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At least 91 records · Page 5Linked to original sources
PubMed1999

Anesthetic profile of dexmedetomidine identified by stimulus-response and continuous measurements in rats.

This study characterizes the anesthetic profile of dexmedetomidine on the basis of steady-state plasma concentrations using defined stimulus-response, ventilatory, and continuous electroencephalographic (EEG) and cardiovascular effect measures in rats. At constant plasma concentrations of dexmedetomidine (range, 0.5-19 ng/ml), targeted and maintained by target-controlled infusion, the whisker reflex, righting reflex, startle reflex (to noise), tail clamp response, hot water tail-flick latency, and attenuation of heart rate (HR) increase associated with tail-flick (sympathoadrenal block) and corneal reflex, were assessed in 22 rats. EEG (power in 0.5- to 3.5-Hz frequency band), mean arterial pressure, and HR were recorded continuously. Blood gas values and arterial drug concentrations were determined regularly. The following steady-state plasma EC(50) values of dexmedetomidine (mean +/- S.E. nanograms per milliliter) were estimated: HR decrease (0.51 +/- 0.04), EEG (1.02 +/- 0.08), whisker reflex (1.09 +/- 0.10), sympathoadrenal block (1.85 +/- 0.80), mean arterial blood pressure increase (1.99 +/- 0.44), righting reflex (2.13 +/- 0.15), tail-flick latency (3.65 +/- 0.87), startle reflex (3.75 +/- 0.64), tail clamp (5.49 +/- 1.34), and corneal reflex (24.5 +/- 12.3). At the EC(50) value of tail clamp, ventilatory depression was minor. In rats, dexmedetomidine creates bradycardia, sedation/hypnosis, sympathoadrenal blocking effects, and blood pressure-increasing effects at plasma concentrations below 2.5 ng/ml. Higher plasma concentrations are needed to loose the startle reflex, tail-flick, tail clamp, and corneal reflex responses. Ventilatory depressant effects are minor. The applied EEG measure seems to reflect sedation/hypnosis but seems to have limited value to predict the deeper levels of analgesia and anesthesia of dexmedetomidine.

Analgesics, Non-Narcotic↗
PubMed2006

Preparation and anesthetic properties of propofol microemulsions in rats.

BACKGROUND: The lipophilicity of propofol has required dispersion in a soybean macroemulsion. The authors hypothesized that the anesthetic properties of propofol are preserved when reformulated as a transparent microemulsion rather than as a turbid macroemulsion and that the dose-response relation can be selectively modified by altering the microemulsion's surfactant type and concentration. METHODS: Microemulsions of propofol were formulated using purified poloxamer 188 (3%, 5%, 7%), and sodium salt of fatty acids (C(8), C(10), C(12)) in saline and characterized using ternary/binary diagrams, particle sizing, and stability upon dilution. Rats received propofol (10 mg . kg(-1) . min(-1)) as either a microemulsion or a conventional macroemulsion to determine these end points: induction (dose; stunned; loss of lash reflex, righting reflex, withdrawal to toe pinch) and recovery (recovery of lash, righting, withdrawal reflexes). After a 14-day recovery period, rats were crossed over into the opposite experimental limb. RESULTS: Forty-eight microemulsions (diameter, 11.9-47.7 nm) were formulated. Longer carbon chain length led to a marked increase in the volume of diluent necessary to break these microemulsions. All rats experienced anesthetic induction with successful recovery, although significantly greater doses of propofol were required to induce anesthesia with microemulsions irrespective of surfactant concentration or type than with macroemulsions. The sodium salt of C10 fatty acid microemulsion required the greatest dose and longest time for anesthetic induction. CONCLUSION: Propofol microemulsions cause induction in rats similar to that from macroemulsions. The surfactant concentration and type markedly affect the spontaneous destabilization and anesthetic properties of microemulsions, a phenomenon suggesting a mechanism whereby dose-response relation can be selectively modified.

Anesthetics, Intravenous↗
PubMed1984

Teratological evaluation of a novel antiabortifacient, dibenzyloxyindanpropionic acid. II. Postnatal morphological and behavioral development.

Dibenzyloxyindanpropionic acid (DIPA) is an antiabortifacient prostaglandin F2 alpha antagonist. Significant protection against prostaglandin F2 alpha-induced abortion in Charles River CD-1 mice is afforded by 50 mg/kg DIPA, administered intramuscularly twice daily from day-15 of gestation, two days prior to prostaglandin F2 alpha challenge. Furthermore, treatment of CD-1 mice with 50 mg/kg DIPA intramuscularly daily throughout gestation or with 50 or 200 mg/kg twice daily only on day-15 of pregnancy, revealed no structural teratological effects nor histopathological anomalies in the offspring. The present behavioral teratological investigation demonstrates that prenatal treatment of CD-1 mice with 50 mg/kg DIPA intramuscularly daily throughout gestation does not adversely affect postnatal morphological development (offspring viability; weight gain; timing of bilateral pinna detachment, eye opening, eruption of mandibular and maxillary incisors, appearance of mamillary ridges, vaginal opening, testicular descent, and appearance of downy fur), postnatal behavioral development (vocalization; auditory startle reflex; corneal reflex; righting reflex and subsequent air righting; cliff avoidance; limb placing response and grip strength; motor coordination; olfactory orientation; locomotion; motor activity; homing instinct; and acquisition and retention of an active avoidance task), or fertility of the progeny. It is concluded that DIPA is an effective and safe antiabortifacient in mice at the doses tested.

Abortifacient Agents↗
PubMed2005

Developmental and neurobehavioral effects of perinatal exposure to polychlorinated biphenyls in mice.

