Effects Of Sodium Pentobarbital Research Articles

Effects of pentobarbital sodium on compound muscle action potentials in rats

Objective To investigate the effects of pentobarbital sodium on compound muscle action potentials (CMAPs) in rats.Methods Ten adult Sprague-Dawley rats (5 males,5 females),aged 8 weeks,weighing 240-260 g,were anesthetized with intraperitoneal 1％ pentobarbital sodium 40 mg/kg.The sciatic nerve was stimulated (intensity 0.50,0.55 and 0.60 V,wave length 0.05 ms,frequency 10 Hz) starting from 8 min after administration.Each intensity was repeated three times at 1 s interval.The stimulation mentioned above was repeated every 5 min.CMAPs from the gastrocnemius muscle were recorded starting from 8 min after administration (T1) and then were recorded every 5 min for 9 times (T2-10),Results The peak value of CMAP was significantly decreased at T3-5 when the intensity was 0.50,0.55 and 0.60 V,and CMAP latency was significantly prolonged at T3-6 when the intensity was 0.50 V,and at T4,5 when the intensity was 0.55 and 0.60 V as compared with those at T1 ( P ＜ 0.05 or 0.01 ).Conclusion Pentobarbital sodium can inhibit CMAPs in rats. Key words: Pentobarbital; Action potentials; Electromyography

Effects of sodium pentobarbital on the components of electroretinogram in the isolated rat retina

Photovoltages, the fast P 3( t) component of electroretinogram (ERG), were registered between two microelectrodes across the rod outer segments. The P 2( t) component, obtained by subtracting the ERGs measured before the application of 50 μM APB from those measured after the application of 50 μM APB, was used as an indicator of depolarizing bipolar cell activity. Measurements of the scotopic threshold response (STR) and the oscillatory potentials (OPs) were used as indicators of third order neuron activity. The slow P 3*( t) component, obtained by subtracting the photovoltages from the transretinal recording in the APB-treated retina was used as an indicator of Müller cell activity. The components of the ERG obtained in normal superfusate medium were compared with those obtained in the presence of 100 μM sodium pentobarbital. We found that sodium pentobarbital slowed the kinetics of the P 2( t) component and increased its latency. The fast P 3( t) component was not affected by pentobarbital. The slow P 3*( t) component was slightly reduced in the presence of pentobarbital. The minor components of the ERG, the STR and the OPs, were strongly suppressed by pentobarbital. These results suggest that in rat retina pentobarbital does not affect photoreceptors, but it does affect bipolar cells and Müller cells, and it suppresses activity of third order neurons.

Differential effects of anesthetics on sympathetic nerve activity and arterial baroreceptor reflex in chronically instrumented rats

The effects of pentobarbital sodium, chloralose, and urethane on sympathetic nerve activity and arterial baroreceptor reflex were examined using rats chronically instrumented for recordings of blood pressure (BP), electrocardiogram and renal sympathetic nerve activity (RSNA). Pentobarbital sodium (30 mg/kg, i.v.) produced a decrease in BP with a transient decrease in heart rate (HR) and no change in RSNA. Chloralose (50 mg/kg, i.v.) also caused a decrease in BP and no change in HR and RSNA until a later increase in HR and RSNA, while urethane (800 mg/kg, i.v.) increased BP, HR, and RSNA. Baroreceptor reflex function was assessed by constructing a logistic function curve compiled from data obtained by intravenous infusion in increasing doses of phenylephrine and sodium nitroprusside. Both pentobarbital sodium and chloralose administration decreased the gain of baroreceptor reflex control of both HR and RSNA. Urethane also decreased the gain of baroreceptor reflex control of HR but elicited no change in that of RSNA. These results suggest that different intravenously administered anesthetics affect the peripheral sympathetic outflows in qualitatively and quantitatively different manners.

