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PubMed1998

Nitric oxide and potassium chloride-facilitated striatal dopamine efflux in vivo: role of calcium-dependent release mechanisms.

Previous studies investigating the calcium-dependency of nitric oxide-facilitated striatal dopamine efflux have produced conflicting results. In the current study, we have investigated the role of extracellular calcium in nitric oxide and potassium chloride-evoked striatal dopamine efflux in vivo using microdialysis. Dialysis probes were implanted in the anterior dorsal striatum of chloral hydrate-anesthetized rats. Intrastriatal infusion (20 min fraction) of the nitric oxide generators sodium nitroprusside (200 microM, 500 microM, or 1 mM) and 3-morpholinosydnonimine (1 mM) increased extracellular dopamine levels. The facilitatory effects of 3-morpholinosydnonimine and potassium chloride on dopamine efflux were attenuated following pretreatment (100 min) and co-infusion of calcium free artificial cerebral spinal fluid containing magnesium chloride. Local potassium chloride infusion (100 mM) administered alone elevated striatal dopamine efflux to a similar degree as potassium chloride (100 mM) delivered 60 min after 3-morpholinosydnonimine infusion. These results demonstrate that like potassium chloride, nitric oxide facilitates striatal dopamine efflux in vivo via a mechanism largely dependent on extracellular calcium. Also, as intrastriatal potassium chloride infusion evoked similar increases in extracellular dopamine levels in controls and subjects receiving pretreatment with the NO-generator 3-morpholinosydnonimine, it is unlikely that the functional integrity of DA nerve terminals is compromised via a neurotoxic disruption of plasma membrane potential following enhanced striatal NO production.

Animals↗
PubMed1999

Lidocaine levels during the first two hours of infiltration of dilute anesthetic solution for tumescent liposuction: rapid versus slow delivery.

BACKGROUND: Tumescent anesthesia for liposuction with dilute lidocaine has been well documented to result in peak serum levels 4-14 hours after infiltration. Pharmacokinetic studies have shown that the rate of lidocaine absorption is related not only to dilution, but also to the speed of subcutaneous infiltration. Early studies with a more concentrated solution of lidocaine (1.0%) have shown that with rapid infusion, peak plasma levels may occur within 30 minutes. OBJECTIVE: To determine whether rapid absorption of lidocaine may occur during infusion of tumescent solution by varying the rate of infusion of dilute lidocaine solution (0.05% or 0.1%) and observing serum levels of lidocaine within the first 2 hours of the procedure. METHODS: Eighteen patients participated in this study and were infused with a standard liposuction tumescent formula consisting of lidocaine either 0.05% or 0.1%. The rates of infusion of tumescent anesthesia ranged from 27.1 mg/min up to 200 mg/min infused over a period of 5 minutes to 2 hours. Total lidocaine infused ranged from 7.4 to 57.7 mg/kg. Serum levels of lidocaine were taken every 15 minutes during the first hour of the procedure and repeated at 2 hours. RESULTS: In all 18 patients, lidocaine levels remained significantly below the toxic range and were always less than 2.0 microgram/ml. In 11 patients, lidocaine levels at all time intervals were less than 0.5 microgram/ml. In seven patients, the lidocaine levels ranged from 0.6 to 1.9 microgram/ml at varying intervals. There was no correlation between the maximum dose of lidocaine (mg/kg) or rate of lidocaine delivered (mg/ml) with plasma levels of lidocaine. CONCLUSION: Despite variability, the serum levels of lidocaine remained well within safety limits during infusion of tumescent solution and the first hours of the procedure when infused in rates up to 200 mg/min with spinal needles and/or small diameter multiholed infusion cannulas.

Adult↗
PubMed1981

Intravenous glucose tolerance test during anaesthesia in dogs: insulin response and glucose clearance.

To evaluate the insulin response and the rates of disappearance of glucose from plasma during high spinal analgesia and various types of general anaesthesia, a series of intravenous glucose tolerance tests was performed in six dogs. Plasma glucose and insulin levels were measured during the intravenous glucose tolerance tests. Insulinogenic indices were calculated. The values obtained during anaesthesia were compared to those obtained during an unanaesthetized state. The insulinogenic index was increased significantly during high spinal analgesia and thiopentone infusion. Halothane and enflurane anaesthesia decreased the insulinogenic index significantly while Innovar-nitrous oxide also decreased it, but not significantly. These findings suggest that insulin secretion in response to hyperglycaemia is stimulated by spinal analgesia and thiopentone anaesthesia, depressed by halothane and enflurane anaesthesia and unchanged during neuroleptanesthesia. A diuresis was observed in the thiopentone anaesthetic and spinal analgesic groups as compared to the other general anaesthetic groups. Urinary losses of insulin and glucose paralleled urinary output; yet the greatest mean urinary loss of glucose did not exceed 4.5 per cent of the load of glucose administered. Accordingly, 95 per cent of the administered glucose remained within the body, presumably available for utilization.

