Disease relevance of Tropin

• The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (p<0.0001), robust bradycardia (135+/-18; p<0.001), and increased sinking (92%; p<0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects [1].
• Despite mild side effects, atropine methonitrate, either alone or in combination with an adrenergic drug, appears to have a place in the treatment of sever reversible airway obstruction not adequately controlled by conventional treatment [2].
• In hypoxia, atropine sulphate and scopolamine hydrobromide again blocked FBM but now scopolamine methylbromide and atropine methylnitrate blocked the FBM in 42% of trials [3].
• During restraint stress, PVN microinjections of DAGO blunted stress-induced tachycardia, apparently by a vagal mechanism as this effect was blocked by atropine methyl nitrate [4].
• In contrast, atropine methylnitrate (2 mg/kg) did not block physostigmine hypothermia in either sex, but markedly decreased physostigmine's protective effect in females [5].

Psychiatry related information on Tropin

• However, the peripherally acting derivative atropine methyl nitrate (2-10 mg/kg) also attenuated all naloxone-induced withdrawal symptoms except jumping, which was not significantly modified [6].
• To investigate the role of gastric contractility in the prepyloric control of meal size, we administered atropine methyl nitrate (3 mg/kg,ip) or saline prior to 30-min tests on 3 separate days in which 0.8 M sucrose was ingested by rats after 1 h of food deprivation [7].

High impact information on Tropin

• To assess the relative contributions of sympathetic and parasympathetic branches of autonomic control to baroreflex functioning, atropine methyl nitrate and atenolol were administered to establish vagal blockade, and cardiac sympathetic blockade, respectively [8].
• Peripheral vagal blockade with atropine methyl nitrate caused a large sudden rise in heart rate, indicating that an increased vagal outflow counteracted the sympathetic activation [9].
• A comparative study of atropine methonitrate, salbutamol, and their combination in airways obstruction [2].
• Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability [10].
• In the three remaining groups, pairing was performed 30 min after an intraperitoneal injection of either 0.5 ml of saline (150 mM NaCl), 100 mg/kg of atropine methyl nitrate (0.5 ml of AMN in saline), or 100 mg/kg of atropine sulfate (0.5 ml of ATS in saline) [11].

Chemical compound and disease context of Tropin

• Bilateral vagotomy, intravenous administration of atropine methylnitrate or practolol pretreatment attenuated the bradycardia [12].
• The influence of residual catecholamines on heart rate was inferred from bradycardia following administration of the beta 1-adrenergic receptor blocking agent, atenolol, in pups pretreated with bretylium, atropine methyl nitrate, and chlorisondamine [13].
• The adrenal catecholamine component of sympathetic control of heart rate was inferred from bradycardia following administration of the ganglion blocking agent, chlorisondamine, to pups pretreated with bretylium and atropine methyl nitrate [13].
• In addition, the tachycardia elicited by (+)-8-OH-DPAT was abolished by the peripheral beta-adrenoceptor antagonist sotalol, but not by atropine methyl nitrate [14].
• Comparative studies of atropine methonitrate and its combination with reproterol in chronic airway obstruction [15].

Biological context of Tropin

• However, atropine methyl nitrate did prevent salivation induced by oxotremorine in the presence of THC [16].
• Administration of atropine sulfate or methylatropine nitrate by sc injection to rats immediately following administration of an LD50 of anguidine and again 4 hr later gave modest but significant protection against anguidine lethality [17].
• Intravenous atropine methylnitrate blocked the bradycardia associated with excitation of the CVLM but did not alter the vascular resistance changes [18].
• In Experiment 1, control rats and rats treated with atropine sulfate or atropine methyl nitrate (50 mg/kg) were trained to escape to a visible platform from different starting points in a swimming pool [19].
• Such histaminergic antagonism also blocked the expression of an established conditioned acid secretory response without effect on conditioned water intake; peripheral cholinergic blockade using atropine methyl nitrate had virtually the same effect as did histaminergic antagonism [20].

