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PubMed1993

Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs.

Effects of saxitoxin (STX; 10 micrograms/kg; i.p.) on cardio-respiratory activities were evaluated in urethane-anesthetized guinea-pigs. Concurrent recordings were made of electrocorticogram (ECoG), bulbar respiratory-related unit activities, diaphragmatic electromyogram (DEMG), electrocardiogram (Lead II ECG), blood pressure, heart rate, end-tidal CO2, arterial O2/CO2 tensions, and arterial pH. The average time to STX-induced respiratory failure was about 10 min. The most striking effect prior to apnea was a state of progressive bradypnea which emerged 5-7 min after the toxin administration. Other noteworthy responses included (i) a time-dependent decrease in ECoG amplitudes which typically began before the development of a bradypneic profile; (ii) an increasing degree of diaphragm neuromuscular blockade; (iii) a state of combined hypercapnia and uncompensated acidemia; (iv) a declining blood pressure; (v) an incrementally dysfunctional myocardial performance; and (vi) an increasingly degenerative central respiratory activity profile which ultimately culminated in a complete loss of central respiratory drive. The therapeutic effect of intratracheally administered oxygen was equivocal in that the cardio-respiratory activities, be they of central of peripheral nature, remained conspicuously dysfunctional and precarious despite 100% oxygen ventilation. What can be inferred from this study is two-fold. First, STX-induced ventilatory insufficiency can be attributed to a loss of functional integrity of both central and peripheral respiratory system components. That is, although diaphragm blockade contributes significantly to STX-induced respiratory failure, analyses of single respiratory unit activity data revealed that the central respiratory rhythmogenic mechanism also appeared to play a pivotal role in the development of a bradypneic profile which promotes, and directly causes, a complete loss of respiratory drive. Second, a state of unabating depression of central respiratory activities, which seemed to be refractory to the effect of O2, suggests STX has a direct and persistent action on medullary rhythmogenic mechanisms. In conclusion, these findings indicate that both central and peripheral cardio-respiratory components are critically involved in STX-induced apnea, dysfunctional cardiovascular performance, and lethality.

Anesthesia↗
PubMed1991

Cocaine-induced respiratory depression in urethane-anesthetized rats: a possible mechanism of cocaine-induced death.

Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7 +/- 0.1 degree C and spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99 +/- 1.40 min (mean +/- SEM). The first set of experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9 +/- 0.3 degrees C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70 +/- 1.24 min, which was significantly (p les than 0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0 +/- 5.7 mmHg to 57.7 +/- 4.6 mmHg, an increase in PaCO2 from 27.7 +/- 2.2 mmHg to 42.7 +/- 3.0 mmHg, and a decrease in pH from 7.467 +/- 0.039 to 7.357 +/- 0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.

Anesthesia↗
PubMed1984

The effect of urethane and thiopental sodium on platelet aggregation in vitro and in vivo.

The potential in vitro (heparinized or citrated PRP) and in vivo effects of urethane and thiopental sodium on arachidonic acid, collagen, or ADP-induced rat platelet aggregation has been investigated. Both anesthetics antagonized platelet aggregation in vitro at concentrations higher than those found in plasma during anesthesia. Neither anesthetic altered the piastrinopenia induced by intravenous administration of these aggregating agents. These findings suggest that both anesthetics are suitable for in vivo platelet aggregation studies.

Adenosine Diphosphate↗
PubMed1986

The nonstop transvesical cystometrogram in urethane-anesthetized rats: a simple procedure for quantitative studies on the various phases of urinary bladder voiding cycle.

A new cystometric procedure that involves a nonstop transvesical (through a needle inserted into the bladder dome) infusion of saline in urethane-anesthetized rats is described. This permits the obtainment of a series of repetitive voiding cycles in both male and female rats. Recording at high-chart speed permits quantitative measurements of the various phases of the voiding cycle. Micturition was almost invariably associated with appearance, during a sustained increase of intravesical pressure, of a series of high-frequency oscillations, which were paralleled by a stream-like emission of the infused fluid. Micturition was not observed after topical tetrodotoxin, after bilateral transection of pelvic nerves, or in acute spinal rats. Intravenous hexamethonium produced a dose-related impairment of the voiding cycle, and, at high doses, suppressed micturition, and overflow incontinence ensued. The experimental procedure described herein appears to be suitable for physiopharmacological studies dealing with regulation of voiding cycle.

