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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urethane-anaesthetized rats were used to investigate the influence of lesions within the locus coeruleus on the inhibition of phasically discharging supraoptic neurones that normally follows the activation of arterial baroreceptors. Carotid sinus baroreceptors were stimulated by the inflation of a blind sac of the carotid bifurcation. A general activation of arterial baroreceptors was evoked by increasing arterial blood pressure following the intravenous injection of the pure alpha-adrenoreceptor agonist phenylephrine. The locus coeruleus of one side only was destroyed either by thermal (radio-frequency) lesions, or by the injection of 6-hydroxydopamine (1 microliter, 0.5 mg/ml). The extent of each lesion was assessed histologically in stained tissue and with fluorescence histochemistry. Lesions in locus coeruleus abolished all baroreceptor input to supraoptic neurones on the side ipsilateral to the lesion. The lesions had no effect on the cardiovascular responses to the stimulus, and did not abolish the excitation of supraoptic neurones after ipsilateral carotid body chemoreceptor activation. 6-Hydroxydopamine lesions (1 microliter, mg/ml) in the rostral part of the ventrolateral A1 catecholamine neurones were less consistent in their abolition of baroreceptor input to the supraoptic nucleus. When the input from ipsilateral carotid sinus baroreceptors was abolished, there was an equivalent effect on the influence of the carotid body chemoreceptors. Input from other arterial baroreceptors, activated by phenylephrine injection, was not affected. From these results, it is proposed that the baroreceptor-induced depression of-phasically discharging supraoptic neurones is mediated via a direct noradrenergic input from the locus coeruleus.
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PMID:Lesions of the locus coeruleus abolish baroreceptor-induced depression of supraoptic neurones in the rat. 643 77

The effects of urethane on the spontaneous and stimulated contractility of isolated strips from rabbit urinary bladder has been investigated to assess if, and at which concentrations, this anaesthetic interferes with the contractility of the bladder smooth muscle. Urethane produces a generalized depression of both spontaneous and stimulated bladder muscle contractility but is expected that, in concentrations similar to those found in plasma during anaesthesia, its effect does not exceed the 10-20% inhibition. Urethane depression of bladder muscle contractility appears attributable, at least in part, to an inhibition of calcium ions mobilization from an intracellular store.
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PMID:The effect of urethane on spontaneous and stimulated contractions of isolated rabbit urinary bladder. 650 36

Anesthetic is thought to depress the energy metabolism or oxygen consumption of the brain as a whole. It has been clear, however, that anesthetic agent may either decrease or increase local metabolic rate of the brain since [14C] 2-deoxyglucose method made one possible to measure local cerebral glucose utilization. In this paper, the authors report the effect of urethane anesthesia on the local cerebral glucose utilization. We measured local cerebral glucose utilization by means of [14C] 2-deoxyglucose method in 87 brain structures of albino rats (about 300 g) under urethane anesthesia, 1 g/kg (n = 5), and conscious state (n = 6). When the whole brain metabolism was computed as a weighted average with the acid of the computerized image-processing system, there was 33% reduction in glucose utilization of the brain as a whole in the rats under urethane anesthesia. Urethane decreased the local rate of glucose metabolism, but the metabolic effect was not homogeneous throughout the brain. The neural structures in which no metabolic depression was observed were entorhinal cortex, many nuclei in hypothalamus, medial habenula-interpeduncular nucleus, nucleus tractus solitarius, and some white matters. The selective metabolic sparing in the habenula-interpeduncular system was also reported to be observed during chloral hydrate and enflurane anesthesia. However, the mechanism involved in the phenomenon remains unclear. In the discussion, we discussed the differential effects of various anesthetics of the local cerebral glucose utilization. We reviewed the literatures on the effects of various anesthetics; barbiturate, chloralose, chloral hydrate, enflurane, ketamine, nitrous oxide and halothane on the local rate of metabolism of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alterations in local cerebral glucose utilization during various anesthesia--the effect of urethane and a review]. 652 17