Anatomical context of Tropin

• In dogs pretreated with hexamethonium (20 mg/kg), propranolol (2 mg/kg), and atropine methylnitrate (3 mg/kg) to produce autonomic nervous system blockade, D-medetomidine also produced an initial pressor response, but no secondary reduction in heart rate or arterial pressure occurred [21].
• Systemic atropine methyl nitrate treatment attenuated bombesin-induced bradycardia, suggesting that bombesin acts within the central nervous system to stimulate cardiac vagal activity [22].
• The combined treatment of ANG II and the quaternary analogue, atropine methyl nitrate (3.25 mg/kg ip), which does not cross the blood-brain barrier, failed to affect the hypothermic responses to ANG II [23].
• Furthermore, atropine methylnitrate prevented the occurrence of gastric erosions following substantia nigra lesions, suggesting that the erosion formation is mediated via parasympathetic-vagal activity [24].
• Parasympathetic nervous system control, as reflected by tachycardic response to muscarinic receptor blockade with atropine methyl nitrate was also unchanged by early NaCl exposure [13].

Associations of Tropin with other chemical compounds

• In addition, the effect of dexmedetomidine in the presence of atropine methylnitrate instead of vagotomy was examined [25].
• The antagonism of ethanol-induced sleep by dibutyryl cyclic adenosine 3', 5'-monophosphate was significantly reduced but not blocked by atropine methyl nitrate [26].
• Neither atropine methyl nitrate nor scopolamine methyl bromide had an appreciable effect upon the specific binding of [3H]clonidine to neural membranes from most brain areas [27].
• In an additional experiment, LAC retained its potency to inhibit feeding in sham-vagotomized rats after an intraperitoneal injection of atropine methylnitrate (5 mg/kg b.wt.0.75) [28].
• Blood pressure (BP) and heart rate (HR) were recorded in conscious rats, before and after a neurohumoral blockade obtained by successive administration of chlorisondamine, enalapril, a V1-vasopressinergic receptor antagonist (Manning compound) and atropine methyl nitrate [29].

Gene context of Tropin

• However, after intracisternal administration of atropine methyl nitrate, TRH no longer caused a significant reduction of sleep, even though TRH antagonism of the ethanol-induced hypothermia was still apparent [26].
• Intravenous injection of atropine methyl nitrate reduced relaxation induced by administration of NPY [30].
• Pretreatment with atropine methyl nitrate attenuated the TRH-induced ulcers in both stress and non-stress situations [31].
• All rats received atropine methyl nitrate (20 mg/kg, ip)+the bispyridinium acetylcholinesterase reactivator HI-6 (125 mg/kg, ip; 1-(((4-(aminocarbonyl)pyridinio) methoxy)methyl)-2-((hydroxyimino)methyl)-pyridinium dichloride) in the same solution 10 min before soman (130 micrograms/kg,sc) [32].
• Atropine methyl nitrate (AMN, 0.05, 0.5 and 25 mg/kg) intraperitoneally increased Fos-like immunoreactivity (Fos-LI) in the myenteric plexus, but not the dorsal vagal complex (DVC, the area postrema (AP), nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV)) in adult, male Sprague-Dawley rats [33].

Analytical, diagnostic and therapeutic context of Tropin

• This effect was curtailed by administration of atropine methyl nitrate (20 mg/kg i.p.) or bilateral cervical vagotomy [34].
• This increased rise in the insulin response to neurocytoglucopenia of BR rats was blocked by previous intravenous injection of atropine methyl nitrate (0.2 mg/100 g body wt) [35].
• Atropine methyl nitrate (0.2 mg/kg) abolished the remaining ECG abnormalities and NM tension [36].
• Male Sprague-Dawley rats were given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 130 micrograms soman/kg sc, and the heart was examined by light and electron microscopy 10, 25, 45, 90, and 180 min after the onset of seizures [37].
• The development of subsensitivity to atropine methylnitrate. A double-blind, placebo-controlled crossover study [38].

References