Effects of anesthetics on norepinephrine release in the hypothalamic paraventricular nucleus region of awake rats

The effects of pentobarbital sodium, chloralose and urethane on norepinephrine (NE) release in the hypothalamic paraventricular nucleus (PVN) region were examined in awake rats. An in vivo microdialysis method was used. Extracellular NE concentrations in the PVN region were measured by high performance liquid chromatography with electrochemical detection. Pentobarbital sodium (30 mg/kg, intravenously (i.v.)) and chloralose (50 mg/kg, i.v.) caused a 30–40% decrease in NE release while urethane (800 mg/kg, i.v.) caused a 50% increase. Plasma NE concentration was not altered after pentobarbital sodium and chloralose administrations, except for its increase in chloralose at 5 h, while the concentration increased significantly ( P<0.01) after urethane. These results suggest that, in the rat, these anesthetic agents have different effects on noradrenergic activity in the PVN region as well as on plasma NE.

Fos expression by naloxone in LHRH neurons of the mediobasal hypothalamus and effects of pentobarbital sodium in the proestrous rat.

Because Fos is thought to be induced in neurons that are activated, we examined whether luteinizing hormone-releasing hormone (LHRH) neurons expressed Fos protein when they were stimulated by an opioid receptor antagonist naloxone (NAL), expecting to identify LHRH neurons which are regulated by opioid neurons directly or indirectly. Further, we examined whether an ovulation-blocking dosage of pentobarbital sodium (PB) would affect the NAL-induced Fos expression. Female rats were infused with naloxone (5 mg/kg/h) for 90 min (10.00-11.30) in the morning of proestrus, during which infusion blood sampling was done, and were killed by i.v. injection with an overdose of PB at 11.30-12.00. Dual immunoperoxidase/immunofluorescence staining for both Fos and LHRH revealed that some LHRH immunoreactive (ir) neurons in the forebrain expressed Fos-ir, associated with an increase in serum LH concentrations, but little co-localization was found in rats in proestrus which were infused with saline as the control. The proportion of LHRH-ir neurons which expressed Fos-ir was about 35-62% in the caudal part of the forebrain including the mediobasal hypothalamus, and this was larger than that (10%) in the rostral part of the forebrain including the preoptic area. PB injection (32 mg/kg bw, i.p.) 15 min prior to the beginning of NAL infusion significantly enhanced the increase in LH secretion due to NAL, and also enhanced Fos-ir expression in LHRH-ir neurons. Together with the well-established fact that PB blocks the LHRH surge generator and our previous findings that NAL stimulates the LHRH pulse generator even in the PB-blocked proestrous rat, these results strongly suggest that the LHRH pulse generator exists in the mediobasal hypothalamus which contains LHRH neurons that are responsive to NAL and express Fos protein.

Effects of Pentobarbital Sodium, Ketamine and Xylazine on Learning Impairment Induced by Transient Global Ischemia in Mongolian Gerbils

Effects of Pentobarbital Sodium, Ketamine and Xylazine on Learning Impairment Induced by Transient Global Ischemia in Mongolian Gerbils

The effect of pentobarbital sodium on the dorsal horn of the spinal cord

The effect of intravenously administered pentobarbital sodium on the activity of single unit in Rexed lamina V of the transected feline lumbar spinal cord was studied using an extracellular microelectrode recording technique. Pentobarbital sodium 1.0 mg·kg(-1), 2.5 mg·kg(-1), and 5.0 mg·kg(-1) administered intravenously suppressed both the spontaneous and the evoked activity in Rexed lamina V cells, known to respond principally to noxious stimuli, in a dose-dependent manner. The maximum depression of cell activity occurred within 5 min after intravenous administration. The recovery of cell activity occurred within 70 min after intravenous administration of pentobarbital sodium. We conclude that pentobarbital sodium intravenously administered has a suppressive effect on single unit activity of cells in Rexed lamina V and probably has an analgesic effect. Its suppressive effect is dose-dependent.

The effect of pentobarbital sodium on the dorsal horn of the spinal cord

The effect of pentobarbital sodium on the dorsal horn of the spinal cord

Pentobarbital sodium inhibits the release of noradrenaline in the medial preoptic area in the rat

The effect of pentobarbital sodium (PB) on noradrenaline (NA) release in the medial preoptic area was studied in ovariectomized rats by a microdialysis method coupled to HPLC. Dialyzates were collected at 6-min intervals before and after the injection in freely moving rats. PB injected i.p. at a dose of 35 mg/kg caused a marked, ∼40–50% decrease in NA release, which became evident 50 min after the injection and lasted for another 60 min during which the observation was performed. The results suggest that the anesthetic effect of barbiturates is related to the reduction in NA release in the brain.

