Vasopressin ameliorates hypotension induced by beach chair positioning in a dose-dependent manner in patients undergoing arthroscopic shoulder surgery under general anesthesia.

BACKGROUND: The beach chair position (BCP) is associated with hypotension that may lead to cerebral ischemia. Arginine vasopressin (AVP), a potent vasoconstrictor, has been shown to prevent hypotension in BCP. It also improves cerebral oxygenation in different animal models. The present study examined the effect of escalating doses of AVP on systemic hemodynamics and cerebral oxygenation during surgery in BCP under general anesthesia. METHODS: Sixty patients undergoing arthroscopic shoulder surgery in BCP under general anesthesia were randomly allocated to receive either saline (control, n = 15) or three different doses of AVP (0.025, 0.05, or 0.075 U/kg; n = 15 each) 2 minutes before BCP. Mean arterial pressure (MAP), heart rate (HR), regional cerebral oxygen saturation (SctO2), and jugular venous oxygen saturation (SjvO2) were measured after induction of anesthesia and before (presitting in supine position) and after BCP. RESULTS: AVP per se given before BCP increased MAP, and decreased SjvO2, SctO2, and HR in all patients (P < 0.05 for all). BCP decreased MAP, the magnitude of which and hence the incidence of hypotension was decreased by AVP in a dose-dependent manner. While in BCP, every dose of AVP reduced the HR and SctO2. Accordingly, it increased the incidence of cerebral desaturation (> 20% SctO2 decrease from the baseline value) with no differences in SjvO2 and the incidence of SjvO2 < 50% or SjvO2 < 40% among the groups. CONCLUSIONS: AVP ameliorates hypotension associated with BCP in a dose-dependent manner in patients undergoing shoulder surgery under general anesthesia. However, AVP may have negative effects on SctO2 before and after BCP and on SjvO2 before BCP.

Propofol attenuates pulmonary injury induced by collapse and reventilation of lung in rabbits.

Propofol is an anesthetic drug with antioxidant and anti-inflammatory properties. We previously found that propofol attenuated lipopolysaccharide-induced acute lung injury in rabbits. This study was performed to evaluate the effects of propofol on lung injury caused by collapse and reventilation in rabbits. The wet/dry weight ratio of the lung, lung injury scores, percentage of polymorphonuclear leukocytes, albumin concentration, malondialdehyde, and interleukin-8 levels in bronchoalveolar lavage fluid were significantly increased in both lungs of the reventilation group. The degree of increase in these parameters was more significant in the right (reventilated) than in the left (non-reventilated) lung. Propofol attenuated these changes. These findings suggest that reventilation of a collapsed lung can cause injury in the contralateral non-reventilated lung as well as the reventilated lung. Propofol may provide a beneficial effect on lung injury induced by collapse and reventilation of the lung.

Cardiovascular and arousal responses to single-lumen endotracheal and double-lumen endobronchial intubation in the normotensive and hypertensive elderly.

BACKGROUND: Endotracheal intubation usually causes transient hypertension and tachycardia. The cardiovascular and arousal responses to endotracheal and endobronchial intubation were determined during rapid-sequence induction of anesthesia in normotensive and hypertensive elderly patients. METHODS: Patients requiring endotracheal intubation with (HT, n = 30) or without hypertension (NT, n = 30) and those requiring endobronchial intubation with (HB, n = 30) or without hypertension (NB, n = 30) were included in the study. Anesthesia was induced with intravenous thiopental 5 mg/kg followed by succinylcholine 1.5 mg/kg. After intubation, all subjects received 2% sevoflurane in 50% nitrous oxide and oxygen. Mean arterial pressure (MAP), heart rate (HR), plasma catecholamine concentration, and Bispectral Index (BIS) values, were measured before and after intubation. RESULTS: The intubation significantly increased MAP, HR, BIS values and plasma catecholamine concentrations in all groups, the peak value of increases was comparable between endotracheal and endobronchial intubation. However, pressor response persisted longer in the HB group than in the HT group (5.1 ± 1.6 vs. 3.2 ± 0.9 min, P < 0.05). The magnitude of increases in MAP and norepinephrine from pre-intubation values was greater in the hypertensive than in the normotensive group (P < 0.05), while there were no differences in those of HR and BIS between the hypertensive and normotensive groups. CONCLUSIONS: Cardiovascular response and arousal response, as measured by BIS, were similar in endobronchial and endotracheal intubation groups regardless of the presence or absence of hypertension except for prolonged pressor response in the HB group. However, the hypertensive patients showed enhanced cardiovascular responses than the normotensive patients.

Maternal and neonatal effects of remifentanil used during induction of general anesthesia in preeclamptic patients undergoing cesarean delivery.