The acute effects of arginine vasotocin (AVT), a putative pineal peptide, on plasma levels of prolactin were investigated in the unanesthetized, estrogen-progesterone-treated male rat. A 10-microgram s.c. injection resulted in significantly increased levels of prolactin while a 1-microgram injection depressed plasma levels of this hormone; an inhibition of release was further suggested by increased levels of pituitary prolactin in rats treated with the lower dose. The same dose administered subcutaneously to urethane-anesthetized rats had no significant effect on plasma prolactin titers while a 10-microgram dose was still stimulatory. In anesthetized rats, no dose of the AVT administered (1 ng to 10 micrograms, s.c., or 1 fg to 1 microgram, i.v.) resulted in inhibition of prolactin release. In the unanesthetized normal male rat, 5 micrograms AVT first increased and then decreased levels of prolactin. Urethane anesthesia appears to mask an inhibitory effect of AVT on plasma prolactin levels in these animal preparations. Since AVT is capable of decreasing plasma prolactin levels, this peptide might be involved in the depression of plasma prolactin levels which appears to (at least partially) mediate pineal-induced gonadal degeneration.
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PMID:Acute effects of arginine vasotocin on plasma and pituitary levels of prolactin in the male rat: influence of urethane anesthesia. 678 80

The effect of the carcinogen urethan on the natural killer (NK) activity of spleen cells from inbred A/J mice was studied. Urethan (1 mg/g) inoculated into 6- to 8-week-old A/J mice produced considerable depression of cytotoxic activity of spleen cells against YAC-1 or RL male 1 tumor cells. This effect was biphasic. Initial depression of NK activity was observed 1 day after urethan treatment, reactivity normalized at 4 days, and then a second, more profound depression was seen around 7-8 days, which persisted for 14-18 days. In contrast, lymphoproliferative responses of spleen cells to mitogens were only transiently depressed after urethan treatment and were in the normal range during the second period of marked depression of NK activity. Urethan appeared to have an even more profound effect on NK activity when given to very young mice (5-17 days old). After one or two injections of urethan, very low splenic NK activity was found 6 and 7 weeks later. The carcinogenic effects of urethan were also more striking in these young recipients, with multiple tumors observed in the lungs at the time of cytotoxicity testing. Inoculation of adult urethan-treated mice with the interferon inducer polyinosinic-polycytidylic acid, boosted NK activity to the same extent as seen with normal mice, which suggested that pre-NK cells are resistant to the effects of urethan. The present data agree with the hypothesis that the ability of a chemical to depress NK cell activity is an important factor in its carcinogenic activity.
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PMID:Inhibition of the activity of mouse natural killer cells by urethan. 693 9

Female B6C3F1 hybrid mice (5-7 weeks of age) were given methyl or ethyl carbamate over a 2 week period and subsequently examined for alterations in various immunological parameters. Exposure to methyl carbamate, a non-carcinogen, did not cause any alterations in the parameters examined. In contrast, exposure to the multipotential carcinogen, ethyl carbamate (urethan) at tumourigenic dosages caused severe myelotoxicity at all dosage levels. Related to the myelotoxicity was a marked depression of natural killer cell activity. Other parameters including susceptibility to tumour cell challenge, humoral immunity, cellular immunity and macrophage function were less affected. These studies indicate that non-toxic, but carcinogenic dosages of urethan, have profound but selective effects on the immune system which can be related to alterations in bone marrow functions.
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PMID:Immune functions in methyl and ethyl carbamate treated mice. 698 8

Urethane-anaesthetised rats were exposed to hypoxia (7% O2 in N2) for 5 min periods while body core temperature (Tbc) was maintained within the normal range (37-38 degrees C) using an abdominal heat exchanger. Animals were exposed to hypoxia and after placement of electrolytic lesions in either the anterior (n = 6) or posterior hypothalamus (n = 6). Neither lesion altered respiration while rats breathed air at either Tbc. At normal Tbc, rats responded to hypoxia with increased ventilation throughout the exposure period. This response was unchanged by lesions in either location. At reduced Tbc rats responded to hypoxia with an initial increase in ventilation followed by depression to below air-breathing levels. This depressive response was unchanged after anterior hypothalamic lesions but eliminated after posterior hypothalamic lesions. It is concluded that neurons either originating in the posterior hypothalamus, or passing through it, play a role in the interaction between cold and hypoxia which leads to inhibition of respiration.
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PMID:Respiratory responses to combined hypoxia and hypothermia in rats after posterior hypothalamic lesions. 801 87