Because behavioral deficits associated with gestational exposure to polychlorinated biphenyls (PCBs) have been a concern, we studied the developmental and neurobehavioral effects of perinatal exposure to Aroclor 1254 (A1254), a commercial mixture of PCBs, in mice. The PCB mixture (A1254; 0, 6, 18, and 54 mg/kg body weight) was administered to pregnant mice (C57BL/6Cr) every 3 days by gavage from gestational day (GD) 6 to postnatal day (PND) 20. Compared with the control, treatment with A1254 did not alter the maternal body weight during the gestation and lactation periods. The body weight of the offspring did not differ among treatments. To assess the effects on offspring following such exposure, physical and neurobehavioral development (i.e., pinna detachment, hair growth, eye opening, incisor eruption, grasp reflex, righting reflex, walking, negative geotaxis, and cliff avoidance) was observed before weaning. At PND 7, poor adult-like responses in negative geotaxis were observed in all exposed groups. When the offspring were at 8-week old, the PCB-treated (18 mg/kg body weight) mice showed a decreased walking speed in the open-field test, and a prolonged time to reach the platform in the water maze test. Spontaneous locomotion activity was not affected by PCB exposure at 9 weeks . These results showed that perinatal exposure to PCBs produces several behavioral alterations in mice. Although dose-dependent changes were not observed, the neurobehavioral effects such as a decreased walking speed in the open-field test and a prolonged time to reach the platform in the water maze test remained in adulthood after the seeming recovery from the transient delay in development before weaning.

Age Factors↗
PubMed1997

Postnatal development and behaviour of Wistar rats after prenatal toluene exposure.

Pregnant Wistar rats were treated with different concentrations of toluene by inhalation (300, 600, 1000 and 1200 ppm) from day 9 to day 21 of pregnancy for 6 h a day in a whole-body inhalation chamber (controls inhaled fresh air only). From day 22, rats were kept single-caged and were allowed to deliver. Besides a detailed evaluation of the physical development of the offspring we performed the following tests: forelimb-grasp reflex, righting reflex, cliff-drop aversion reflex, maintainance of balance on a rotating rod, measurement of locomotor activity and learning ability in a discrimination learning test. A toluene exposure of 1200 ppm resulted in a reduced body weight of rat dams and offspring and a higher mortality until weaning. The physical development (incisor eruption, eye opening and vaginal opening) was retarded in this group. There were no clear-cut and concentration-dependent differences in the development of reflexes, rota rod performance and locomotor activity between the offspring of animals exposed to toluene and the controls. Likewise, no effects were found on learning ability in the operant conditioning task. Compared to the controls there were no differences in mating, fertility and pregnancy indexes in the F1-generation. The tests performed have provided no evidence that toluene exposures < or = 1200 ppm induce adverse effects on the behaviour of rat offspring exposed during late embryonic and fetal development.

Animals↗
PubMed1986

Effects of chronic dietary administration of the cholinergic false precursor N-amino-N,N-dimethylaminoethanol on behavior and cholinergic parameters in rats.

The choline analog, N-amino-N,N-dimethylaminoethanol (NADe), was fed ad libitum (chloride salt; 0.5%) to weanling rats in a low choline, low methionine synthetic diet. Control rats were fed choline chloride (0.5%) in place of NADe. Initial observation and behavioral screen tests of grasp strength, startle reflex, righting reflex, analgesia (hot plate test) and body temperature did not reveal any toxic effects caused by NADe, although both experimental and control groups gained weight more slowly than rats fed standard lab chow. After 25 days on the diet, the performance of rats fed NADe in a one-trial passive avoidance test was significantly impaired compared to control rats. There was no difference between experimental and control rats in sensitivity to foot shock or in activity monitored in a closed field. A subjective, 6-component behavioral rating scale indicated rats fed NADe were resistant to handling but not aggressive. These behavioral results were similar in two separate feeding experiments using deuterium-labeled and unlabeled NADe. The twitch response of isolated rat phrenic nerve-diaphragms during stimulation did not show any impairment of neuromuscular function in rats fed NADe. Receptor binding experiments indicated there were no differences between experimental and control rats in tritiated quinuclidinyl benzilate [( 3H]QNB) binding capacity in cortex, heart and ileum. Competitive [3H]QNB binding with carbachol indicated there was no difference in the IC50's measured in cortex homogenates. Acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities in cortex were similar in experimental and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1992

Histologic examination of the rat central nervous system after intrathecal administration of human beta-endorphin.

The objective of this study was to evaluate histologically the toxicity of human beta-endorphin on the rat central nervous system after intrathecal administration. Animals received a single injection of 5 micrograms (n = 9) or 50 micrograms (n = 10) on each of four consecutive days, while others received 50 micrograms (n = 8) as a single dose. The control groups received either physiologic saline (n = 10) during each of four consecutive days or had sham operations (n = 4). Tests for nociception (tail-flick latency), motor function, and reflexes (righting reflex, eye-blink reflex, and inclined plane) were performed 5, 15, 30, 60, and 120 min after injection. Both dosages produced a dose-dependent impact on these parameters. In the 50-micrograms group, there were no significant differences in analgesia between the first and the fourth doses injected. The 50-micrograms dose produced catalepsy in some animals. All changes returned to baseline within 24 h. One animal in the 50-micrograms group developed hind limb paralysis after a single injection. Histologic sections from brain, brain stem, and spinal cord were prepared. No changes in histology were found except for that in the paretic animal, which had anoxic changes in the hippocampus and other cortical areas. Human beta-endorphin produced no neurotoxicity. The effect on nociception, reflexes, and motor function confirmed the results of previous studies.

Animals↗