bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuroprotective Effects of Dexmedetomidine in the Gerbil Hippocampus after Transient Global Ischemia
Authors: Kuhmonen Johanna , Pokorny Jaroslav , Miettinen Riitta , Haapalinna Antti , Jolkkonen Jukka , Riekkinen Paavo Sr. , Sivenius Juhani 
Published: November 2003

Background
Cerebral ischemia induces a massive release of norepinephrine associated with neuronal death in the brain. It has been demonstrated that alpha2-adrenoceptor agonists decrease the release and turnover of noradrenaline, and this might prove advantageous in counteracting the neurodegeneration in ischemic brain. Therefore, in the present study, the authors tested whether dexmedetomidine, a selective alpha2-receptor agonist, has neuroprotective effects in a gerbil transient global ischemia model.

Methods
Ischemia was induced by bilateral carotid occlusion for 5 min in diethylether-anesthetized normothermic gerbils. Dexmedetomidine was administered subcutaneously in four different treatment paradigms (6-8 animals/group): 3 or 30 microg/kg 30 min before and thereafter at 3, 12, 24, and 48 h after the occlusion, or 3 or 30 microg/kg at 3, 12, 24, and 48 h after the occlusion. Control animals were subjected to forebrain ischemia but received only saline injections. One week after occlusion, animals were transcardially perfused for histochemistry. Neuronal death in the CA1 and CA3 regions of the hippocampus and in the hilus of the dentate gyrus was evaluated in silver-stained 60-microm coronal sections.

Results
Compared with saline-treated ischemic animals, dexmedetomidine at a dose of 3 microg/kg given before and continued after the induction of ischemia reduced the number of damaged neurons in the CA3 area (2 +/- 3 vs. 17 +/- 20 degenerated neurons/mm2; P < 0.05). Also in the dentate hilus, the number of damaged neurons was reduced by dexmedetomidine (3 microg/kg) given before and continued after ischemia (5 +/- 7 vs. 56 +/- 42 degenerated neurons/mm2; P < 0.01).

Conclusions
The present data demonstrate that dexmedetomidine effectively prevents delayed neuronal death in CA3 area and in the dentate hilus in gerbil hippocampus when the management is started before the onset of ischemia and continued for 48 h after reperfusion. Inhibition of ischemia-induced norepinephrine release may be associated with neuroprotection by dexmedetomidine.
In Vitro Negative Inotropic Effect of Plasma Collected at the Time of Reperfusion in Humans undergoing Liver Transplantation
Authors: Chemla Denis , Jayais Pascal , Ecoffey Claude , Declere Adrien Descorps , Lecarpentier Yves 
Published: November 2003

Background
During orthotopic liver transplantation (OLT), acute depression of myocardial contractility has been suspected at the time of the graft reperfusion.

Methods
The authors tested the hypothesis that plasma collected at the time of reperfusion in OLT patients exerted a negative inotropic effect on isolated rat myocardium. Plasma from 13 OLT patients was collected either before surgical incision (group 1, n = 8) or 3-5 min after vena cava and portal vein unclamping (group 2, n = 9). Six patients had their pre- and postincision plasma analyzed. A postreperfusion syndrome was observed in 3 of 13 patients. Left ventricular rat papillary muscles were studied at baseline (T0), 30 min after the addition of plasma (T30), and 60 min after the addition of plasma (T60). The authors recorded contraction parameters (maximum unloaded shortening velocity [Vmax], peak extent of systolic shortening at preload [deltaL], maximum active isometric tension [AFi], positive peak tension derivative [+dFi/dt], time-to-peak shortening [TPS], and time-to-peak force [TPF]) and relaxation parameters (maximum lengthening velocity at preload [VI], negative peak tension derivative [-dFi/dt], index of load sensitivity of relaxation [tRi]).

Results
In group 1, contraction parameters remained unchanged, with the exception of a decreased Vmax at T30 and AFi at T60 (each P < 0.05). In group 2, all contraction parameters were significantly decreased at T30 and at T60, with the exception of AFi at T60. Both types of plasma decreased V1 and altered tRi at T30 and T60, whereas only reperfusion plasma decreased -dFi/dt at T30 and T60. At T30, deltaL, -dFi/dt, and tRi were significantly more impaired in group 2 than in group 1. There was no relationship between inotropic changes and mean arterial pressure decrease at the time of reperfusion.

