Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Urethane”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 595 records · Page 33Linked to original sources
PubMed2006

Roles of glutamatergic and serotonergic mechanisms in reflex control of the external urethral sphincter in urethane-anesthetized female rats.

This study was conducted to examine reflex mechanisms that mediate urinary bladder and external urethral sphincter (EUS) coordination in urethane-anesthetized female Sprague-Dawley rats. We investigated the properties of EUS reflexes elicited by electrical stimulation of pelvic nerve afferent axons (pelvic-EUS reflex). The changes in the reflexes induced by bladder distension and administration of agonists or antagonists for glutamatergic or serotonergic receptors were examined. The reflexes consisted of an early response (ER, 18- to 22-ms latency) and a late, long-duration (>100-ms latency) response (LR), which consisted of bursts of activity at 20- to 160-ms interburst intervals. In a few experiments, a reflex with an intermediate (40- to 70-ms) latency was also identified. With the bladder empty, the ER, but not the LR, was detected in the majority of experiments. The LR was markedly enhanced when the bladder was distended. The ER remained, but the LR was abolished, after spinal cord transection at T8-T9. The ER and LR were significantly decreased 75 and 35%, respectively, by the N-methyl-D-aspartate receptor antagonist MK-801 (0.3 mg/kg iv), but only decreased 18 and 14%, respectively, by the alpha-amino-5-methylisoxazole-4-propionate receptor antagonist LY-215490 (3 mg/kg iv). The serotonin (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (1 mg/kg iv) enhanced spontaneous EUS activity and the pelvic-EUS reflex. WAY-100635 (0.1-1 mg/kg iv), a 5-HT1A antagonist, reversed the effect of 8-hydroxy-2-(di-n-propylamino)-tetralin and suppressed EUS activity and the pelvic-EUS reflex. These results indicate that glutamatergic and serotonergic mechanisms are important in the reflex pathways underlying bladder- sphincter coordination in rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Analysis of factors involved in determining urinary bladder voiding cycle in urethan-anesthetized rats.

The mechanism(s) involved in determining the voiding cycle of the rat urinary bladder have been investigated in urethan-anesthetized animals. Fluid emission is almost confined to that phase of the voiding cycle which is characterized by the presence of a series of high-frequency oscillations in intraluminal pressure (IPHFO). During this phase the mean urethral flow rate reached a maximum and fluid was expelled in a stream-like fashion. The index obtained by multiplying the amplitude of IPHFO by their duration was significantly related to the maximal value of urethral flow rate. The IPHFO were selectively abolished by administration of d-tubocurarine at a dose that barely affects detrusor contractility. Moreover, d-tubocurarine reduced mean urethral flow rate and increased residual volume. The reflex (hexamethonium sensitive) mechanism(s) responsible for the generation of IPHFO is more developed in male than female rats. This mechanism, which involves activation of skeletal muscle, plays a significant role in determining bladder voiding in this species.

Anesthesia↗
PubMed1988

Physiological changes during thermoregulation and fever in urethan-anesthetized rats.

Adult male Wistar rats were anesthetized with urethan (1.5 g/kg). They were unable to maintain body temperature (Tb) in a warm (32 degrees C) or cool (9 degrees C) environment or at a laboratory room temperature of 22 degrees C. Tb was allowed to fall to 35.8, 34.5, or 33.3 degrees C, and prostaglandin E1 (PGE1, 400 ng) was delivered into a lateral cerebral ventricle. An immediate feverlike rise in Tb resulted, accompanied by vigorous shivering. Animals were vasoconstricted throughout. When Tb was raised to and maintained at 38.3 or 39.5 degrees C, animals also responded with a fever; however, the magnitude of the fever diminished as the starting Tb increased. In a series of experiments in which Tb was maintained (36.8-37.4 degrees C) by means of a heating pad, PGE1 delivered into a lateral cerebral ventricle or into the anterior hypothalamus caused a dose-dependent change in Tb, which was similar in time of onset, magnitude, and duration to that observed in conscious animals. This fever was accompanied by shivering and increased O2 uptake, heart rate, arterial blood pressure, respiratory rate, and intracranial pressure during the rising phase of the fever, and vasodilation of the paws occurred during defeveresence. Animals were also able to develop a dose-dependent rise in Tb in response to purified human interleukin 1.

Alprostadil↗
PubMed2003

Beta and gamma oscillations in the olfactory system of the urethane-anesthetized rat.

