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Results for “Ganglionic Blockers”

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At least 1,009 records · Page 56Linked to original sources
PubMed1991

Vagally mediated acid hypersecretion and lesion formation in anesthetized rat under hypothermic conditions.

The pathophysiological changes associated with hypothermia were investigated in the rat stomach under anesthetized conditions. The animal was placed in a styrene foam box and the core body temperature was kept between 24 and 36 degrees C using a heat lamp and refrigerant pack. Lowering of body temperature (less than 30 degrees C) produced acid hypersecretion and induced hemorrhagic lesions in the gastric mucosa; these responses reached the maximum at 28 degrees C, and a significant relationship was found between acid output and lesion score. Hypothermia (28 degrees C) also caused a marked increase of gastric contractile activity and mucosal blood flow (MBF), but the ratio of acid output to MBF became greater when compared to that obtained under normothermic conditions. These changes induced by hypothermia (28 degrees C) were completely blocked by vagotomy and were significantly inhibited by atropine, hexamethonium, clonidine, or TRH antiserum. However, lowering body temperature did not significantly affect acid secretory, motility, and ulcerogenic responses induced by carbachol in the vagotomized rat, excluding local mechanisms (suppression of the inhibitory nerves) in the hypothermia-induced changes. We conclude that hypothermia alone stimulates vagally dependent acid secretion and motility, resulting in damage in the gastric mucosa. These changes may be centrally mediated by TRH, which is released in association with the thermogenic response to hypothermia.

Animals↗
PubMed1995

Contribution of alpha- and beta- adrenoceptors and neuropeptide-Y to autonomic dysreflexia.

Modest increases in urinary bladder pressure result in acute hypertensive episodes in humans with spinal cord lesions above T5. The underlying mechanisms of this condition, referred to as autonomic dysreflexia, are not well understood. The aim of this study was to characterize the contribution of alpha- and beta-adrenoceptors as well as circulating neuropeptide-Y (NPY) to the pressor response to bladder distension in conscious cervical spinal rats. Rats were chronically instrumented with arterial and venous catheters. After 2-3 days, a complete spinal transection (C7) was performed, and the urinary bladder was catheterized: 24 h later, mean arterial pressure (MAP) responses to 5 min bladder distensions (+40) were measured under control conditions and after administration of specific autonomic antagonists. To assess the contribution of alpha and beta adrenergic mechanisms the alpha antagonist prazosin (0.45 mg/kg i.v.) and beta antagonist, propranolol (4 mg/kg i.v.), were administered individually or together. Blood samples were taken before, during and after bladder distension for determination of plasma NPY by radioimmunoassay. The pressor response to bladder distension was approximately 30 mmHg under control conditions. The response was attenuated (-38%), but not abolished, by prazosin. A similar attenuation (-41%) was observed with propranolol. There were no changes in plasma NPY in response to bladder distension. Finally, the pressor response was completely abolished by combined alpha- and beta-adrenergic blockade. These results suggest that autonomic dysreflexia is mediated exclusively by adrenergic receptors in the spinal rat. Moreover, both alpha and beta adrenergic receptors contribute to the pressor response induced by bladder distension in the conscious cervical spinal rat.

Animals↗
PubMed1994

Acid secretory and duodenal ulcerogenic responses induced by mepirizole in anesthetized rats. Relation to body temperature.