Anesthesia↗
PubMed1990

Dissociation of mu opioid tolerance from receptor down-regulation in rat spinal cord.

The effect of continuous intrathecal infusions of opioids was studied in rats. Chronic intrathecal infusion of the highly selective mu agonist, [NMPhe3, D-Pro4]morphiceptin produced a rapid onset of tolerance to the drug in the analgesic test. However, membrane prepared from the spinal cords of the rats chronically infused with a low dose of the drug showed no statistically significant change in the number of mu or delta receptor binding sites. In addition, membrane prepared from rats challenged with a single high-dose bolus injection of [NMPhe3, D-Pro4]morphiceptin did not produce alterations in the receptor binding number. If the chronically treated rats were challenged with an acute bolus dose of [NMPhe3, D-Pro4]morphiceptin, there was a significant decrease in the number of binding sites. The reduced binding site number was observed for the mu ligand but not for the delta ligand. A similar decrease of receptor binding can also be achieved by chronic infusion of the drug at high doses. Scatchard plot showed a decrease of maximum mu binding sites in the membranes prepared from the combined chronic infusion-acute injection treated rats. Brain tissue from the same rats showed no change in the number of mu and delta receptor binding sites, indicating that the down-regulation of mu receptors was confined to the spinal cord only. Morphine did not induce receptor down-regulation by acute, chronic or combined treatments. These results suggest that in the rat spinal cord, tolerance can be induced without apparent receptor down-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Release of immunoassayable neurohypophyseal peptides from rat spinal cord, in vivo.

The subarachnoid space of the spinal cord was perfused in vivo in urethane-anesthetized rats and perfusates were assayed for arginine-vasopressin (AVP) and oxytocin immunoreactivity. In control perfusates, oxytocin concentrations were 3 times those of AVP. Electrical stimulation of the paraventricular nucleus (PVN) of the hypothalamus, but not of other hypothalamic areas, yielded increased amounts of immunoassayable peptides in the spinal cord perfusates. Intravenous infusion of AVP did not elevate AVP concentrations in the cord perfusates. These data suggest that electrical stimulation of PVN neurons caused release of AVP and oxytocin from spinal cord terminals and support the concept that these peptides are neurotransmitters in the cord.

Animals↗
PubMed2001

Randomized controlled study of colloid preload before spinal anaesthesia for caesarean section.

We randomized women having elective Caesarean section to receive either no preload (control group, n=33) or 4% gelatin solution (Gelofusine) 15 ml kg(-1) (colloid group, n=35) i.v. before spinal anaesthesia. Intravenous metaraminol was titrated at 0.25-0.75 mg min(-1) to maintain systolic arterial pressure (SAP) in the target range 90-100% of baseline after the spinal injection. The control group required more vasopressor in the first 10 min [median 1.7 (range 0-2.9) mg vs 1.4 (0-2.8), P=0.02] at a greater maximum infusion rate [0.5 (0-0.75) vs 0.25 (0-0.5) mg min(-1), P=0.0005] and had a lower minimum SAP [90 (51-109) vs 101 (75-127) mm Hg, P=0.006] than the colloid group. Nausea was less frequent in the colloid group (6 vs 24%) but neonatal outcome was similar in the two groups. Colloid preload improved haemodynamic stability but did not affect neonatal outcome when arterial pressure was maintained with an infusion of metaraminol during spinal anaesthesia for Caesarean section.

Adult↗
PubMedDate not supplied

Comparison of remifentanil and propofol infusions for sedation during regional anesthesia.

