Visceral fat, but not subcutaneous fat, is associated with lower core temperature during laparoscopic surgery.

BackgroundPrevious studies suggest that lower BMI is a risk factor for intraoperative core hypothermia. Adipose tissue has a high insulation effect and is one of the major explanatory factors of core hypothermia. Accordingly, determining the respective influence of visceral and subcutaneous fat on changes in core temperature during laparoscopic surgery is of considerable interest.MethodsWe performed a prospective study of 104 consecutive donors who underwent laparoscopic nephrectomy. Temperature data were collected from anesthesia records. Visceral and subcutaneous fat were calculated by computed tomography (CT) or ultrasound. For ultrasound measurements, preperitoneal fat thickness was used as an index of visceral fat. Multiple linear regression analysis was performed at 30, 60, and 120 minutes after the surgical incision to identify the predictive factors of body temperature change. The potential explanatory valuables were age, sex, BMI, visceral fat, and subcutaneous fat.ResultsBMI (β = 0.010, 95%CI: 0.001-0.019, p = 0.033) and waist-to-hip ratio (β = 0.424, 95%CI: 0.065-0.782, p = 0.021) were associated with increased core temperature at 30 minutes after the surgical incision. Ultrasound measured-preperitoneal fat was significantly associated with increased core temperature at 30 and 60 minutes after the surgical incision (β = 0.012, 95%CI: 0.003-0.021, p = 0.009 and β = 0.013, 95%CI: 0.002-0.024, p = 0.026). CT-measured visceral fat was also associated with increased core temperature at 30 minutes after the surgical incision (β = 0.005, 95%CI: 0.000-0.010, p = 0.046). Conversely, subcutaneous fat was not associated with intraoperative core temperature. Male sex and younger age were associated with lower intraoperative core temperature.ConclusionsVisceral fat protects against core temperature decrease during laparoscopic donor nephrectomy

Perioperative Management of Blood Coagulation : Monitoring of Coagulation Disorder and Fibrinolysis

手術が安全に行われるようになった現在でも周術期における重大な合併症の主な原因は出血に伴うものが多くを占めている1)．日本麻酔科学会の麻酔関連偶発症例調査によると周術期の30 日以内の死亡の原因の第1 位は「術前合併症としての出血性ショック」，第2 位が「手術が原因の大出血」であり，これらを合わせると約半数が出血に関連した死亡である2)．このように周術期は出血を如何にコントロールするかが重要であるが，一方塞栓症の危険性も高い時期でもあり，止血凝固管理は大きな課題の一つである

Ventricular tachycardia without preceding electrocardiogram change after hypertonic mannitol administration: a case report

Abstract Background Mannitol is widely used during neurosurgery, but it has a serious complication including lethal arrhythmia due to mannitol-induced hyperkalemia. Case presentation We report on a 62-year-old man scheduled for the clipping of an unruptured cerebral artery aneurysm. During surgery, approximately 20 min after the end of 200-mL 20% hypertonic mannitol administration, ventricular tachycardia (VT) occurred without preceding electrocardiogram (ECG) change, such as peaked T waves, and VT was recovered to sinus rhythm after chest compression. A potassium concentration after recovery from VT was 6.4 mEq/L, which was normalized by the administration of calcium gluconate, furosemide, and insulin with glucose. Conclusions Physicians must be aware that VT without preceding ECG change can occur after hypertonic mannitol administration

Direct Effect of Remifentanil and Glycine Contained in Ultiva® on Nociceptive Transmission in the Spinal Cord: In Vivo and Slice Patch Clamp Analyses.

BACKGROUND:Ultiva® is commonly administered intravenously for analgesia during general anaesthesia and its main constituent remifentanil is an ultra-short-acting μ-opioid receptor agonist. Ultiva® is not approved for epidural or intrathecal use in clinical practice. Previous studies have reported that Ultiva® provokes opioid-induced hyperalgesia by interacting with spinal dorsal horn neurons. Ultiva® contains glycine, an inhibitory neurotransmitter but also an N-methyl-D-aspartate receptor co-activator. The presence of glycine in the formulation of Ultiva® potentially complicates its effects. We examined how Ultiva® directly affects nociceptive transmission in the spinal cord. METHODS:We made patch-clamp recordings from substantia gelatinosa (SG) neurons in the adult rat spinal dorsal horn in vivo and in spinal cord slices. We perfused Ultiva® onto the SG neurons and analysed its effects on the membrane potentials and synaptic responses activated by noxious mechanical stimuli. RESULTS:Bath application of Ultiva® hyperpolarized membrane potentials under current-clamp conditions and produced an outward current under voltage-clamp conditions. A barrage of excitatory postsynaptic currents (EPSCs) evoked by the stimuli was suppressed by Ultiva®. Miniature EPSCs (mEPSCs) were depressed in frequency but not amplitude. Ultiva®-induced outward currents and suppression of mEPSCs were not inhibited by the μ-opioid receptor antagonist naloxone, but were inhibited by the glycine receptor antagonist strychnine. The Ultiva®-induced currents demonstrated a specific equilibrium potential similar to glycine. CONCLUSIONS:We found that intrathecal administration of Ultiva® to SG neurons hyperpolarized membrane potentials and depressed presynaptic glutamate release predominantly through the activation of glycine receptors. No Ultiva®-induced excitatory effects were observed in SG neurons. Our results suggest different analgesic mechanisms of Ultiva® between intrathecal and intravenous administrations

