer pain in rats. These findings may improve our understanding of the underlying mechanisms of BCP and provide a novel target for the treatment of BCP.