Chloral hydrate, pentobarbitone and urethane were evaluated and compared for onset, duration and depth of anaesthesia, cardiovascular and respiratory effects, nociception and mortality in adult male rats. Chloral hydrate (300 and 400 mg/kg) severely depressed the cardiovascular and respiratory systems. Duration of anaesthesia was linearly related to dose, and anaesthetic depth and analgesia were excellent. Pentobarbital (40 mg/kg) produced a short period of light surgical anaesthesia. Moderate to severe respiratory and cardiovascular depression occurred. Duration of anaesthesia was not related to dose. Urethane (1.2 and 1.5 g/kg) caused moderate cardiovascular depression. In addition, mortality was high at the 1.5 g/kg dose. Duration of anaesthesia was greater than 24 h for most animals. Anaesthesia depth and analgesia were excellent.
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PMID:Anaesthetic effects of chloral hydrate, pentobarbitone and urethane in adult male rats. 836 72

Interleukin-1 beta stimulates oxytocin and vasopressin release in conscious, male rats and causes a rise in blood pressure. These experiments were done to : A) examine the effect of i.c.v. interleukin-1 beta (1 ng/microliter) on circulating levels of vasopressin in female rats at different stages of lactation and B) determine if alpha-adrenergic mechanisms and/or prostaglandins were involved as mediators. Urethane-anaesthetized nonlactating rats and rats at Day 7, 10, 20 and 26 of lactation were set up for arterial blood sampling and i.c.v. injections. One mL blood samples were obtained in one min periods before, and at 1, 2.5, 5, 10, 30, 60 and 120 min after the following treatments: i.c.v. treatment with either interleukin-1 beta (1 ng in 1 microliter PBS-BSA) or PBS-BSA (1 microliter) as a vehicle control; or i.c.v. treatment with interleukin-1 beta following pretreatment with either phentolamine (1.7 micrograms/microliter i.c.v.) or indomethacin (1 microgram/microliter i.c.v.). As blood was sampled, isotonic saline was infused (1 mL per min) and blood pressure was monitored to minimize any hypovolemic effects due to sampling. Extracted plasma was assayed using a specific vasopressin radioimmunoassay. Interleukin-1 beta i.c.v. stimulated the release of vasopressin above that elicited by PBS-BSA alone in non-lactating rats resulting in an approximate 1.2 to 2-fold increase in plasma hormone levels. Throughout the first half of lactation, vasopressin responsiveness to i.c.v. interleukin-1 beta treatment was markedly attenuated. In latter stages of lactation, the response recovered and resembled that of non-lactators around the time of weaning. Prostaglandins consistently mediate a stimulatory action of interleukin-1 beta on vasopressin release whereas alpha-adrenergic mechanisms mediate a depression of interleukin-1 beta-induced vasopressin release during the early to middle stages of lactation. It is possible that the depression in interleukin-1 beta-stimulation of vasopressin release in early to mid-lactation is conducive for nursing to occur and that the increase in vasopressin responsiveness towards the latter stages of lactation represents a component of the weaning process.
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PMID:Changing effect of i.c.v. IL-1 beta on vasopressin release in anaesthetized, female rats at different stages of lactation: role of prostaglandins and noradrenaline. 895 69

The present study was designed to investigate the relative contributions of arterial P(O(2)), local cerebral blood flow, and oxygen delivery to the adenosine A(1) receptor-mediated depression of evoked synaptic transmission recorded in the rat hippocampus. Urethane-anesthetized rats were given a unilateral common carotid artery occlusion and then placed in a stereotaxic apparatus for stimulation and recording of bilateral hippocampal field excitatory postsynaptic potentials (fEPSPs). Arterial blood gases, mean arterial blood pressure (MAP), and bilateral hippocampal blood flow (HBF) were also measured. Arterial P(O(2)), HBF, and oxygen delivery were manipulated using normoxic hypotension, hypoxic hypotension, and hypoxic normotension. Both hypoxic hypotension and normoxic hypotension resulted in decreased HBF, decreased oxygen delivery, and a depression of the evoked fEPSP limited to the hippocampus ipsilateral to the occlusion. The enhanced HBF and oxygen delivery associated with increased MAP resulted in a restoration and maintenance of hippocampal fEPSPs despite sustained hypoxemia. The adenosine A(1) receptor-mediated depression of the fEPSP was more strongly correlated with changes in HBF and oxygen delivery than with arterial P(O(2)). We propose that adenosine plays an important role mediating the depression of neuronal activity associated with reduced oxygen delivery characteristically observed in ischemic brain tissue.
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PMID:The effect of acute hypoxemia and hypotension on adenosine-mediated depression of evoked hippocampal synaptic transmission. 1289 63


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