Fast oscillations in the beta (15-40 Hz in awake rats) and gamma (50-100 Hz) frequency ranges are prominent in field potentials induced by odorants in the mammalian olfactory bulb (OB) and piriform cortex (PC). Whereas the gamma oscillation has been studied for >50 yr, the beta oscillation has attracted attention only recently, and its origin, mechanism, and relationship to gamma are unknown. To address these questions, we have examined responses induced by odorants in the urethane-anesthetized rat-a preparation well-suited for the analysis of mechanisms. We found that both oscillations could be induced by odorants in a concentration-dependent manner. Analysis with a concentration series and spectral methods revealed that the beta and gamma oscillations were distinct and not harmonically related, indicating generation by independent mechanisms. The beta oscillation was synchronous at sites < or =4 mm apart in the OB, the greatest distance tested. In contrast, the gamma oscillation was synchronous in some experiments and asynchronous in others (frequency differed slightly at different sites, resulting in progressive phase shifts). Current source-density analysis indicated that, for both oscillations, the field potentials in the OB were generated by synaptic currents in granule cells. The two oscillations were differently affected by surgical interruption of the lateral olfactory tract. This lesion abolished the beta oscillation, whereas the gamma oscillation was still induced in the OB. Our results confirm previous reports that the gamma oscillation is generated within the OB but indicate that the beta oscillation requires the participation of PC.

Anesthesia, Intravenous↗
PubMed1990

Hemodynamic changes that accompany the pressor response to propranolol in urethane anesthetized rats subjected to alpha-blockade.

It has been shown that a paradoxical pressor response to a beta-blocker occurs in rats given an alpha-blocker. The dual-isotope microsphere technique was used to investigate the hemodynamic changes that accompany the pressor response to propranolol in phentolamine-treated, urethane-anesthetized rats. Rats were divided into four groups (n = 8 per group): group I received 10 min of saline infusion; group II received intravenous infusion of phentolamine (300 micrograms/kg/min) for 10 min; group III received intravenous injection of propranolol (100 micrograms/kg) after 20 min of phentolamine infusion, and group IV received intravenous injection of saline after 20 min of phentolamine infusion. In groups I and IV, saline did not cause any significant hemodynamic changes. In group II, phentolamine decreased the mean arterial pressure (MAP) and total peripheral resistance (TPR) by 34 +/- 3 mm Hg and 0.28 +/- 0.07 mm Hg/min/ml, respectively. Arterial conductances in the skeletal muscle and skin were increased to 157 and 165% of control values, respectively. Cardiac output and conductances in other tissues and organs were not significantly affected. In rats given phentolamine (group III), propranolol raised MAP (+40 +/- 2 mm Hg) by increasing TPR (+0.41 +/- 0.03 mm Hg/min/ml). Vascular conductances in the skeletal muscle, skin and kidneys were decreased to 38, 57 and 69% of control values, respectively. Conductances in other tissues and organs were not significantly affected. Our results show that propranolol raised MAP by increasing flow resistance, primarily via the reversal of the vasodilator effects of phentolamine in the muscle and skin.

Adrenergic alpha-Antagonists↗
PubMed1978

Adrenergic and dopaminergic control of growth hormone secretion in urethan anesthetized adult male rats.

The effects of drugs which interfere with alpha-adrenergic and dopaminergic mechanisms, involved in GH and PRL secretion, have been analyzed in urethane anesthetized rats. Clonidine induced a dose-dependent release of GH (0.0032--0.1 mg/kg i.v.) as well as of PRL (0.032--1.0 mg/kg i.v.). The lowest dose of clonidine, when given into the third ventricle, provoked a very pronounced release of GH. Phentolamine, given intravenously, inhibited the clonidine-induced GH release in a dose-dependnet manner. L-Dopa administered intravenously and apomorphine administered intravenously or intraventricularly did not affect basal secretion of GH bu- produced a dose-dependnet inhibition of clonidine-induced GH release. Pimozide did not change basal GH secretion. Furthermore pimozide did not attenuate the inhibition of clonidine-induced GH secretion seen after apomorphine administration, however, it completely reversed apomorphine-induced PRL inhibition. These findings demonstrate that an alpha-adrenoceptor-mediated stimulatory mechanism is involved in GH and PRL secretion. An inhibitory dopaminergic mechanism is confirmed for PRL secretion and suggested for GH secretion.

Animals↗
PubMed1976

Selective effect on T and B cell subpopulations in rat lymphoid organs after urethan treatment.