BACKGROUND: Endotracheal intubation elicits cardiovascular and arousal responses. The present study was aimed to determine whether remifentanil affects these responses in patients with preeclampsia. METHODS: Thirty preeclamptic women who were scheduled to undergo cesarean delivery under general anesthesia were randomly assigned to receive either remifentanil 1 microgram/kg (n = 15) or saline (n = 15) before induction of anesthesia. Systolic arterial pressure (SBP), heart rate (HR) and bispectral index (BIS) value as well as plasma catecholamine concentrations were measured. Neonatal effects were assessed using Apgar score and umbilical cord blood gas analysis. RESULTS: Induction with thiopental caused a reduction in SBP and BIS (P < 0.01) in both groups. Following the tracheal intubation SBP and HR increased in both groups, the magnitude of which was lower in the remifentanil group. BIS values also increased, of which magnitude did not differ between the groups. Norepinephrine concentrations increased significantly following the intubation in the control, while remained unaltered in the remifentanil group. The neonatal Apgar scores (5 min), and umbilical gas values were similar in the two groups except for higher incidence of Apgar score < 7 at 1 min in the remifentanil group. CONCLUSIONS: Remifentanil 1 microgram/kg effectively attenuates hemodynamic and catecholamine but not BIS responses to tracheal intubation in preeclamptic patients undergoing cesarean delivery. However, remifentanil may cause mild neonatal depression and thus should be used when adequate facilities for neonatal resuscitation are available.

Antinociceptive effects and synergistic interaction with morphine of intrathecal metabotropic glutamate receptor 2/3 antagonist in the formalin test of rats.

Spinal metabotropic glutamate receptors (mGluRs) have been known to be involved in the modulation of nociception. While the antinociceptive effects of the mGluR1/5 have been demonstrated, the role of mGluR2/3 for nociception is less clear. This study investigated the effects of an intrathecal mGluR2/3 agonist, APDC, and a mGluR2/3 antagonist, LY341495, for inflammatory and acute pain in the formalin test and thermal stimulation test. We also examined their interaction with intrathecal morphine for the antinociceptive effect. APDC had little effect on the formalin-induced nociception. In contrast, LY341495 caused a dose-dependent suppression of the phase 2 flinching response to the formalin stimulus without affecting phase 1 flinching response. Furthermore, the suppression of pain behavior by LY341495 during phase 2 was reduced significantly by pretreatment with APDC. LY341495 and morphine also showed synergistic drug interaction for antinociception during phase 2 in the formalin test.

Evaluation of interaction between intrathecal adenosine and MK801 or NBQX in a rat formalin pain model.

Adenosine and excitatory amino acids have been known to be involved in modulating nociceptive transmission at the spinal level. The authors assessed the characteristics of the interaction of the adenosine-excitatory amino acid antagonist combinations in the spinal cord of rats on the formalin-induced nociception. Intrathecal NMDA antagonist ((5R, 10S)-(+)-5-methyl-10,11-dihydro-(5)H-dibenzo[a[,]d]cyclohepten-5,10-imine hydrogen maleate, MK801, 30 microg) and AMPA antagonist (2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[F]quinoxaline-7-sulfonamide, NBQX, 3 microg) decreased the total number of flinches during both phases in the formalin test. Intrathecal adenosine (300 microg) had little effect on the phase 1 flinching response, but decreased the phase 2 response. The fixed dose analysis and the isobolographic analysis revealed that adenosine interacts additively with MK801 and NBQX in the spinal cord.

Lack of the nitric oxide-cyclic GMP-potassium channel pathway for the antinociceptive effect of intrathecal zaprinast in a rat formalin test.

Zaprinast is a phosphodiesterase inhibitor that is active in various models of pain when administered locally. In addition, the antinociception of zaprinast is involved in the nitric oxide (NO)-cGMP pathway. However, the effect of zaprinast administered spinally has not been examined. Therefore, this study examined the effect of zaprinast on the formalin-induced nociception at the spinal level. Next, the role of the NO-cGMP-potassium channel pathway on the effect of zaprinast was further clarified. Catheters were inserted into the intrathecal space of male Sprague-Dawley (SD) rats. Pain was induced by applying 50 microl of a 5% formalin solution to the hindpaw. The change in the zaprinast-induced effect was examined after an intrathecal pretreatment with a NO synthase inhibitor (l-NMMA), a guanylyl cyclase inhibitor (ODQ) or a potassium channel blocker (glibenclamide). Zaprinast produced an antinociceptive effect during phase 1 and phase 2 in the formalin test. Intrathecal l-NMMA, ODQ and glibenclamide did not reverse the antinociception of zaprinast in either phase of the formalin test. These results suggest that zaprinast is effective against both acute pain and the facilitated pain state at the spinal level. However, the NO-sensitive cGMP-potassium channel pathway is not contributable to the antinociceptive mechanism of zaprinast in the spinal cord.