BACKGROUND AND OBJECTIVES: Patients treated with regional anesthesia often require concomitant medication for comfort and sedation. Propofol is widely used for this purpose. Remifentanil, a new ultra-short-acting opioid, exhibits at low doses distinct sedative properties that may be useful for supplementation of regional anesthesia. This study compared the effectiveness of remifentanil and propofol infusions for providing sedation during regional block placement and surgery. METHODS: In an open, prospective trial, 28 patients were randomly allocated to receive continuous infusions of remifentanil (6 microg/kg/h) or propofol (3 mg/kg/h) for sedation during spinal or axillary regional anesthesia. Infusion rates were titrated to maintain a sedation level > or = 2 as assessed with the Observer's Assessment of Alertness Scale. Vital signs were measured continuously, during and for 2 hours after ending study drug infusion. RESULTS: Similar scores for comfort and sedation were obtained in both groups during placement of the regional block and during surgery. Degree of sedation correlated with drug infusion rate of remifentanil (P < .002) but not for propofol. Respiratory rate decreased in the remifentanil group in absence of surgery (P < .05). Mean arterial pressure and heart rate were 20% lower in the propofol group (P < .05). Return to alertness occurred after 10 +/- 6 minutes in the remifentanil group and after 16 +/- 15 minutes in the propofol group. Similar incidences of hypotension, bradycardia, and nausea and vomiting were found in both groups, but intraoperative respiratory depression and nausea were more prominent in the remifentanil group. CONCLUSIONS: When titrated to the same sedation level, remifentanil provided a smoother hemodynamic profile than propofol during regional anesthesia. The frequent occurrence of remifentanil-induced respiratory depression requires cautious administration of this agent. The incidence of adverse reactions seen with both agents during and after their administration makes the management of such sedative infusion techniques difficult.

Adult↗
PubMed1975

Clearance of some quaternary amines from the spinal subarachnoid space.

The spinal subarachnoid space was perfused with artificial cerebrospinal fluid (CSF) from the low lumbar level to the middle thoracic level or to the cisterna magna in anesthetized rabbits. 3-H-choline, 3-H-methyl-atropine or 3-H-decamethonium with carrier in different concentrations was added to the perfusate together with 14-C-inulin, the latter serving as a marker of the dilution of the perfusate by original CSF. Choline was eliminated from the perfusate partly by a saturable mechanism probably by an uptake into the spinal cord. About 15 per cent of the radioactivity of the choline infused was recovered from the spinal cord mainly as phosphorylcholine, betaine, and phospholipids. Amphetamine decreased the elimination of choline from ventriculocisternal perfusates and partly inhibited the uptake of choline in rabbit choroid plexus in vitro. In contrast, amphetamine did not influence the saturable elimination of choline in the lumbothoracic perfusion. Neither methylatropine nor decamethonium was eliminated from the perfusate by a saturable mechanism in the lumbothoracic perfusions. However, in perfusions including the cisterna magna methylatropine was partly eliminated by such a mechanism. The concentration of radioactivity in fourth ventricular choroid plexa suggested this structure to be responsible for the saturable part of the elimination. In conclusion, there is no active removal of quaternary amines in general from spinal CSF like the choroid plexus mediated clearance from ventricular CSF.

Animals↗
PubMed1982

Agonist regulation of muscarinic acetylcholine receptors in rat spinal cord.

In vitro studies with cultured cells originating from nervous tissue have shown that chronic exposure to muscarinic agonists results in a loss of muscarinic receptors. To determine whether this type of regulation of muscarinic receptor number also occurs in vivo, we infused carbachol into the spinal cords of rats. A single carbachol injection into the lumbar spinal cord caused a significant increase in the nociceptive threshold. This effect of carbachol diminished to control levels after 12 h of repeated agonist injections every 4 h and was blocked by atropine. The desensitization to the antinociceptive effects of carbachol was associated with a loss of muscarinic receptors as determined by the binding of the muscarinic antagonist [3H]quinuclidinyl benzilate. After a 24-h exposure to carbachol given every 4h, there was about a 60% loss of binding sites. The loss of muscarinic receptors was also blocked by atropine and was reversible. These results represent direct evidence that a muscarinic agonist can regulate receptor number in the central nervous system and suggest that this loss of receptors is associated with a desensitization to the antinociceptive effects of carbachol injected into the spinal cord.

Animals↗
PubMed1998

Brain-derived neurotrophic factor stimulates hindlimb stepping and sprouting of cholinergic fibers after spinal cord injury.