Sodium pentobarbital: sensory and associative effects in classical conditioning of the rabbit nictitating membrane response.

Four experiments were conducted to determine the effects of sodium pentobarbital (0, 3, 9, and 15 mg/kg) on the acquisition of the rabbit's classically conditioned nictitating membrane response (NMR) and to determine the locus of the drug's effects on sensory, motor, associative, and nonassociative processes. In experiment 1, classical conditioning of the NMR was accomplished by pairing tone and light conditioned stimuli (CSs) with paraorbital shock as the unconditioned stimulus (US). The experiment revealed that pentobarbital retarded the acquisition of conditioned responses (CRs) to both tone and light CSs. Experiment 2, employing unpaired CS, UCS presentations, indicated small but significant drug effects on NMR base rate and nonassociative NMRs to the CS. Experiment 3 revealed no significant drug effect on the psychophysical functions relating UCS intensity to UCR frequency or amplitude, nor on the UCS intensity threshold for eliciting UCRs. On the other hand, in experiment 4, the drug significantly impaired CR frequency over an extended range of CS intensities and raised CS intensity threshold. It was concluded that pentobarbital's attenuation of CS intensity also operated to impair CR acquisition.

Pentobarbital produces dissimilar changes in glucose influx and utilization in brain

The effects of pentobarbital sodium on local cerebral glucose utilization (LCGU) and 3-O-methylglucose (3-MG) influx were measured by quantitative autoradiography in 52 brain areas of control and treated rats. Pentobarbital (50 mg/kg ip) lowered LCGU to a relatively uniform rate (approximately 35 mumol.100 g-1.min-1) in 24 of 25 forebrain areas. Among the 18 hindbrain areas, LCGU was decreased by pentobarbital by 15-55% (range 50-157 and 28-110 mumol.100 g-1.min-1 in control and treated rats, respectively). In contrast, pentobarbital lowered the 3-MG influx rate constant and permeability-surface area product by 20-30% in nearly all brain structures. The 3-MG results fit a model in which both the half-saturation constant and the maximal velocity of the glucose carrier are decreased by pentobarbital. After pentobarbital treatment, the ratio of local cerebral plasma flow (LCPF) to LCGU was the same as in controls for brain areas in which LCGU was less than 35 mumol.100 g-1.min-1 but was higher in brain areas where LCGU exceeded 35 mumol.100 g-1.min-1. Pentobarbital produced dissimilar changes in LCGU, 3-MG influx, and LCPF; these processes may thus not be closely linked during pentobarbital anesthesia.

Augmentation of GABA-induced current in frog sensory neurons by pentobarbital

The effect of pentobarbital sodium (PB) on the gamma-aminobutyric acid (GABA)-induced macroscopic and microscopic Cl- currents (ICl and iCl, respectively) was studied in the soma membrane of isolated frog sensory neurons using a rapid concentration-jump and patch-clamp technique. The GABA-induced ICl was composed of a transient peak and a steady plateau. PB shifted the concentration-response curve of the GABA-induced peak ICl to the left without affecting the maximum value. The apparent dissociation constant (KD) decreased from 13 microM at control to 8.0, 4.8, and 2.9 microM by adding 10, 30, and 100 microM PB, respectively. PB also shifted the concentration-response curve for the plateau ICl to the left and augmented the maximum value of the plateau, indicating an increase in the available receptor-channel complex. The Hill coefficient (n = 2) in concentration-response curves of both peak and plateau responses was not changed by adding PB. Both the activation and desensitization phases of GABA-induced ICl consisted of two exponential components. PB significantly increased the time constant of slow desensitization component at all concentrations of GABA used. In the "inside-out" configuration, PB markedly increased the open probability (Po) of a GABA-gated single Cl- channel having a conductance of 14.57 +/- 2.3 pS (n = 123) without affecting the single-channel conductance. The increase of Po was due to the prolongation of mean open time (tau of the tau os) and shortening of mean closed time (tau cf and tau cs), resulting in the increase of channel-opening events.(ABSTRACT TRUNCATED AT 250 WORDS)

Pentobarbital inhibits hippocampal neurons by increasing potassium conductance.