Anesthesia↗
PubMed1981

Role of metabolic activation in the sister chromatid exchange-inducing activity of ethyl carbamate (urethane) and vinyl carbamate.

Ethyl carbamate (EC, urethane) at 10(-2) M concentration induced more sister chromatid exchanges (SCEs) in cultured human peripheral blood lymphocytes in the absence of S9 mix than did 10(-2) M vinyl carbamate (VC), a possible proximate carcinogenic metabolite (Dahl et al., 1978) of EC. VC itself doubled SCE frequency over the control. In the presence of native S9 mix from Aroclor-induced rat liver, the SCE-inducing activity of VC was highly increased whereas that of EC was suppressed. This opposite effect of S9 mix on VC and EC seems to be due to two different factors. Activation of VC by the S9 fraction seems to be due to the presence of mixed-function oxidases in the S9 mix, because neither the native S9 fraction in the absence of co-factors nor the heat-inactivated S9 fraction in the incubation mixture led to the activation of VC. Deactivation of EC by S9 mix, on the other hand, seems to involve the presence of excess protein and/or substances of low molecular weight in the incubation mixture, because this deactivating effect did not change considerably when the S9 fraction was supplied in the absence of co-factors or when it originated from non-induced rat liver. Heat denaturation of the S9 fraction led to an increased deactivating effect on the SCE-inducing ability of EC. This result is in line with the assumption that reactive -SH groups in the S9 protein are at least partly responsible for the deactivation of EC by S9. Heat denaturation of the S9 fraction led to an about 1.5-fold increase in reactive -SH groups.

Animals↗
PubMed1992

Ontogeny of hippocampal afterdischarges in the urethane-anesthetized rat.

Experimental studies have shown that seizure manifestations vary as the brain develops. This study investigated the characteristics of afterdischarges in the hippocampal circuits at various ages in the developing rat. Rats from the following post-natal periods were tested: PN 10-11, PN 14-15, PN 17-19, PN 21-23 and PN 25-27. Animals were anesthetized with urethane and recording electrodes placed in the hippocampus bilaterally. Stimulating electrodes were placed in the left CA3 region and in the angular bundle. Afterdischarges were produced in all animals using stimulus trains of 20 or 50 Hz. Rats in the PN 10-11 and 14-15 age groups had afterdischarges that consisted of population spikes in CA1 and broad positive potentials in the dentate gyrus. Between PN 17 and 19, maximal dentate activation, which consists of bursts of large amplitude population spikes in the dentate gyrus, first appeared in response to 20 Hz stimulation to CA3 or either 20 or 50 Hz stimulation to the angular bundle. Rats older than 21 days had afterdischarge patterns like those recorded in the adult. These data indicate that, in the rat, the seizure capabilities of the limbic circuits go through a major transition period around PN 17-19. The appearance of maximal dentate activation marks the ability of the developing rat brain to produce and sustain reverberatory seizure discharges.

Animals↗
PubMed1986

Oxytocin inhibits ACTH and peripheral catecholamine secretion in the urethane-anesthetized rat.

Oxytocin (OT) generally has a stimulatory effect on ACTH secretion both in vitro and in vivo. As part of a study of ACTH-releasing factors in hypophysial portal blood, the effects of i.v. OT administration on plasma ACTH levels were tested in urethane-anesthetized rats. Surprisingly, i.v. injection of 10 micrograms OT lowered plasma ACTH levels by about 35% (P less than 0.01). It was reasoned that this paradoxical inhibition of ACTH secretion by OT might be mediated by inhibition of the unusually high rate of peripheral catecholamine secretion in this model. Measurement of plasma catecholamines before and after i.v. administration of 10 micrograms OT revealed a 53% inhibition of EPI (P less than 0.01) and 43% inhibition of NE (P less than 0.05). Administration of the beta-adrenergic antagonist propranolol (400 micrograms) 15 min before the beginning of the experiment completely blocked the inhibitory effects of OT on ACTH secretion and in fact unmasked the stimulatory effects of OT normally seen in conscious animals and in vitro. Superfused bisected adrenal glands exposed to 10(-6) M OT for 10 min secreted more than 30% less EPI and NE than control adrenals suggesting that the inhibition of EPI and NE secretion by OT in vivo occurs, at least in part, directly at the level of the adrenal. The data support the hypothesis that peripheral catecholamines may at times be directly involved in the control of ACTH secretion and also suggest that OT, which has recently been identified in the adrenal medulla, may have important paracrine functions in the regulation of adrenal catecholamine secretion.