Neurotrophic factors have been proposed as a therapeutic treatment for traumatic brain and spinal cord injury. The present study determined whether exogenous administration of one such factor, brain-derived neurotrophic factor (BDNF), could effect behavioral recovery and/or histopathological changes after spinal cord injury. Adult rats received a mild or moderate contusion injury or complete transection of the mid-thoracic spinal cord. Immediately thereafter, they were infused intrathecally with vehicle or BDNF for 28 days. Behavioral recovery was evaluated for 6 weeks after injury, at which time the rats were sacrificed and the spinal cord tissue was examined histologically. The infusion of BDNF resulted in acute stimulation of hindlimb activity. These effects included activation of alternating airstepping in injured rats when the hindlimbs were unloaded as well as slight improvements in the rate of recovery in open field locomotion score. BDNF infusion was also associated with enhanced growth of cholinergic fibers at the injury epicenter, but did not affect white matter sparing or density of serotonergic axons at or below the injury site. Based on immunohistochemical detection of BDNF protein distribution, these described effects are likely to be mediated by the activation of cells and axons within the central injury region and the along the peripheral rim of the spinal cord. Together, these findings demonstrate that the exogenous infusion of BDNF after spinal trauma can influence postinjury outcome through mechanisms that include acute stimulation of hindlimb activity and neuritogenesis at the injury site.

Animals↗
PubMed2002

Histologic characterization of acute spinal cord injury treated with intravenous methylprednisolone.

OBJECTIVE: Many substances have been investigated for attenuation of spinal cord injury after acute trauma; however, pharmacologically only steroid administration has shown clinical benefits. This study attempts to characterize local spinal cord histologic response to human dose equivalent (HDE) intravenous methylprednisolone (MP) administration in a rodent model of acute spinal cord injury. DESIGN: Forty-eight Sprague-Dawley rats were divided equally into control and experimental groups. Each group was subdivided into eight sets of three animals each, according to postinjury intervals. Paraplegia after lower thoracic laminectomy was achieved using a standardized weight drop technique. INTERVENTION: Within one hour, experimental animals were treated with HDE MP followed by 23-hour continuous infusion of HDE MP. Spinal cords were harvested at variable intervals postinjury and prepared for histologic/immunohistochemistry examination. MAIN OUTCOME MEASUREMENTS: Edema, necrosis, and glial fibrillary acidic protein (GFAP) positivity in the specimens from treated/control groups were graded by microscopy and immunohistochemistry staining and compared in a blinded manner by a qualified neuropathologist and senior authors. RESULTS: Minimal differences were observed between control and MP-treated animals at zero and four hours. At eight hours, increased white matter and medullary edema was evident in control versus MP-treated rats. This trend continued through twelve, sixteen, twenty-four, forty-eight, and seventy-two hours. No difference was observed in the astrocytic response to injury by GFAP immunohistochemistry between the groups. CONCLUSIONS: Histologically, MP reduces the development of severe edema and preserves spinal cord architecture adjacent to the site of injury. In contrast, MP does not alter the development of spinal cord necrosis or astrocytic response at the zone of injury.

Acute Disease↗
PubMed2002

Epinephrine markedly improves thoracic epidural analgesia produced by a small-dose infusion of ropivacaine, fentanyl, and epinephrine after major thoracic or abdominal surgery: a randomized, double-blinded crossover study with and without epinephrine.

UNLABELLED: We have shown that epinephrine markedly improves the analgesic effect of a thoracic epidural infusion of bupivacaine and fentanyl. Ropivacaine has an intrinsic vasoconstrictive effect, and epinephrine may therefore not have the same pharmacokinetic interaction in a ropivacaine-fentanyl infusion; but a possible spinal cord alpha(2)-agonist effect of epinephrine would give the same positive pharmacodynamic interaction with ropivacaine and fentanyl during epidural analgesia. In a prospective, randomized, crossover study, a thoracic epidural infusion of ropivacaine 1 mg/mL and fentanyl 2 microg/mL with or without epinephrine 2 microg/mL was given to 12 patients in a double-blinded manner after major thoracic or upper abdominal surgery. Main outcome measures were pain intensity at rest and when coughing, evaluated on a visual analog scale. Extent of sensory blockade was evaluated by determining dermatomal hypoesthesia to cold. Pain increased (P < 0.001) and hypoesthetic dermatomal segments decreased (P < 0.001) when epinephrine was omitted from the triple epidural infusion. After 3 h without epinephrine, pain intensity when coughing was unacceptable despite rescue analgesia. After restarting the triple epidural mixture with epinephrine, pain was again reduced to mild pain when coughing, and the sensory blockade was restored. The mixture with epinephrine caused less nausea and facilitated mobilization. We conclude that epinephrine improves the pain relief and reduces the side effects of a thoracic epidural infusion of ropivacaine and fentanyl after major thoracic or upper abdominal surgery. IMPLICATIONS: Epidural epinephrine markedly improves the pain relief and sensory blockade of a small-dose thoracic epidural infusion of ropivacaine and fentanyl. Nausea was reduced, and mobilization of the patients was facilitated.

