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Although rectus sheath block (RSB) is routinely used in laparoscopic surgeries to reduce mid-abdominal pain, whether RSB should be performed before or after surgery remains unclear. Herein, the optimal timing for RSB in patients undergoing laparoscopic surgery was investigated. This retrospective cohort study analyzed the data of patients who underwent RSB during laparoscopic procedures at our hospital between January 2013 and December 2018. The primary outcome was the time to rescue analgesia within 24 hours postanesthesia. The patients were divided into preoperative (pre-) and postoperative (post-) RSB groups. A multivariable Cox proportional hazards regression model was used to analyze the time to rescue analgesia in the unmatched and propensity score (PS)-matched patient populations. In total, 609/14,284 patients were included (pre-RSB group, 227 patients; post-RSB group, 382 patients). After PS matching, 97 patients were assigned to both groups. Although the time from extubation to the first analgesic request was not significantly different between the 2 groups (322 vs 294 minutes, P = .57), the patients in the pre-RSB group showed a lower risk of postoperative first analgesic administration after PS matching (adjusted hazard ratio, 0.71; 95% confidence interval, 0.53–0.95; P = .023). Among patients undergoing laparoscopic surgery, those in the pre-RSB group tended to have a longer time to the first analgesic request and had a lower risk of analgesic administration within the first 24 hours than those in the post-RSB group. Thus, performing RSB preoperatively may be preferable.

Anesthetic pre- and postconditioning pharmacologically reduces ischemia/reperfusion injury. Mitochondria play a central role in these myocardial protective salvage effects. In the preconditioning, low levels of reactive oxygen species, which are produced by anesthetics in the mitochondria, act as a trigger to prevent cardiomyocytes death and modify intracellular signaling mechanisms. In the postconditioning, decreased mitochondrial matrix pH, which was caused by anesthetics, triggers the onset of a rapid protective effect. The mitochondrial membranes have several ion channels that act as major determining factors of cellular life and death under pathophysiological conditions. In these channels, the mitochondrial adenosine triphosphate-sensitive K+ channels, the mitochondrial Ca2+-activated K+ channels and mitochondrial permeability transition pores play critical roles in cardioprotection against ischemia/reperfusion injury. Mitochondrial permeability transition pores are end effectors, which contribute to myocardial preconditioning and postconditioning. Activation of intracellular signaling and acidification of mitochondrial matrix pH prevent the mitochondrial permeability transition pore opening, and therefore, preserve the mitochondrial function to supply adenosine triphosphate, resulting in myocardial protection due to the maintenance of intracellular homeostasis.

We examined the cardioprotective profile of the new A(3) adenosine receptor (AR) agonist CP-532,903 [N(6)-(2,5-dichlorobenzyl)-3'-aminoadenosine-5'-N-methylcarboxamide] in an in vivo mouse model of infarction and an isolated heart model of global ischemia/reperfusion injury. In radioligand binding and cAMP accumulation assays using human embryonic kidney 293 cells expressing recombinant mouse ARs, CP-532,903 was found to bind with high affinity to mouse A(3)ARs (K(i) = 9.0 +/- 2.5 nM) and with high selectivity versus mouse A(1)AR (100-fold) and A(2A)ARs (1000-fold). In in vivo ischemia/reperfusion experiments, pretreating mice with 30 or 100 microg/kg CP-532,903 reduced infarct size from 59.2 +/- 2.1% of the risk region in vehicle-treated mice to 42.5 +/- 2.3 and 39.0 +/- 2.9%, respectively. Likewise, treating isolated mouse hearts with CP-532,903 (10, 30, or 100 nM) concentration dependently improved recovery of contractile function after 20 min of global ischemia and 45 min of reperfusion, including developed pressure and maximal rate of contraction/relaxation. In both models of ischemia/reperfusion injury, CP-532,903 provided no benefit in studies using mice with genetic disruption of the A(3)AR gene, A(3) knockout (KO) mice. In isolated heart studies, protection provided by CP-532,903 and ischemic preconditioning induced by three brief ischemia/reperfusion cycles were lost in Kir6.2 KO mice lacking expression of the pore-forming subunit of the sarcolemmal ATP-sensitive potassium (K(ATP)) channel. Whole-cell patch-clamp recordings provided evidence that the A(3)AR is functionally coupled to the sarcolemmal K(ATP) channel in murine cardiomyocytes. We conclude that CP-532,903 is a highly selective agonist of the mouse A(3)AR that protects against ischemia/reperfusion injury by activating sarcolemmal K(ATP) channels.

Although indwelling urinary catheters (IUCs) are used intraoperatively and may cause complications (e.g., delirium), only few robust studies have investigated the association between intraoperative IUC use and complications. We hypothesized that IUC use might increase the postoperative incidence of altered mental status and/or urinary catheter infection.