The effects of sodium pentobarbital were studied using intracellular recordings from CA1 and CA3 pyramidal cells in slices of guinea pig hippocampus. Drugs were applied either by perfusion or by pressure ejection at concentrations of 10(-6), 10(-5), and 10(-4) M. Pentobarbital at all concentrations caused neuronal hyperpolarization, decreased spontaneous activity, and sometimes decreased input resistance. Hyperpolarization also occurred in zero calcium perfusate or with tetrodotoxin in the perfusate. The postspike train long-lasting afterhyperpolarization, which is an intrinsic calcium-mediated potassium conductance, was increased at all doses. gamma-Aminobutyric acid induced depolarizing dendritic responses were augmented only at 10(-4) M pentobarbital. It is proposed that one of the important mechanisms of pentobarbital neuronal inhibition, particularly at lower doses, is an increase in potassium conductance.

Hemodynamic characterization of chronic bile duct-ligated rats: effect of pentobarbital sodium.

Systemic and splanchnic hemodynamics of the chronic bile duct-ligated rat were characterized by radioactive microspheres. Conscious and pentobarbital sodium-anesthetized, bile duct-ligated and sham-operated rats had cardiac output and regional organ blood flows determined. The conscious bile duct-ligated rat compared with the sham-operated showed a hyperdynamic circulation with an increased cardiac output (153.3 +/- 9.8 vs. 112.6 +/- 6.0 ml/min, P less than 0.005) and portal tributary blood flow (21.32 +/- 1.43 vs. 12.79 +/- 1.47 ml/min, P less than 0.005). Pentobarbital sodium anesthesia induced marked hemodynamic changes in both sham-operated and bile duct-ligated rats. The latter group was especially sensitive to its effects; thus, comparison of cardiac output and portal tributary blood flow between anesthetized bile duct-ligated and sham-operated rats showed no significant differences. We conclude that the rat with cirrhosis due to chronic bile duct ligation is an excellent model for hemodynamic investigations but should be studied in the conscious state, since pentobarbital sodium anesthesia eliminates the hyperdynamic circulation.

Effect of sodium pentobarbital on behavioral thermoregulation in rats and mice

In this study on behavioral thermoregulation, male Sprague-Dawley rats were given intraperitoneal (IP) injections of sodium pentobarbital in doses of 0, 1, 5, 10 or 15 mg/kg and male CBA/J mice were given doses of 0, 5, 10, 15 or 30 mg/kg. The animals were immediately placed in a temperature gradient which allowed them to select their preferred ambient temperature (T a). The preferred T a of rats increased following an injection of 10 mg/kg sodium pentobarbital, whereas, the barbiturate had no effect on the preferred T a of mice. In another study, male rats and mice were given sodium pentobarbital in doses of 0, 5, 10 and 15 mg/kg and then placed into a temperature-controlled environmental chamber set at 30°C for mice and 25°C for rats (i.e., their approximate preferred T a when dosed with sodium pentobarbital). Colonic temperatures were taken one hour after injection. Sodium pentobarbital induced dose dependent hypothermia in rats at 25°C and hyperthermia in mice at 30°C. These data suggest a direct or indirect block of heat gain/conserving effectors in rats treated with sodium pentobarbital which results in hypothermia and an appropriate compensatory selection of a warmer T a.

Effects of sodium pentobarbital on release of gonadotropins in ewes immediately after ovariectomy and after treatment with gonadotropin-releas ing hormone