Conclusion
Plasma collected at the time of graft reperfusion in OLT patients exerted negative effects on contraction and relaxation performance in isolated rat left ventricular papillary muscle.
Postoperative Inflammatory Response after Autologous and Allogeneic Blood Transfusion
Authors: Avall Anders , Hyllner Monica , Bengtson Jan Peter , Carlsson Lars , Bengtsson Anders 
Published: November 2003

Background
Allogeneic blood transfusions cause immunosuppression. The aim of this study was to determine whether complement anaphylatoxins, cytokines, or both are released in the recipient, after blood transfusions in general, and after autologous blood transfusions in particular.

Methods
Thirty-one patients having total hip joint replacement surgery were randomized to receive either allogeneic red blood cells (n = 15) or predeposited autologous whole blood transfusion (n = 16). Plasma concentrations of the anaphylatoxins C3a and C5a, the terminal C5b-9 complement complex, and cytokines IL-6 and IL-8 in the recipients were repeatedly analyzed before, during, and after surgery.

Results
Significantly increased concentrations of IL-6 and IL-8 appeared in both groups, with a significantly greater increase in the autologous blood group. Patients in both groups developed a moderate but significant increase of C3a without a significant difference between them. C5a and terminal C5b-9 complement complex were not greatly changed.

Conclusions
The study showed a greater increase in cytokine concentration after autologous blood transfusion than after allogeneic blood transfusion. The lower response in the latter may result from transfusion-induced suppression of cellular immunity.
Reducing Pain after Inguinal Hernia Repair in Children
Authors: Splinter William M. , Reid Craig W. , Roberts David J. , Bass Juan 
Published: November 2003

Background
The optimal method to achieve analgesia after inguinal hernia repair in children is unknown. This study compared the analgesic efficacy, adverse events, and the costs associated with supplementation of local anesthesia (infiltration of the wound) with either intravenous ketorolac or caudal analgesia in children having inguinal hernia repair.

Methods
With parental consent and institutional review board approval, children aged 2-6 yr having elective, outpatient inguinal hernia repair were studied in this randomized, single-blinded investigation. Anesthesia was induced by inhalation with nitrous oxide and halothane or intravenously with propofol. Anesthesia was maintained with nitrous oxide and halothane. Patients were randomly assigned to receive caudal analgesia (1 ml/kg 0.20% bupivacaine with 1/200,000 epinephrine) or intravenous ketorolac (1 mg/kg) immediately after induction of anesthesia. Both groups received field blocks with 0.25% bupivacaine administered by the surgeon under direct vision during operation. Patients were assessed for 24 h. In-hospital pain was assessed using a behavior-based pain score. Parents assessed pain with a visual linear analog pain scale with anchors of 0 (no pain) and 100 (worst pain imaginable).

Results
The authors studied 164 children, with 84 patients in the ketorolac group. The groups had similar demographic data. In-hospital analgesic requirements and pain scores were almost identical in both groups. Pain at home was significantly less in the ketorolac group, with visual linear analog pain scale scores of 10 (0-80) compared with 20 (0-80) (median [range]) for ketorolac versus caudal (P = 0.002 by the Mann-Whitney U test). The ketorolac group also had a lower incidence of vomiting, ambulated more rapidly, and micturated earlier (P < 0.05).

Conclusion
The use of intravenous ketorolac to supplement local anesthesia infiltrated by the surgeon during pediatric inguinal hernia repair is superior to supplementation with caudal analgesia.
Correlation between Evoked Motor Response of the Sciatic Nerve and Sensory Blockade
Authors: Benzon Honorio T. , Kim Charles , Benzon Hazel P. , Silverstein Mark E. , Jericho Barbara , Prillaman Katherine , Buenaventura Ricardo 
Published: November 2003

Background
Incomplete sensory blockade of the foot after sciatic nerve block in the popliteal fossa may be related to the motor response that was elicited when the block was performed. We investigated the appropriate motor response when a nerve stimulator is used in sciatic nerve block at the popliteal fossa.

Methods
Six volunteers classified as American Society of Anesthesiologists' physical status I underwent 24 sciatic nerve blocks. Each volunteer had four sciatic nerve blocks. During each block, the needle was placed to evoke one of the following motor responses of the foot: eversion, inversion, plantar flexion, or dorsiflexion. Forty milliliters 1.5% lidocaine was injected after the motor response was elicited at < 1 mA intensity. Sensory blockade of the areas of the foot innervated by the posterior tibial, deep peroneal, superficial peroneal, and sural nerves was checked in a blinded manner. Motor blockade was graded on a three-point scale. The width of the sciatic nerve and the orientation of the tibial and common peroneal nerves were also examined in 10 cadavers.