Antinociceptive effect of selective G protein-gated inwardly rectifying K+ channel agonist ML297 in the rat spinal cord.

The G protein-gated inwardly rectifying K+ (GIRK) channels play important signaling roles in the central and peripheral nervous systems. However, the role of GIRK channel activation in pain signaling remains unknown mainly due to the lack of potent and selective GIRK channel activators until recently. The present study was designed to determine the effects and mechanisms of ML297, a selective GIRK1/2 activator, on nociception in the spinal cord by using behavioral studies and whole-cell patch-clamp recordings from substantia gelatinosa (SG) neurons. Rats were prepared for chronic lumber catheterization and intrathecal administration of ML297. The nociceptive flexion reflex was tested using an analgesy-meter, and the influence on motor performance was assessed using an accelerating rotarod. We also investigated pre- and post-synaptic actions of ML297 in spinal cord preparations by whole-cell patch-clamp recordings. Intrathecal administration of ML297 increased the mechanical nociceptive threshold without impairing motor function. In voltage-clamp mode of patch-clamp recordings, bath application of ML297 induced outward currents in a dose-dependent manner. The ML297-induced currents demonstrated specific equilibrium potential like other families of potassium channels. At high concentration, ML297 depressed miniature excitatory postsynaptic currents (mEPSCs) but not their amplitude. The ML297-induced outward currents and suppression of mEPSCs were not inhibited by naloxone, a μ-opioid receptor antagonist. These results demonstrated that intrathecal ML297 showed the antinociceptive effect, which was mediated through direct activation of pre- and post-synaptic GIRK channels. Selective GIRK channel activation is a promising strategy for the development of new agents against chronic pain and opioid tolerance

Identification of Spinal Inhibitory Interneurons Required for Attenuating Effect of Duloxetine on Neuropathic Allodynia-like Signs in Rats

Neuropathic pain is a chronic pain condition that occurs after nerve damage; allodynia, which refers to pain caused by generally innocuous stimuli, is a hallmark symptom. Although allodynia is often resistant to analgesics, the antidepressant duloxetine has been used as an effective therapeutic option. Duloxetine increases spinal noradrenaline (NA) levels by inhibiting its transporter at NAergic terminals in the spinal dorsal horn (SDH), which has been proposed to contribute to its pain-relieving effect. However, the mechanism through which duloxetine suppresses neuropathic allodynia remains unclear. Here, we identified an SDH inhibitory interneuron subset (captured by adeno-associated viral (AAV) vectors incorporating a rat neuropeptide Y promoter; AAV-NpyP+ neurons) that is mostly depolarized by NA. Furthermore, this excitatory effect was suppressed by pharmacological blockade or genetic knockdown of α1B-adrenoceptors (ARs) in AAV-NpyP+ SDH neurons. We found that duloxetine suppressed Aβ fiber-mediated allodynia-like behavioral responses after nerve injury and that this effect was not observed in AAV-NpyP+ SDH neuron-selective α1B-AR-knockdown. These results indicate that α1B-AR and AAV-NpyP+ neurons are critical targets for spinal NA and are necessary for the therapeutic effect of duloxetine on neuropathic pain, which can support the development of novel analgesics

1-kHz high-frequency spinal cord stimulation alleviates chronic refractory pain after spinal cord injury: a case report

Abstract Background Patients with spinal cord injury (SCI) frequently complain of intractable pain that is resistant to conservative treatments. Here, we report the successful application of 1-kHz high-frequency spinal cord stimulation (SCS) in a patient with refractory neuropathic pain secondary to SCI. Case presentation A 69-year-old male diagnosed with SCI (C4 American Spinal Injury Association Impairment Scale A) presented with severe at-level bilateral upper extremity neuropathic pain. Temporary improvement in his symptoms with a nerve block implied peripheral component involvement. The patient received SCS, and though the tip of the leads could not reach the cervical vertebrae, a 1-kHz frequency stimulus relieved the intractable pain. Conclusions SCI-related symptoms may include peripheral components; SCS may have a considerable effect on intractable pain. Even when the SCS electrode lead cannot be positioned in the target area, 1-kHz high-frequency SCS may still produce positive effects