In vitro phytohemagglutinin (PHA) and concanavalin A (Con A) responsiveness of thymus and bone marrow cells, and E, EA, and EAC rosette-forming cells (E, EA, EAC) of these organs and spleen were studied in Fisher rats at various time intervals following a carcinogenic treatment with urethan (UR). Immediately after treatment, organ cellularities were drastically reduced with a progressive recovery as time passed. 1 day after treatment, the response of thymocytes to PHA showed a fourfold increase while organ cellularity dropped to 1%. This response fell below normal values after 7 days with an overshoot after days 14 and 21. UR-treated bone marrow cells showed a response to PHA below normal values after 1 and 7 days, a twofold increase after 3 days and an overshoot after 14 and 21 days. The responsiveness to Con A of both organs was affected by UR treatment to a much lesser extent, although following a pattern similar to that of PHA. E were never found, whether in normal nor in UR-treated animals. As far as the B-cell compartment is concerned, UR causes a progressive diminution of EAC, while the number of EA remains unaffected. The data are discussed in terms of selective effect on T- and B-cell subpopulations.

Animals↗
PubMed1991

Role of sympathetic nerve activity in the generation of vascular nitric oxide in urethane-anesthetized rats.

The aim of the present study was to examine the involvement of the sympathetic nervous system in the generation or release of vascular nitric oxide. In urethane-anesthetized rats, the administration of the novel nitric oxide synthesis inhibitor L-N-nitro arginine (LNA) (0.02 mmol/kg i.v.) increased mean arterial pressure and renal, mesenteric, and hindquarter vascular resistances. The intravenous administration of L-arginine (60 mg/kg plus 12 mg/kg/min i.v.) produced small reductions in arterial pressure and vascular resistances and abolished the hemodynamic effects of LNA. Pretreatment with the ganglion blocking agent chlorisondamine lowered mean arterial pressure and vascular resistances, abolished the LNA-induced pressor and renal vasoconstrictor response, and attenuated the increases in mesenteric and hindquarter resistances. In contrast, the vasodilator hydralazine lowered mean arterial pressure and vascular resistances to levels equivalent to that of ganglionic blockade; however, the subsequent administration of LNA still produced significant increases in arterial pressure and regional vascular resistances. In ganglion-blocked rats in which pressure and vascular resistances were returned to normal levels by infusion of arginine vasopressin or phenylephrine, the pressor and vasoconstrictor effects of LNA were restored. However, phenylephrine was significantly more efficacious and markedly exaggerated the action of LNA. These results suggest that the sympathetic nervous system plays an important role in modulating the synthesis or release of vascular nitric oxide through the effects of 1) normal sympathetic discharge, 2) humoral activation of alpha-adrenergic receptors, and 3) vascular tone per se.

Animals↗
PubMedDate not supplied

Mice with focal pulmonary fibrosis caused by monocrotaline are insensitive to urethane induction of lung tumorigenesis.

To establish the characteristics of an optimized pulmonary fibrosis model, male ICR mice were given 4 weekly sc injections of 150 or 0 mg/kg monocrotaline (MCT) and maintained without further treatment for 33 wk (Experiment 1). The final mortality in the MCT group was 64%. Epithelial cells with large bizarre nuclei and an increased incidence of alveolar/bronchiolar hyperplasias were typically observed. In areas of pulmonary fibrosis, the PCNA labeling index (LI) in the alveolar/airway epithelium was significantly elevated. DNA content analysis demonstrated a larger range (4-8C) for the ploidy pattern of alveolar epithelium with large bizarre nuclei than in the normal epithelium (2C). In Experiment 2, the relationship between pulmonary fibrosis development and lung tumorigenesis was investigated. Mice were given 4 weekly sc injections of 150 and 0 mg/kg MCT, followed by a single i.p. injection of 1,000 or 500 mg/kg urethane (UR) on week 7, then maintained without further treatment for an additional 15 wk. UR following MCT-induced inflammatory changes, fibrosis, and epithelia with large bizarre nuclei but no tumorous lesions, in spite of the fact that treatment with UR alone caused a high incidence of pulmonary tumors. Hyperplasias were seen in all groups, but the multiplicity in the combined groups tended to be decreased by the MCT pretreatment. The present study demonstrated that this new protocol is more suitable than previous one for the experimental production of pulmonary fibrosis. Furthermore, the induction of lung tumors by UR was completely depressed in mice with MCT-induced pulmonary fibrosis, suggesting that alveolar epithelial cells are resistant to this lung carcinogen under these conditions.