Results
A significantly greater number of posterior tibial, deep peroneal, superficial peroneal, and sural nerves were blocked when inversion or dorsiflexion was seen before injection than after eversion or plantar flexion (P < 0.05). Motor blockade of the foot was significantly greater after inversion. Anatomically, the tibial and common peroneal nerves may be separate from each other throughout their course. The sciatic nerve ranged from 0.9-1.5 cm in width and was divided into the tibial and common peroneal nerves at 8 +/- 3 (range, 4-13) cm above the popliteal crease.

Conclusions
Inversion is the motor response that best predicts complete sensory blockade of the foot. Incomplete blockade of the sciatic nerve may be a result of the size of the sciatic nerve, to separate fascial coverings of the tibial and common peroneal nerves, or to blockade of either the tibial or common peroneal nerves after branching from the sciatic nerve.
The Effect of Clonidine on Cerebral Blood Flow Velocity, Carbon Dioxide Cerebral Vasoreactivity, and Response to Increased Arterial Pressure in Human Volunteers
Authors: Lee Hye-Won , Caldwell James E. , Dodson Barbara , Talke Pekka , Howley Joan 
Published: November 2003

Background
Because patients may be taking clonidine chronically or may be receiving it as a premedication before surgery, the authors investigated its effect on cerebral hemodynamics.

Methods
In nine volunteers, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO2 vasoreactivity was measured before clonidine administration (preclonidine), 90 min after clonidine, 5 microg/kg orally, then following restoration of mean arterial pressure (MAP) to the preclonidine level. In addition, Vm was measured after a phenylephrine-induced 30-mmHg increase in MAP.

Results
After clonidine administration, Vm decreased from 62 +/- 9 to 48 +/- 8 cm/s (P < 0.01), and MAP decreased from 86 +/- 10 to 63 +/- 5 mmHg (P < 0.01; mean +/- SD). Clonidine decreased the CO2 vasoreactivity slope from 2.2 +/- 0.4 to 1.2 +/- 0.5 cm x s(-1) x mmHg(-1) (P < 0.05); restoring MAP to the preclonidine level increased the slope to 1.60 +/- 0.5 cm x s(-1) x mmHg(-1), still less than the preclonidine slope (P < 0.05). CO2 vasoreactivity expressed as a percentage change in Vm, decreased after clonidine, 3.5 +/- 0.8 versus 2.4 +/- 0.8 %/mmHg (P < 0.05); this difference disappeared after restoration of MAP, 3.1 +/- 1.2 %/mmHg. With a 30-mmHg increase in MAP, Vm increased by 13% before and after clonidine (P < 0.05).

Conclusions
Clonidine, 5 microg/kg orally, decreases Vm and slightly attenuates cerebral CO2 vasoreactivity, therefore decreased cerebral blood flow and mildly attenuated CO2 vasoreactivity should be anticipated.
Doxycycline Reduces Early Neurologic Impairment after Cerebral Arterial Air Embolism in the Rabbit
Authors: Reasoner Daniel K. , Hindman Bradley J. , Dexter Franklin , Subieta Alberto , Cutkomp Johann , Smith Tom 
Published: November 2003

Background
Previous studies indicate leukocytes play a role in the pathogenesis of cerebral arterial air embolism. Because doxycycline inhibits numerous leukocyte activities, the authors hypothesized doxycycline would decrease neurologic impairment after cerebral arterial air embolism.

Methods
New Zealand White rabbits anesthetized with methohexital received either intravenous saline (n = 7) or 10 mg/kg doxycycline (n = 7) 1 h before administration of 100 microl/kg of air into the internal carotid artery. Somatosensory-evoked potentials (SSEPs) were recorded at 30-min intervals for the next 2 h. After the final recording, the anesthetic was discontinued, and animals recovered. Animals were neurologically evaluated 4 h after air embolism on a scale of 0 (normal) to 99 (coma) points.