The role of body temperature in the acid stimulatory mechanism by mepirizole, a duodenal ulcerogen, was investigated in urethane-anesthetized rats. Subcutaneous administration of mepirizole (60 and 200 mg/kg) increased acid secretion in a dose-dependent manner and resulted in duodenal lesions within 8 hr. The acid secretory and ulcerogenic responses induced by mepirizole were inhibited completely by vagotomy and significantly reduced by subcutaneous pretreatment with atropine (1 mg/kg), hexamethonium (10 mg/kg), or clonidine (1 mg/kg). During anesthesia, body temperature was decreased to 34 degrees C in control rats but further reduced to 31 degrees C after administration of mepirizole. When body temperature was maintained at 36 degrees C during a test period, mepirizole caused significantly less effect on acid secretion and produced less damage in the duodenum. In addition, intracisternal administration of antiserum of thyrotropin-releasing hormone (TRH: 5 mu1/rat) also significantly inhibited acid hypersecretion and development of duodenal lesions in response to mepirizole. When acid output induced by mepirizole was plotted against duodenal lesion score from one group to another, a significant linear relationship was found between these two values (r = 0.814, P < 0.05). We conclude that mepirizole induced vagally mediated acid secretion and duodenal lesions in anesthetized rats. These responses may occur centrally in association with lowering of body temperature, which potentiates the acid stimulatory effect of mepirizole, probably through a TRH-dependent mechanism.

Animals↗
PubMed1994

Adrenergic, purinergic, and endothelial mediators and modulators of norepinephrine-induced mesenteric autoregulatory escape.

We evaluated the effects of potential factors in autoregulatory escape from norepinephrine-induced vasoconstriction in rat anterior mesenteric artery. We determined mesenteric artery blood flow velocity with a pulsed Doppler, sonic flowmeter, and systemic arterial blood pressure with a transducer. A 4-min norepinephrine infusion (0.125-1.0 x 10(-8) M/min) intravenously evoked a dose-dependent, initial vasoconstriction that was followed by rapid escape of blood flow toward or above the control value during sustained norepinephrine administration. Neonatal capsaicin treatment enhanced vasoconstrictor responses to norepinephrine but failed to affect escape parameters. Propranolol decreased norepinephrine-induced escape dose dependently. Adenosine deaminase attenuated escape, and the combination of this enzyme plus propranolol nearly abolished escape from norepinephrine-induced vasoconstriction. Methylene blue also diminished autoregulatory escape. These findings suggest that norepinephrine-induced autoregulatory escape involves simultaneous beta-adrenoceptor, purinergic, and endothelial mediation. Norepinephrine-evoked mesenteric vasoconstriction appears to involve predominantly alpha 2-adrenoceptors and is modulated by peptidergic sensory nerves and adenosine.

Adenosine Deaminase↗
PubMed1997

6-[18F]fluorodopamine positron emission tomographic scanning in the assessment of cardiac sympathoneural function--studies in normal humans.

Thoracic positron emission tomographic (PET) scanning after injection of 6-[18F]fluorodopamine ([18F]-6F-DA) visualizes cardiac sympathetic innervation. We tested whether changes in curves relating myocardial [18F]-6F-DA-derived radioactivity with time (time-activity curves, TACs) can reflect changes in important aspects of cardiac sympathetic function. Thoracic PET scans were obtained after intravenous administration of [18F]-6F-DA or the perfusion imaging agent [13N]ammonia into normal volunteers. Ganglion blockade with trimethaphan (TRI) was used to decrease sympathoneural traffic, desipramine (DMI) to block neuronal uptake of catecholamines, and tyramine (TYR) to displace vesicular amines. After [18F]-6F-DA administration, myocardial concentrations of [18F]-6F-DA-derived radioactivity declined bi-exponentially from the peak value. TRI increased the y-intercept (yo) value for the early phase (p = 0.01), and DMI decreased the yo for the late phase (p = 0.01). The TRI effect did not result from increased arterial [18F]-6F-DA concentrations or from increased myocardial perfusion. TYR infusion, begun 90 min after [18F]-6F-DA administration, accelerated the decline of myocardial radioactivity by 2.6-fold (p = 0.003). Alterations in post-ganglionic sympathoneural traffic, neuronal catecholamine uptake, and vesicular turnover of monoamines produce distinct changes in myocardial TACs after [18F]-6F-DA injection. [18F]-6F-DA PET scanning may therefore enable assessments of effects of stressors, drugs, and neurocardiological disorders on specific aspects of cardiac sympathoneural function.

Adrenergic Uptake Inhibitors↗