Animals↗
PubMed1984

Spontaneous and urethan-induced tumor incidence in B6C3F1 versus B6CF1 mice.

The incidences of spontaneous tumors of the murine hybrids (C57BL/6J X C3Hf)F1 (B6C3F1) and (C57BL/6J X BALB/c)F1 (B6CF1) were compared in untreated mice kept until 110 weeks of age. Male B6C3F1 and B6CF1 mice had respectively 16% and 20% incidence of lymphomas, 26% and 4% of liver tumors and 12% and 22% of lung tumors. Among B6C3F1 and B6CF1 females, a 36% and 12% incidence of lymphomas, a 6% and zero incidence of liver tumors, and a 4% and 16% of lung tumors were observed. A few other tumors were seen in both hybrids. Groups of male and female mice of the 2 hybrids received 5 i.p. injections of 1000 mg/kg urethan once every other day starting at 10 days of age, and were kept under observation until 65-80 weeks of age. Treated B6C3F1 mice had an earlier mortality than B6CF1 mice due to tumor development. The statistical analysis, allowing for survival, showed a significantly higher lymphoma incidence in male and female B6C3F1 than B6CF1 mice, which had instead a higher incidence of lung tumors. Hepatocellular tumors were seen in both sexes of the 2 hybrids, with a higher frequency in B6C3F1 mice. Male mice of both hybrids had a higher incidence of liver tumors than females.

Animals↗
PubMed1986

Desferrioxamine administered intravenously by infusion causes a reduction in the electroretinogram in rabbits anaesthetized with urethane.

In rabbits anaesthetized with urethane, intravenous infusion of the iron-chelating drug desferrioxamine causes a reduction in the amplitude of the electroretinogram. This is most pronounced for weak light intensities, but the change is more complex than a mere reduction in sensitivity. In experiments lasting up to 3 days the effect is reversible and is not accompanied by electron-microscopical histological changes.

Anesthesia↗
PubMed2006

Dose-different effects of orexin-A on the renal sympathetic nerve and blood pressure in urethane-anesthetized rats.

Previous studies have demonstrated that central injection of orexin-A affects renal sympathetic nerve activity (RSNA) and blood pressure (BP) in both anesthetized and unanesthetized rats. In the present study, we examined, using urethane-anesthetized rats, the dose-dependent effects of intravenous (iv) or intralateral cerebral ventricular (LCV) injection of various doses of orexin-A on RSNA and BP. We found that injection of a low dose of orexin-A (10 ng iv or 0.01 ng LCV) suppressed RSNA and BP significantly. Conversely, a high dose (1000 ng iv or 10 ng LCV) of orexin-A elevated both RSNA and BP significantly. Pretreatment with either iv or LCV injection of thioperamide, a histaminergic H(3)-receptor antagonist, eliminated the effects of a low dose of orexin-A on both RSNA and BP. Both iv and LCV injection of diphenhydramine, a histaminergic H(1)-receptor antagonist, abolished the effects of a high dose of orexin-A on RSNA and BP. Furthermore, bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) abolished the effects of both low and high doses of orexin-A on RSNA and BP. These findings suggest that orexin-A affects RSNA and BP in a dose-dependent manner and that the SCN and histaminergic nerve may be involved in the dose-different effects of orexin-A in rats.

Anesthetics, Intravenous↗
PubMed1975

Pasma growth hormone responses to thyrotropin-releasing hormone in the urethane-anesthetized rat.

Intravenous injection of synthetic thyrotropin-releasing hormone (TRH) resulted in a significant and dose-related increase in plasma growth hormone (GH) in the urethane anesthetized rat. The minimum effective does of TRH was 40 ng per 100 g body wt when administered intravenously. The maximum responses of plasma GH to TRH were observed at 5 min following TRH, whereas those of plasma TSH were obtained at 10 min. Pretreatment with either T3 (50 mug/100 g body wt ip) significantly suppressed both plasma GH and TSH responses to TRH. The GH release induced by TRH was significantly inhibited by somatostatin (5 mug/100 g body wt iv) which was injected 5 min and immediately before the injection of TRH.

Anesthesia, General↗
PubMed2001

Azo-containing urethane analogues for colonic drug delivery: synthesis, characterization and in-vitro evaluation.