Results
At 4 h, doxycycline animals had lesser neurologic impairment (46 +/- 23; median, 41) than animals that received saline (77 +/- 20; median, 81); P = 0.007. SSEP amplitude was greater in the doxycycline group at 60, 90, and 120 min after air embolism; P = 0.001, 0.006, 0.026, respectively. SSEP amplitudes at 30, 60, 90, and 120 min inversely correlated with 4 h neurologic impairment; tau = -0.43, -0.75, -0.85, -0.79, respectively.

Conclusions
Doxycycline decreased electrophysiologic and neurologic abnormalities after cerebral air embolism. Because groups could be distinguished electrophysiologically as soon as 1 h after air embolism and because SSEP amplitude inversely correlated with neurologic impairment, doxycycline appears to inhibit a key early (approximately 1 h) process in the pathophysiology of cerebral air embolism.
Leukocyte-Endothelium Interaction in the Rat Mesenteric Microcirculation during Halothane or Sevoflurane Anesthesia
Authors: Morisaki Hiroshi , Suematsu Makoto , Wakabayashi Yoshiyuki , Moro-oka Shigeaki , Fukushima Kazuaki , Ishimura Yuzuru , Takeda Junzo 
Published: November 2003

Background
The effects of inhalational anesthetics on the microcirculation, including leukocyte dynamics, remain to be clarified. The authors investigated halothane and sevoflurane anesthesia to determine if these agents evoked leukocyte adhesion through endothelial cell-dependent mechanisms involving such adhesion molecules.

Methods
Rats were anesthetized with halothane or sevoflurane in 100% oxygen and the lungs were mechanically ventilated. Leukocyte behavior in mesenteric venules was recorded through intravital video microscopy under monitoring microvascular hemodynamics. To examine the mechanisms for leukocyte rolling and adhesion, these studies were repeated after animals were pretreated with a monoclonal antibody against P-selectin (MAb PB1.3) or against intracellular adhesion molecule-1 (ICAM-1; MAb 1A29): P-selectin required for rolling of circulating leukocytes and ICAM-1 for firm adhesive interactions with leukocyte integrins.

Results
Under baseline anesthetic conditions (1 minimum alveolar concentration [MAC]), venular wall shear rates, an index of the disperse force on marginating leukocytes, in the sevoflurane-treated rats were about two times higher than those with halothane. At 2 MAC, halothane caused a marked arteriolar constriction and decreasing shear rates concurrent with an increasing density of venular leukocyte adhesion. Sevoflurane at 2 MAC induced leukocyte rolling and adhesion, which were attenuated by PB1.3 and 1A29, without alterations in the wall shear rates. Halothane-induced leukocyte adhesion was not prevented by PB1.3 but it was by 1A29.

Conclusions
Halothane or sevoflurane anesthesia induces venular leukocyte rolling and adhesion: P-selectin upregulation plays a crucial role in leukocyte rolling and adhesion during sevoflurane anesthesia, whereas low-flow perfusion is likely to evoke ICAM-1-dependent leukocyte adhesion during halothane anesthesia.
Effects of Desflurane in Rat Myocardium
Authors: Gueugniaud Pierre-Yves , Hanouz Jean-Luc , Vivien Benoit , Lecarpentier Yves , Coriat Pierre , Riou Bruno 
Published: November 2003

Background
The cardiovascular effects of desflurane have been investigated in several in vivo animal and human studies. To determine the possible contributions of myocardial depression, the effects of desflurane on various contractile parameters in isolated cardiac papillary muscles were compared with those of isoflurane and halothane.

Methods
The effects of desflurane, isoflurane, and halothane (0.5-2.5 minimum alveolar concentration [MAC]) were studied in rat left ventricular papillary muscles (29 degrees C; pH 7.40; stimulation frequency, 12 pulses/min). The inotropic effects were compared under low (isotony) and high (isometry) loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions.

Results
Desflurane has no significant inotropic effect (AF at 2.5 MAC: 95 +/- 11% of control values; NS) in contrast with halothane and isoflurane (AF at 2.5 MAC: 37 +/- 14 vs. 65 +/- 10%, respectively; P < 0.05). After alpha- and beta-adrenoceptor blockade or pretreatment with reserpine, desflurane induced a negative inotropic effect (AF at 2.5 MAC: 83 +/- 11 vs. 89 +/- 8%, respectively) that was not significantly different from that of isoflurane (AF at 2.5 MAC: 80 +/- 12%). Halothane induced a negative lusitropic effect under low load, which was significantly greater than those of isoflurane and desflurane. In contrast to halothane, isoflurane and desflurane induced no significant lusitropic effect under high load and did not modify postrest potentiation. These results suggest that desflurane did not impair sarcoplasmic reticulum function.

