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Biomedical subjects

E Wei

Publications and source records attributed to E Wei.

15 recordsLinked to original sources

Cardiovascular effects of hypertonic sodium chloride solutions when injected into the liquor space of anaesthetized cats.

1 In cats anaesthetized with chloralose, hyper- and hypotonic solutions were injected into the cisterna magna (in 0.5 ml) or into a lateral cerebral ventricle (in 0.2 to 0.3 ml), with aqueduct cannulated to prevent the injected solution from entering the subarachnoid space, and the effects on blood pressure and heart rate were examined. 2 Cisternal injections of hyper- and hypotonic solutions of NaCl (0.51 M and 0.05 M), glucose (1.03 M and 0.10 M), or sucrose (1.02 M and 0.10 M), as well as distilled water produced a rise in arterial blood pressure with tachycardias. Isotonic solutions of NaCl, glucose or sucrose were ineffective. 3 Ventricular injections of the hypertonic NaCl solution, also produced a pressor response with tachycardia effects when injected in this way. 4 The pressor responses and the tachycardias occurred after bilateral vagotomy and resulted from a sympathetic discharge which, on cisternal injection, originated from structures reached from the subarachnoid space, and on ventricular injection, from structures in the ventricular walls, probably in the hypothalamus. 5 The stimuli responsible for the discharge, were, on cisternal injection, the changes in osmolarity and on ventricular injection, the sodium ions.

Anesthesia

Endorphins may function in heat adaptation.

Administration of the opiate antagonist naloxone to rats after acute or chronic heat exposure precipitates an increase in colonic temperature, an increase in escape attempts, and a decrease in body weight. These changes are accompanied by signs associated with hyperthermia such as salivation, diarrhea, and an abnormal extended posture. Although brain endorphin involvement is possible, hypophysectomy diminishes the intensity and magnitude of these naloxone effects, indicating that the naloxone effect in intact animals may be due to a functional antagonism of pituitary endorphins. These observations suggest that endorphins attenuate physiological responses to thermal and noxious stimuli triggered in common neuroanatomical pathways by heat.

Adaptation, Physiological

Quinoline: conversion to a mutagen by human and rodent liver.

Quinoline, a hepatocarcinogen in rats, and 23 quinoline derivatives were tested for mutagenic activity with the Ames Salmonella typhimurium assay. Quinoline, 5-hydroxyquinoline, and 8-hydroxyquinoline were mutagenic in strain TA 100 when Aroclor 1254-induced rat (male outbred Sprague-Dawley) liver homogenate was present in the incubation mixture. Enzyme preparations from rats pretreated with P-448-dependent aryl hydrocarbon hydroxylase inducers [3-methylcholanthrene (MCA) and beta-naphthoflavone] and MCA-treated "responsive" C57BL mice also metabolized quinoline to a mutagen, but phenobarbital and pregnenolone-16alpha-carbonitrile pretreatment did not yield active preparations. The mutagenicity of quinoline was blocked by the in vitro addition of menadione, butylated hydroxytoluene, alpha-naphthoflavone, vitamin A acetate, and glutathione to the test system. Depletion of glutathione by diethyl maleate pretreatment in vivo enhanced the mutagenic potential of the liver enzyme preparation. Mutagenic activity was correlated to the formation of water-soluble quinoline metabolites, and we suggested that the reactive quinoline intermediate is quinoline-2,3-epoxide. Microsomal enzymes isolated from human liver tissue, but not lung tissue, also converted quinoline to a mutagen.

Animals

Airborne mutagens bioassayed in Salmonella typhimurium.

Particulate airborne pollutants, collected in Buffalo, New York, and Berkeley, California, were asayed for mutagenic activity in the Ames Salmonella typhimurium test system. Mutagens requiring liver enzymes for activation, as well as direct acting mutagens, were readily detected in the Buffalo sample. By contrast, only direct acting mutagens were detected in the Berkeley sample.

Air Pollutants

Physical dependence of opiate-like peptides.

Methionine-enkephalin and beta-endorphin, endogenous peptides with activities similar to those of opiates, were infused for 70 hours into the periaqueductal gray-fourth ventricular space of the rat brain. When challenged with a naloxone, a specific opiate antagonist, these animals manifested a typical morphine-like withdrawal syndrome. These results show that such peptides can cause physical dependence.

Animals

Potency of the N3im-methyl analog of TRH in the induction of shaking movements in the rat.

The relative potencies of TRH analogs in provoking a shaking response in rats were determined. Bilateral administration of 0.011-2.0 mug TRH analog into the periaqueductal-fourth ventricular spaces of the barbiturate-anesthetized rat showed that N3im-methyl TRH was approximately 10X more potent than TRH, whereas N1im-methyl TRH was approximately 10X less potent than TRH. These results indicate that the potencies of the TRH analogs in inducing shaking parallel their thyrotropin-releasing activities.

Animals

beta-endorphin is a potent analgesic agent.

beta-Endorphin, an opiate-like peptide, has potent antinociceptive properties when it is administered directly into the brain and assayed in the the tail-flick, hot-plate, and writhing tests in mice and in the wet shake test in rats. On a molar basis, beta-endorphin is 18 to 33 times more potent than morphine and its actions are blocked by the specific opiate antagonist, naloxone hydrochloride. The activity of beta-endorphin in vivo is also compared to other peptides that show opiate-like activity in assays in vitro.

Analgesics, Opioid

Regional sensitivity of the rat brain to the inhibitory effects of morphine on wet shake behavior.

The aim of this investigation was to determine the brain regions which were most sensitive to the inhibitory effects of morphine on the shaking response of pentobarbital-anesthetized rats to ice water. The median inhibitory dose (ID50) of morphine sulfate administered intraventricularly was found to be 0.35 mug/rat. When morphine was bilaterally injected into different regions of the brain, the ID50 values ranged from 0.04 to 17.9 mug/rat. The lowest ID50 values (0.04-0.20 mug) were found in the periaqueductal gray, the medial preoptic area and the locus ceruleus. The ID50 values ranged from 0.65 to 1.6 mug for areas around the nucleus accumbens, the fasciculus retroflexus, the medical thalamus and the septal area; from 5.6 to 7.3 mug for various hypothalamic nuclei; and from 11.0 to 17.9 mug for the basal ganglia, reticular formation substantia nigra and the reticular nucleus of the thalamus. The brain areas with the lowest ID50 values are known to have thermoregulatory functions. The similarity of the shaking response to shivering is discussed. It is concluded that the central inhibitory effects of morphine on shaking are subserved by discrete neuroanatomical substrates located in medial subcortical structures.

Anesthesia

Central sites of naloxone-precipitated shaking in the anesthetized, morphine-dependent rat.

Naloxone hydrochloride, an opiate antagonist, administered via the intracranial or parenteral route precipitates shaking behavior in the morphine-dependent rat. We made localized bilateral injections of naloxone HCl, 1.5 mug/rat, into 60 subcortical sites of the pentobarbital-anesthetized, morphine-dependent rat and found that two circumscribed areas of the brain, the medial hypothalamus and the periaqueductal-4th ventricular spaces, were selectively sensitive to naloxone-precipitated shaking. In the nondependent rat, morphine injections into the anterior diencephalon inhibited the shaking response to ice water; injections of morphine into the medial diencephalon were less effective. However, naloxone antagonized the morphine-inhibited shaking more effectively when injections of naloxone were made in the medial diencephalon than when injections were made in the anterior diencephalon. These results suggest that the reciprocal relationship of morphine and morphine-naloxone effects on shaking behavior may be regulated by topographically different structures in the diencephalon.

Animals