A urethane-based analogue containing an azo aromatic linkage in the backbone was synthesized for use in colon-specific delivery systems by reacting toluene-2,6-diisocyanate with a mixture of an aromatic azo diol, (bis-4-hydroxyphenyl)-4,4'-diazobiphenyl, poly(ethylene glycol) (Mn = 4000; number-average molecular weight) and 1,2-propanediol (propylene glycol). The resultant compounds (UR-1 and UR-2) were characterized by IR spectroscopy, 1H NMR spectroscopy, DSC studies, X-ray diffraction studies and molecular weight determination by gel permeation chromatography. The compounds exhibited low molecular weight, lacked film-forming properties and crystallinity in the structure. An in-vitro bacterial degradation test to demonstrate the susceptibility of azo bond to bacterial enzymes was performed using media inoculated with lactobacillus culture. The results indicated degradation of films by azoreductase. In-vitro permeation of 5-aminosalicylic acid was studied in control and lactobacilli-treated films. The permeability of the lactobacilli treated films was significantly increased suggesting the potential of these compounds for application in colonic targeting.

Antineoplastic Agents↗
PubMed1983

Involvement of liver aldehyde oxidase in conversion of N-hydroxyurethane to urethane.

The present study provides the evidence that liver aldehyde oxidase in the presence of its electron donors can catalyze the reduction of N-hydroxyurethane to urethane under anaerobic conditions. Guinea pig liver 9000 X g supernatant and cytosol, but not liver microsomes, exhibited N-hydroxyurethane reductase activity in the presence of acetaldehyde or 2-hydroxypyrimidine. The cytosolic enzyme was precipitated with ammonium sulfate between 30 and 45% ammonium sulfate saturation. The N-hydroxyurethane reductase and aldehyde oxidase activities of the precipitate were similarly susceptible to inhibition by a variety of chemicals. When the precipitate was chromatographed on a DEAE-cellulose column, the elution peak position of N-hydroxyurethane reductase was entirely identical with that of aldehyde oxidase. Furthermore, purified rabbit liver aldehyde oxidase also exhibited a significant N-hydroxyurethane reductase activity in the presence of acetaldehyde or 2-hydroxypyrimidine.

Aldehyde Oxidase↗
PubMed1985

Centrally inhibitory effect of adrenaline on cardiovascular and sympathetic nerve system in urethane anesthetized rat.

The present study was undertaken to determine the central effect of adrenaline. Adrenaline was administered to the cisterna magna in urethane anesthetized rats. Following the intracisternal injections, the blood pressure dropped and reached a plateau after 15 min, the hypotensive effect continuing for at least 30 min. The heart rate also slowed concomitantly with the depressor effect. The vehicle treated rats did not show any cardiovascular responses. The cardiovascular responses in the experimental rats were accompanied by an inhibition of the sympathetic nerve activity. Pressor responses to electrical stimulation of the posterior hypothalamus were partly inhibited, while pressor responses to intravenous injections of noradrenaline remained unchanged. In DOCA hypertensive rats, the depressor responses to intracisternal injections of adrenaline were augmented. These findings suggest that adrenaline in the brain could contribute to the inhibitory mechanism of the cardiovascular system accompanied by inhibition of the sympathetic nerve system, and that this mechanism may be attenuated in DOCA hypertensive rats.

Anesthesia↗
PubMed1978

Relationship between gastric secretion and serum gastrin levels in dogs anesthetized with morphine and urethane.

The serum levels of immunoreactive gastrin (IRG) and secretion of gastric juice were simultaneously determined in dogs anesthetized with morphine and urethane. There was a significant positive linear correlation between secretion and serum IRG level in these dogs. Serum IRG level and gastric secretion were reduced by bilateral vagotomy at the neck. The amount of gastric juice was reduced dose-dependently by an intravenous injection of atropine (0.001--0.016 mg/kg), hexamethonium (0.064--1 mg/kg) and secretin (2--8 U/kg). The reduction of gastric secretion paralleled that of the serum IRG level. However, the reduction of gastric secretion did not parallel that of serum IRG level under the influence of prostaglandin E1 (0.002--0.008 mg/kg i.v.) and duodenal acidification. Prostaglandin E1 and duodenal acidification reduced gastric secretion without the reducing serum IRG level. These findings were discussed in relation to the mechanism of gastric juice stimulation by morphine, and it is suggested that endogenous gastrin release through the vagal and non-vagal pathways participates in morphine-induced gastric secretion. The difference in inhibitory effect between duodenal acidification and secretin suggests the possibility that substances other than secretin may participate in the regulation of gastric secretion in dogs.

Anesthesia↗