Conclusions
When compared with isoflurane, desflurane induced a moderate positive inotropic effect related to intramyocardial catecholamine release. After adrenoceptor blockade, desflurane induced a negative inotropic effect comparable with that induced by isoflurane.
Opioid-induced Delay in Gastric Emptying
Authors: Murphy D. B. , Sutton J. A. , Prescott L. F. , Murphy M. B. 
Published: November 2003

Background
Opioids delay gastric emptying, which in turn may increase the risk of vomiting and pulmonary aspiration. Naloxone reverses this opiate action on gastric emptying, but it is not known whether this effect in humans is mediated by central or peripheral opiate antagonism. The importance of peripheral opioid receptor antagonism in modulating opioid-induced delay in gastric emptying was evaluated using methylnaltrexone, a quaternary derivative of the opiate antagonist naltrexone, which does not cross the blood-brain barrier.

Methods
In a randomized, double-blind, crossover placebo-controlled study, 11 healthy volunteers were given either placebo (saline), 0.09 mg/kg morphine, or 0.09 mg/kg morphine plus 0.3 mg/kg methylnaltrexone on three separate occasions before ingesting 500 ml deionized water. The rate of gastric emptying was measured by two methods: a noninvasive epigastric bioimpedance technique and the acetaminophen absorption test.

Results
The epigastric bioimpedance technique was sufficiently sensitive to detect opioid-induced changes in the rate of gastric emptying. The mean +/- SD time taken for the gastric volume to decrease to 50% (t0.5) after placebo was 5.5 +/- 2.1 min. Morphine prolonged gastric emptying to (t0.5) of 21 +/- 9.0 min (P < 0.03). Methylnaltrexone given concomitantly with morphine reversed the morphine-induced delay in gastric emptying to a t0.5 of 7.4 +/- 3.0 (P < 0.04). Maximum concentrations and area under the concentration curve from 0 to 90 min of serum acetaminophen concentrations after morphine were significantly different from placebo and morphine administered concomitantly with methylnaltrexone (P < 0.05). No difference in maximum concentration or area under the concentration curve from 0 to 90 min was noted between placebo and methylnaltrexone coadministered with morphine.

Conclusions
The attenuation of morphine-induced delay in gastric emptying by methylnaltrexone suggests that the opioid effect is mediated outside the central nervous system. Methylnaltrexone may have the potential to decrease the side effects of opioid medications, which are mediated peripherally, while maintaining the central analgesia effect of the opioid.
The Addition of Phenylephrine Contributes to the Development of Transient Neurologic Symptoms after Spinal Anesthesia with 0.5% Tetracaine
Authors: Sakura Shinicki , Sumi Mariko , Sakaguchi Yasuko , Saito Yoji , Kosaka Yoshihiro , Drasner Kenneth 
Published: November 2003

Background
Recent reports indicate that transient neurologic symptoms commonly occur after single-injection spinal anesthesia with lidocaine. Information regarding tetracaine has been limited to a single case report. In addition, little is known about the cause of these symptoms or the cofactors that affect their occurrence. The present study sought to determine whether the presence of phenylephrine or the concentration of glucose in the anesthetic solution affects the incidence of transient neurologic symptoms after spinal anesthesia with 0.5% tetracaine.

Methods
One-hundred sixty patients classified as American Society of Anesthesiologists physical status I or II who were scheduled for elective surgery on a lower limb or perineum were sequentially assigned to one of four equal groups to receive intrathecal 0.5% tetracaine in 7.5% or 0.75% glucose, with or without 0.125% phenylephrine. Patients were evaluated on postoperative day one for the presence of pain, dysesthesia, or both in the legs or buttocks by an investigator unaware of the drug given.

Results
Symptoms were present in 10 patients (12.5%) receiving a spinal anesthetic containing phenylephrine, but in only one patient (1.3%) receiving spinal anesthesia without phenylephrine. There was no significant difference in the incidence of symptoms between groups receiving 7.5% glucose and those receiving 0.75% glucose (8.8% and 5% of patients, respectively).

Conclusions
These results suggest that adding phenylephrine to tetracaine for spinal anesthesia increases the potential for transient neurologic symptoms, but that the concentration of glucose does not affect their occurrence.