Under general anesthesia arginine vasopressin prevents hypotension but impairs cerebral oxygenation during arthroscopic shoulder surgery in the beach chair position.

BACKGROUND: Patients undergoing surgery in the beach chair position (BCP) are at a risk of cerebral ischemia. We evaluated the effect of arginine vasopressin (AVP) on hemodynamics and cerebral oxygenation during surgery in the BCP. METHODS: Thirty patients undergoing shoulder surgery in BCP under propofol-remifentanil anesthesia were randomly allocated either to receive IV AVP 0.07 U/kg (AVP group, N = 15) or an equal volume of saline (control group, N = 15) 2 minutes before taking BCP. Mean arterial blood pressure (MAP), heart rate (HR), jugular venous bulb oxygen saturation (SjvO2), and regional cerebral tissue oxygen saturation (SctO2) were measured after induction of anesthesia and before (presitting in supine position) and after patients took BCP. RESULTS: AVP itself given before the positioning increased MAP and decreased SjvO2 and SctO2 (P < 0.0001), with HR unaffected. Although MAP was decreased by BCP in both groups, it was higher in the AVP group (P < 0.0001). While in BCP, HR remained unaltered in the control and decreased in the AVP group. SjvO2 in BCP did not differ between the groups. SctO2 was decreased by BCP in both groups, which was more pronounced in the AVP group until the end of study. The incidence of hypotension (13% vs 67%; P = 0.003) was less frequent, and that of cerebral desaturation (>20% SctO2 decrease from presitting value) (80% vs 13%; P = 0.0003) was higher in the AVP group. The incidence of jugular desaturation (SjvO2 <50%) was comparable between the groups. CONCLUSIONS: A prophylactic bolus administration of AVP prevents hypotension associated with BCP in patients undergoing shoulder surgery under general anesthesia. However, it was associated with regional cerebral but not jugular venous oxygen desaturation on upright positioning.

Remifentanil decreases sevoflurane requirements to block autonomic hyperreflexia during transurethral litholapaxy in patients with high complete spinal cord injury.

BACKGROUND: An inhaled anesthetic concentration required to block autonomic hyperreflexia (AHR) is high enough to cause severe hypotension in patients with high spinal cord injury (SCI). We determined the effects of remifentanil on the sevoflurane requirement to block AHR in SCI. METHODS: The study involved 96 patients with chronic, complete SCI scheduled to undergo transurethral litholapaxy during general anesthesia. Anesthesia was induced with thiopental, and sevoflurane concentrations in 50% nitrous oxide were adjusted to maintain a bispectral index of 40 to 50. Whether the patient develops an AHR [an increase of systolic blood pressure (SBP) >20 to 40 mm Hg] was first examined by distending the bladder with glycine solution (the first trial). Patients who developed AHR were then allocated to receive no remifentanil infusion (control, n = 31), a target-controlled plasma concentration of 1 ng/mL (n = 25), or 3 ng/mL remifentanil (n = 24). After baseline hemodynamics had recovered, the target sevoflurane and remifentanil concentrations were maintained for at least 20 minutes and the procedure was resumed (the second trial). Each target sevoflurane concentration was determined by the up-and-down method based on changes (15% increase or more) of SBP in response to the bladder distension. SBP, heart rate, and bispectral index were measured before and during the bladder distension during the trials, and plasma concentrations of catecholamines during the first trial. RESULTS: Eighty-two (85.4%) of 96 patients developed AHR during the first trial, in which 2 were excluded because of hypotension (mean arterial blood pressure <50 mm Hg) developed during target-controlled drug administration. During the second trial, the end-tidal concentrations of sevoflurane to prevent AHR were reduced to 2.6% (95% confidence interval 2.5% to 2.8%, P < 0.01) and 2.2% (2.1% to 2.4%, P < 0.0001) in the groups receiving 1 and 3 ng/mL remifentanil, respectively, in comparison with 3.1% (2.9% to 3.3%) in the control. When considering minimum anesthetic concentration (MAC) values and the contribution of 50% nitrous oxide (0.48 MAC), the combined MAC values, expressed as multiples of MAC, were 2.27, 1.98, and 1.75 in the control, 1 ng/mL remifentanil, and 3 ng/mL remifentanil groups, respectively. CONCLUSIONS: Target-controlled concentrations of 1 and 3 ng/mL remifentanil would reduce the requirement of sevoflurane combined with 50% nitrous oxide to block AHR by 16% and 29%, respectively, in SCI patients undergoing transurethral litholapaxy.

Urinary trypsin inhibitors afford cardioprotective effects through activation of PI3K-Akt and ERK signal transduction and inhibition of p38 MAPK and JNK.

BACKGROUND: We determined the effect of urinary trypsin inhibitors (UTI) in regional myocardial ischemia/reperfusion (I/R) injury and its underlying mechanisms involving the role of prosurvival kinases such as phosphatidylinositol-3-OH kinases (PI3K)-Akt and extracellular signal-regulated kinases (ERK 1/2) and apoptotic kinases such as p38 and JNK. METHODS: The rats were anesthetized and subjected to an I/R insult consisting of 30-min left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size was measured after 120 min of reperfusion. UTI was given alone or along with wortmannin (inhibitor of PI3K) or PD098059 (inhibitor of ERK1/2) before LAD occlusion. The phosphorylation of Akt, ERK1/2, p38 and JNK was determined by immunoblotting after 5 min of reperfusion. UTI was administered 10 min before LAD occlusion, and wortmannin and PD098059 were administered 20 min before LAD occlusion. RESULTS: UTI significantly reduced the infarct size compared with the control. Wortmannin or PD098059 alone did not affect the infarct size, but they abolished the UTI-induced cardioprotective effect. UTI significantly reduced the phosphorylation of p38 and JNK, while it enhanced that of Akt and ERK1/2. CONCLUSIONS: UTI has a protective effect against regional myocardial I/R injury through activation of survival kinases PI3K-Akt and ERK1/2 and attenuation of p38 and JNK.