Adrenocorticotropic Hormone↗
PubMed1994

Effect of D-Ala-D-beta Nal-Ala-Trp-D-Phe-Lys-NH2 (KP-102) on GH secretion in urethan-anesthetized rats.

The effect of a newly developed growth hormone (GH)-releasing hexapeptide (KP-102) on GH secretion was studied in urethan-anesthetized adult male rats. Although KP-102 alone exerted a small influence on GH secretion, it produced a large plasma GH response in the presence of exogenous GH-releasing factor (GRF). During the continuous infusion of GRF, the somatotropes became refractory to a large bolus dose of GRF, but KP-102 induced a marked increase of plasma GH. The GH response to KP-102 alone or KP-102 with GRF was significantly augmented when antiserum to somatostatin (ASS) was previously administered. Although KP-102 and GRF acted synergistically on GH secretion in control animals, they acted additively in ASS-administered rats. The KP-102 effect on plasma GH was significantly attenuated in control animals and ASS-administered rats by prior i.v. injection of antiserum to GRF. Taken together, KP-102 stimulates GH secretion dependent on GRF and appears to act synergistically with GRF by antagonizing the SS effect.

Animals↗
PubMedDate not supplied

CRF-evoked bradycardia in urethane-anesthetized rats is blocked by naloxone.

CRF, injected IV at a dose of 6 nmol/kg, produced a fall in blood pressure and in heart rate in urethane-anesthetized rats. The CRF-bradycardia was not obtained in hypophysectomized animals, in animals pretreated with dexamethasone, or in animals pretreated with the narcotic antagonist, naloxone (1 mg/kg, IV). By contrast, the hypotensive effects of CRF were not affected by these procedures. Vagotomy or pretreatment with a low dose of N-methylnaloxone did not affect the CRF-bradycardia, indicating that the slowing of the heart was not due to parasympathetic stimulation or due to a peripherally mediated opioid chemoreflex. The results suggested that the CRF-bradycardia was mediated by the release of opioid peptides from the pituitary.

Animals↗
PubMed1987

Evaluation of autologous cancellous bone grafting of mandibular discontinuity defects in dogs using a Dacron-urethane prosthesis.

Reconstruction of 2 cm discontinuity defects using autologous cancellous bone chips and a Dacron-urethane prosthesis was evaluated in four canine mandibles. Histologic studies were performed on specimens taken six and 12 months after bone grafting. All four grafts were completely incorporated, producing a reconstruction that conformed precisely to the desired shape. Remodeling resulted in a trabecular pattern similar to that of the normal mandible. The prosthesis was well tolerated and did not elicit an inflammatory response.

Animals↗
PubMed1981

Reduced prevalence and growth rate of urethane-induced lung adenomas in ageing adult strain A mice.

Following administration of 1.0 mg of urethane/g body wt the average diameter and prevalence of lung adenomas in adult strain. A mice were found to be progressively smaller in animals of progressively greater age at initiation of treatment. Reduction of tumor diameters below detectibility in animals in the older treatment groups could not account for the concurrent reduction in prevalence. Explanations for the observed data in ageing animals based on considerations of reduced immunocompetence or on decreased urethane metabolism or distribution were also considered insufficient. Possible mechanisms for the observed data are discussed.

Adenoma↗
PubMed1980

Naloxone inhibits arginine vasotocin- (AVT) induced prolactin release in urethane-anesthetized male rats in vivo.

Arginine vasotocin (AVT) (1 microgram) elicited a two-fold increase in serum prolactin (Prl) levels 10 min following its i.v. injection into urethane-anesthetized adult male rats. At 20 min after AVT administration serum Prl concentrations had essentially returned to preinjection levels. Prior treatment of the animals with 0.2 mg/kg body weight of naloxone (Nal), an opiate antagonist, completely blocked the Prl response to a single injection of AVT. Nal itself did not alter the titers of Prl at any time point. The results suggest that the in vivo Prl-releasing effect of AVT is mediated via an interaction with opiate receptors.