Two experiments were conducted with ewes 9 to 11 days after estrus to determine whether the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are controlled differentially. In experiment 1, gonadotropin-releasing hormone (GnRH) was injected (100 (μg/ewe) at time = 0 min into ewes in four treatment groups. The treatment groups (9 ewes/group) were: 1) periodic iv sodium pentobarbital (NaPen) vehicle from 0 min; 2) periodic iv NaPen from 0 min; 3) vehicle iv for 120 min then iv NaPen from 120 min; 4) vehicle iv for 150 min then iv NaPen from 150 min. A surgical plane of anesthesia was maintained from the initiation of NaPen injection until the experiment ended. Jugular blood was sampled at 30-min intervals from −30 to + 210 min for LH and FSH assays, and profiles of hormone concentrations were compared by time-trend analyses. GnRH released LH (P<.001) and FSH (P<.001), but NaPen did not affect the profiles of hormone concentrations; this indicated that NaPen did not reduce the ability of the pituitary to secrete gonadotropins in response to GnRH. Experiment 2 was a 2x2 factorial with ovariectomy (time = 0 hr) and NaPen as the main effects. One group of ovariectomized (n = 6) and one group of sham ovariectomized (n = 6) ewes were anesthetized only during surgery, while a group of ovariectomized (n = 7) and a group of sham ovariectomized (n = 6) ewes were kept at a surgical plane of anesthesia until 10 hr after surgery. Patterns of LH and FSH were compared in jugular blood collected hourly from 0 hr until 10 hr after surgery and in samples collected at 24 hr intervals from -24 to +72 hr of surgery. After ovariectomy, LH increased (P<.001) hourly and daily, but anesthesia suppressed (hourly, <.001 and daily, P<.005) these increases, which resulted in an interaction (hourly, P<.001 and daily, P<.01) of ovariectomy and anesthesia. FSH after ovariectomy increased hourly and daily (hourly, P<.02 and daily, P<.001), but the effect of anesthesia and interaction of ovariectomy and anesthesia were not significant. Because NaPen did not alter secretion of LH or FSH after exogenous GnRH in experiment 1 while it blocked the postovariectomy increase in LH but not FSH in experiment 2, we concluded that the postovariectomy increase in LH resulted from increased hypothalamic secretion of GnRH. The mechanisms responsible for the postovariectomy increase in FSH secretion are not identical to those for LH. The mechanisms that control the postovariectomy secretion of FSH might involve factors that are not suppressible by NaPen or, alternatively, the differences in LH and FSH release after ovariectomy might reflect the removal of ovarian factors that suppress FSH but not LH secretion in intact ewes.

Follicular response of adult rats to PMSG and effect of sodium pentobarbital on number of ova shed in superovulation treated rats.

Follicular response of adult rats to PMSG and effect of sodium pentobarbital on number of ova shed in superovulation treated rats.

Effect of pentobarbital sodium on tracheal pressure increase induced by vagus nerve stimulation in anesthetized dogs

Effect of pentobarbital sodium on tracheal pressure increase induced by vagus nerve stimulation in anesthetized dogs

THE EFFECT OF SODIUM PENTOBARBITAL AND STORAGE TIME ON PRESERVATION OF RAM SPERMATOZOA MOTILITY AT 5 °C

The effect of sodium pentobarbital (0, 50, 100, 150, 200 and 300 mg/L of diluent) on the survival of ram spermatozoa stored at 5 °C for up to 7 days was studied. Although spermatozoa motility in diluent containing 150 mg of sodium pentobarbital was higher [Formula: see text] than in the remaining diluents, the magnitude of the difference was small. The average motility percent and rating of 73% and 4.0 for all sodium pentobarbital concentrations observed at the beginning of the storage period declined gradually to 22% and 2.1, respectively, after 7 days of storage. The pregnancy and lambing rates of 70% and 63.3% in ewes inseminated at synchronized estrus with semen extended and stored for 24 h with sodium pentobarbital (150 mg/L of diluent) did not differ significantly (P &gt; 0.05) from the respective rates of 73% and 66.7% in the control ewes.

Pentobarbital induces a naloxone-reversible decrease in mesolimbic self-stimulation threshold

The effects of sodium pentobarbital and naloxone were tested on intracranial self-stimulation (ICSS) in rats implanted with electrodes in the ventral tegmental area. Threshold for ICSS was determined using a rate-independent current titration paradigm. A low dose of pentobarbital (5 mg/kg) did not have a significant effect on ICSS thresholds, while a high dose (20 mg/kg) rendered the subjects too ataxic to respond reliably in the operant task. An intermediate dose (10 mg/kg) induced a highly significant lowering of threshold (17% below saline baseline levels) without apparent deterioration in response capability. The concurrent administration of naloxone (2 mg/kg) significantly reversed the pentobarbital-induced threshold decrease, while naloxone treatment alone had no effect on the ICSS threshold.