Anaesthetic requirements and stress hormone responses in acute cord-injured patients undergoing surgery of the injured spine.

BACKGROUND AND OBJECTIVE: Neuraxial anaesthesia has been shown to produce a sedative and anaesthetic-sparing effect. The purpose of the present study was to determine the effects of acute spinal cord injury on sevoflurane requirement and stress hormone responses during spinal surgery at the level of the injury. METHODS: Thirty-five patients with traumatic complete spinal cord injury undergoing spinal surgery at the level of the injury were studied. They were grouped into quadriplegics (above C7, n = 20) and paraplegics (below T1, n = 15) according to the level of injury. Patients (n = 35) with spine trauma without neurological impairment undergoing spinal surgery at the respective level served as controls. The bispectral index score was maintained at 40-50 throughout the surgery. Measurements included end-tidal sevoflurane concentrations, mean arterial pressure, heart rate, and plasma concentrations of catecholamines and arginine vasopressin. RESULTS: During the surgery, the mean arterial pressure was significantly lower in both quadriplegics and paraplegics (P < 0.05). The heart rate did not differ significantly in the quadriplegics, but was higher in the paraplegics, compared with their controls. However, end-tidal sevoflurane concentrations and bispectral index score were comparable with controls in both quadriplegics and paraplegics. Throughout the study, the plasma arginine vasopressin concentrations were not altered, although norepinephrine and epinephrine concentrations were lower in the quadriplegics. There were no significant differences in stress hormones between the groups having thoraco-lumbar surgery. CONCLUSION: Spinal cord injury neither alters the anaesthetic requirement regardless of the level of injury during spinal surgery at the level of the injury, nor enhances arginine vasopressin release. However, it blunts catecholamine responses in quadriplegics.

Bispectral index values during sevoflurane-nitrous oxide general anesthesia in women undergoing cesarean delivery: a comparison between women with and without prior labor.

BACKGROUND: An end-tidal concentration of 1% sevoflurane (1% ET(SEVO)) in 50% nitrous oxide (N(2)O) during elective cesarean delivery has been associated with bispectral index (BIS) values >60, which are associated with an increased risk of awareness. We hypothesized that BIS values during sevoflurane-N(2)O general anesthesia for cesarean delivery would be lower in women with prior labor compared with women without prior labor. METHODS: Forty patients undergoing cesarean delivery were enrolled in this observational study. One group had urgent surgery after labor (labor group, n = 20) and the other had elective surgery without labor (control group, n = 20). General anesthesia was induced with thiopental 4 mg/kg, followed by succinylcholine 1.5 mg/kg, and maintained with 1% ET(SEVO) and 50% N(2)O in oxygen. BIS values, systolic arterial blood pressure, heart rate, plasma stress hormone concentrations, Apgar scores, and postoperative analgesia variables were assessed and compared between groups. RESULTS: BIS values during the period between intubation and delivery were lower in the labor group than in the control group (P < 0.001). Plasma norepinephrine concentrations increased at delivery compared with baseline in both groups. They were higher in the labor group than in the control group both at baseline and at delivery. Systolic arterial blood pressure, heart rate, Apgar scores, surgical characteristics, and plasma concentrations of vasopressin and cortisol were not different between groups. Postoperative visual analog scale pain scores were similar between groups, while the labor group consumed less analgesics (P < 0.01) during the first 24 h after the operation. CONCLUSIONS: Prior labor was associated with lower intraoperative BIS values during sevoflurane/N(2)O general anesthesia and reduced postoperative analgesic consumption in women undergoing cesarean delivery compared with women without prior labor.

Sevoflurane concentrations required to block autonomic hyperreflexia during transurethral litholapaxy in patients with complete spinal cord injury.

BACKGROUND: Autonomic hyperreflexia (AHR) is a potentially life-threatening hypertensive condition that occurs in patients with high spinal cord injury (SCI). The current study was aimed to determine sevoflurane concentrations that block AHR in SCI patients. METHODS: The study involved 28 patients with chronic, complete SCI scheduled to undergo transurethral litholapaxy during general anesthesia. Nine patients without SCI served as controls post hoc. Anesthesia was induced with thiopental, and sevoflurane concentrations in 50% nitrous oxide were adjusted to maintain a Bispectral Index of 40-50. When a patient developed AHR during bladder distension, the target sevoflurane concentration was maintained for at least 10 min, and then the procedure was resumed. Systolic blood pressure, heart rate, and Bispectral Index as well as plasma concentrations of catecholamines and arginine vasopressin were measured before and during the bladder distension. Each target concentration was determined by the up-and-down method based on changes (15% increase or more) of systolic blood pressure in response to bladder distension. RESULTS: In SCI, systolic pressure increased by 67 +/- 33 mmHg, whereas heart rate decreased by 13 +/- 8 beats/min during the first trial (P < 0.01). The hypertensive event was associated with increases of norepinephrine concentrations, but not of epinephrine or vasopressin concentrations. Systolic pressure, heart rate, and norepinephrine concentrations did not change significantly in the control patients. The end-tidal concentrations of sevoflurane to prevent AHR were EC50 of 3.12% and EC95 of 3.83%. CONCLUSION: The EC95 for sevoflurane in 50% nitrous oxide to block AHR during transurethral litholapaxy in patients with SCI was 3.83%.