Animals↗
PubMed1987

Intrathecally administered apomorphine or LY171555 reduces nociceptive responses recorded from ventrobasal thalamic neurones in urethane anaesthetised rats.

The effects of intrathecal injections of the D2 agonists apomorphine and LY171555 were studied on responses of ventrobasal neurones responding to noxious stimulation in the urethane anaesthetised rat. At a dose of 75 micrograms/kg the D2 agonists had little effect on a total of 18 thalamic neurones. A higher dose (100 micrograms/kg) produced a reversible reduction of thalamic nociceptive responses on 15 occasions. A transient fall in blood pressure usually accompanied the intrathecal injection of the agonists. These results suggest that dopamine can modulate the transmission of nociceptive information to the thalamus and also suggests a role in the processing of autonomic function.

Afferent Pathways↗
PubMed1986

GABA A receptor mediated neurogenic inhibition of motility in the small intestine of urethane-anaesthetized rats.

Intravenous GABA (0.1-3 mg/kg) induced transient relaxation of the duodenum in urethane anaesthetized rats. The effect of GABA was mimicked by homotaurine and antagonized by bicuculline, suggesting the involvement of GABA A receptors in this type of response. Duodenal relaxation induced by GABA was unaffected by i.v. hexamethonium, phentolamine propranolol or 6-hydroxydopamine but was prevented in preparations pretreated with topical tetrodotoxin thus indicating its neurogenic origin. The ability of GABA to induce neurogenic relaxation decreased rapidly when increasing the distance from the duodenum while relaxations induced by DMPP or noradrenaline were observed throughout the whole rat small intestine.

Anesthesia↗
PubMed1992

Effect of the GABAB antagonist, phaclofen, on baclofen-induced inhibition of micturition reflex in urethane-anesthetized rats.

The effect of intrathecal or intracerebroventricular administration of the GABAB receptor agonist, baclofen, on rhythmic contractions induced by distension of the urinary bladder (micturition reflex) was evaluated in urethane-anesthetized rats. Baclofen inhibited bladder motility acting at central nervous system sites (spinal and supraspinal) with a comparable potency. The inhibitory effect of i.t. baclofen (0.1-10 nmol) was blocked by i.t. phaclofen (200 nmol) while i.c.v. phaclofen did not affect i.c.v. baclofen (0.1-1 nmol). The inhibition of the micturition reflex induced by bladder distension observed after i.t. administration of baclofen was unaffected by systemic capsaicin pretreatment (50 mg/kg s.c., four days before). On the other hand, i.t. baclofen suppressed, in a phaclofen-sensitive manner, the reflex bladder contraction evoked by chemical stimulation (topical capsaicin) of capsaicin-sensitive bladder afferents. Intrathecal baclofen did not affect the hexamethonium-resistant tonic contraction produced by topical application of capsaicin on to the urinary bladder, which is ascribable to local peptide release from sensory nerves. Bladder motility inhibition by i.t. or i.c.v. baclofen (1 nmol) was unchanged by previous administration of p-chlorophenylalanine, indicating that the serotonergic pathways do not play a role in its action. Baclofen (100 microM) suppressed the release of calcitonin gene-related peptide-like immunoreactivity evoked by electrical field stimulation from the dorsal half of the rat spinal cord. This response was also abolished by in vitro capsaicin desensitization or tetrodotoxin, indicating that baclofen suppresses transmitter release from central endings of capsaicin-sensitive primary afferents. The present findings indicate that baclofen acts at both spinal and supraspinal sites to inhibit, with different mechanisms, the micturition reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Establishment of epithelial cell strains from normal adult mouse lung resembling a urethane-induced lung adenoma cell strain and a metastasizing mouse lung carcinoma cell line.

Epithelial cell strains, designated NAL, have been established from normal lungs of adult female Balb/c mice. The ultrastructural characteristics, effect of dexamethasone on cellular morphology and proliferation rate, and the cytoskeletal protein pattern of NAL suggests that these cell strains may be related to a urethane-induced mouse lung adenoma cell strain NUL and to a metastasizing mouse lung tumour cell line CMT. NAL exhibited no anchorage-independent growth under normal conditions, however extensive passaging in the presence of 5 X 10(-6)M dexamethasone resulted in a colony forming efficiency in soft agar of 8.4% at passage number 30.

Adenoma↗