Adjuvants, Anesthesia↗
PubMed1989

Arterial gas embolism as a pathophysiologic mechanism for spinal cord decompression sickness.

A continuous infusion of air (1.0 ml.min-1) was delivered via a fine aortic cannula into the arterial circulation of 7 anesthetized dogs until no spinal cord function could be elicited by somatosensory evoked potentials. The animals were then rapidly perfusion-fixed and the spinal cords removed for histological examination. The appearance of the embolized cords differed substantially from eight spinal cords injured by fulminant decompression sickness (DCS). The embolized cords appeared essentially normal whereas the DCS cords featured extravascular, nonstaining, space-occupying lesions (SOLs) scattered throughout the cord, mainly in the white matter. Two spinal cords injured by DCS with a delayed onset (30 min from surfacing) appeared similar to the embolized cords. These findings are compatible with the hypothesis that two mechanisms are involved in the onset of spinal cord DCS. Fulminant disease is associated with SOLs, which are probably caused by the in situ evolution of a gas phase. Disease with a delayed onset is more likely to be caused by an ischemic mechanism, which in the acute phase is histologically indistinguishable from gas embolism.

Animals↗
PubMed1979

Stimulation of phrenic nerve activity by salicylate.

To assess the possibility that salicylate stimulates VE by direct excitation of phrenic motoneurons, we compared two groups of anesthetized vagotomized dogs with respect to increases in phrenic nerve activity elicited by a large dose of sodium salicylate (225 mg/kg). The sole difference between the two groups of animals was the condition of the spinal cord (SC); SC remained intact in one group of animals (i.e., intact animals) whereas the other group of animals (i.e., T1 spinal-transected animals) underwent complete transection of the SC at the first thoracic level. Both groups of animals were ventilated by a respirator and arterial PCO2 was maintained constant throughout all experiments. Following salicylate infusion, intact animals exhibited two- to threefold increases in the frequency of phrenic nerve bursts and three- to fivefold increases in moving average minute phrenic activity (i.e., the summation of peak integrated burst activity per minute). In contrast, salicylate infusion into T1 spinal-transected animals elicited no statistically significant increase in the frequency of phrenic nerve bursts while increases in minute phrenic activity were limited to 32 +/- 8%. Since T1 spinal transection markedly diminishes increases in phrenic nerve activity elicited by salicylate, we conclude that salicylate stimulates VE by a reflex mechanism whose afferent pathways originate in metameres below T1.

Action Potentials↗
PubMed1995

An intact glutamatergic trigeminal pathway is essential for the cardiac response to simulated diving.

Nasal water flow plus concomitant expiratory apnea in anesthetized (Innovar-Vet), paralyzed, and artificially ventilated rats produces immediate bradycardia. To investigate the origin of this response, four procedures were used to block the trigeminal pathway. 1) Trigeminal receptors within the nasal passages were anesthetized by infusing local anesthetic through the external nares. 2) Trigeminal nerves that innervate the nasal passages were sectioned bilaterally as they passed through the orbit. 3) The trigeminal neural pathway was blocked within the brain stem by either electrolytically lesioning or infusing local anesthetic into the spinal trigeminal nucleus interpolaris (Sp5I). 4) Synaptic transmission within Sp5I was prevented by infusing glutamate receptor antagonists D-2-amino-7-phosphonoheptanoic acid and 6,7-dinitroquinoxaline-2,3-dione. After each of the procedures was completed, the cardiovascular responses to nasal water flow plus apnea were either attenuated or eliminated. The major conclusion of this study is that an intact glutamatergic trigeminal pathway is required for manifestation of the cardiovascular responses to nasal stimulation. Evidence also suggests that N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors are both required for synaptic neurotransmission within Sp5I.

Animals↗
PubMedDate not supplied

Spinal anesthesia: practical applications.

The recent widespread popularity of spinal anesthesia can be traced to two events. One is the appreciation that, when used for operations below the level of the umbilicus, anesthetically induced physiologic trespass is less with spinal than with general anesthesia. The other is the recognition that modest hypotension with peripheral vasodilation, that may be seen with spinal anesthesia or intravenous infusion of nitroprusside, is, unlike hypotension associated with hypovolemia, unaccompanied by physiologically significant changes in peripheral distribution of cardiac output or changes in the balance between tissue oxygen supply and demand in the myocardium or elsewhere. Spinal anesthesia also has special advantages specific to urinary tract surgery in the geriatric patient.

Age Factors↗