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At least 1,225 records · Page 68Linked to original sources
PubMed1998

Zaprinast, a type V phosphodiesterase inhibitor, dilates capacitance vessels in anaesthetised rats.

The effects of zaprinast (a type V phosphodiesterase inhibitor) on mean arterial pressure, heart rate, cardiac output, mean circulatory filling pressure, arterial and venous resistances were compared to those of sodium nitroprusside in three groups, each of intact or ganglion-blocked, Inactin-anaesthetised rats. In intact rats, zaprinast (1.5, 3.0 mg kg(-1) min(-1)) and sodium nitroprusside (8.0, 64.0,microg kg(-1) min(-1)) dose-dependently reduced mean arterial pressure and arterial resistance, but did not alter cardiac output and venous resistance. Both increased heart rate, with the effect of zaprinast less than that of sodium nitroprusside. Mean circulatory filling pressure was elevated by both doses of zaprinast but only the high dose of sodium nitroprusside. In rats given mecamylamine (3.7 micromol kg(-1), i.v. bolus) and noradrenaline (7.3 nmol kg(-l) min(-1)), zaprinast and sodium nitroprusside elicited dose-dependent reductions in mean arterial pressure, arterial and venous resistances, and mean circulatory filling pressure. Both increased cardiac output, with the effect of zaprinast greater than that of sodium nitroprusside at the low dose. Zaprinast but not sodium nitroprusside reduced heart rate. Our results indicate that zaprinast, similar to sodium nitroprusside, dilates both resistance and capacitance vessels in ganglion-blocked rats infused with noradrenaline to restore vasomotor tone. Zaprinast but not sodium nitroprusside has a direct, negative chronotropic effect on the heart.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1999

Delta9-tetrahydrocannabinol inhibits gastric motility in the rat through cannabinoid CB1 receptors.

We investigated involvement of the autonomic nervous system in gastric motor and cardiovascular responses to delta9-tetrahydrocannabinol (delta9-THC) in anesthetized rats. Intravenously administered delta9-THC evoked long-lasting decreases in intragastric pressure and pyloric contractility, bradycardia, and hypotension. The changes in gastric motor function and bradycardia were abolished by vagotomy and ganglionic blockade, whereas spinal cord transection prevented the hypotensive response. Administered intravenously alone, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-met hyl-1H-pyrazole-3-carboxamide, a putative cannabinoid CB1 receptor antagonist, evoked transient decrease in intragastric pressure, and hypertension that was associated with bradycardia. However, this agent completely blocked the gastric motor and cardiovascular responses to intravenous delta9-THC. Application of delta9-THC to the dorsal surface of the medulla resulted in small and short-lasting decreases in gastric motor and cardiovascular function. We conclude that the decrease in gastric motor function and bradycardia are partially due to an action of delta9-THC in the dorsal medulla and that intact vagal nerves are required. The hypotension was mediated through sympathetic pathways. Both gastric motor and cardiovascular effects of peripherally administered delta9-THC seem to be mediated through cannabinoid CB1 receptors.

Animals↗
PubMed2003

Postoperative ileus is maintained by intestinal immune infiltrates that activate inhibitory neural pathways in mice.

BACKGROUND AND AIMS: Postoperative ileus after abdominal surgery largely contributes to patient morbidity and prolongs hospitalization. We aimed to study its pathophysiology in a murine model by determining gastric emptying after manipulation of the small intestine. METHODS: Gastric emptying was determined at 6, 12, 24, and 48 hours after abdominal surgery by using scintigraphic imaging. Intestinal or gastric inflammation was assessed by immune-histochemical staining and measurement of tissue myeloperoxidase activity. Neuromuscular function of gastric and intestinal muscle strips was determined in organ baths. RESULTS: Intestinal manipulation resulted in delayed gastric emptying up to 48 hours after surgery; gastric half-emptying time 24 hours after surgery increased from 16.0 +/- 4.4 minutes after control laparotomy to 35.6 +/- 5.4 minutes after intestinal manipulation. The sustained delay in gastric emptying was associated with the appearance of leukocyte infiltrates in the muscularis of the manipulated intestine, but not in untouched stomach or colon. The delay in postoperative gastric emptying was prevented by inhibition of intestinal leukocyte recruitment. In addition, postoperative neural blockade with hexamethonium (1 mg/kg intraperitoneally) or guanethidine (50 mg/kg intraperitoneally) normalized gastric emptying without affecting small-intestinal transit. The appearance of intestinal infiltrates after intestinal manipulation was associated with increased c-fos protein expression in sensory neurons in the lumbar spinal cord. CONCLUSIONS: Sustained postoperative gastroparesis after intestinal manipulation is mediated by an inhibitory enterogastric neural pathway that is triggered by inflammatory infiltrates recruited to the intestinal muscularis. These findings show new targets to shorten the duration of postoperative ileus pharmacologically.

Animals↗
PubMed1991

Evidence for the existence of a urethro-urethral excitatory reflex in urethane anesthetized rats: involvement of peripheral ganglionic structures.

In urethane-anesthetized rats urethral distension with saline at the level of the external urethral sphincter elicited a series of slow phasic contractions with an amplitude between two and 18 mm. Hg. Contractions having an amplitude lower than four mm Hg were unaffected by i.v. or topical hexamethonium (HEX) or by topical tetrodotoxin (TTX). HEX or TTX transiently abolished or reduced the distension-evoked contractions having an amplitude between four and 18 mm. Hg. Administration of d-tubocurarine (d-Tc), atropine, bilateral section of pudendal nerves, spinalization (T12-S1) or bilateral removal of the major pelvic ganglia did not modify the distension-induced rhythmic urethral activity. In rats desensitized to capsaicin (four days before), both amplitude and frequency of urethral contractions did not differ from control value. In rats pretreated with atropine, administration of HEX still inhibited the distension-induced urethral contractions. Intravenous dimethylphenylpiperazinium (DMPP) triggered a rapid phasic contraction with an amplitude ranging between 15 and 25 mm. Hg. This effect was inhibited by previous administration of HEX. In accordance with histochemical studies showing spherical ganglionic cell bodies between the outermost striated muscle layer and the smooth muscular coat, present data indicate that distension of the external urethral sphincter reflexly activates urethral contractions, possibly through a local mechanism.

Anesthesia↗
PubMed1979

Further observation on the denervation supersensitivity of the urethra in patients with chronic neurogenic bladders.

The response of the urethra in patients with chronic neurogenic bladders to autonomic stimulation was investigated by urethral pressure profile. A consistent supersensitivity to alpha-adrenergic stimulation was documented. Experiments with various autonomic blocking drugs confirmed that this response is alpha-adrenergically mediated via the short neuron system. The results appear to offer pharmacological evidence for the recently evolving intricate innervation pattern of the urethra including its distal portion, where the alpha-adrenergic system is believed to be important.

Adrenergic Agonists↗
PubMed1977

Complications of autonomic dysreflexia.

Autonomic dysreflexia can be a life-threatening problem if not promptly recognized and treated. Since the most common cause is bladder distension it is essential that the urologist be familiar with this syndrome. Several patients with serious complications owing to autonomic dysreflexia, including 1 mortality, are presented. The complications of autonomic dysreflexia result from a sudden marked rise in blood pressure, which may be severe enough to rupture single or multiple cerebral blood vessels or lead to a considerable increase in intracranial pressure. The neurophysiology, clinical features and therapeutic measures are discussed.

Adolescent↗
PubMed1999

Altered baroreflex control of heart rate in bradykinin B2-receptor knockout mice.

Recently, we have shown that a knockout mouse strain lacking the bradykinin B2-receptor gene exhibits an accelerated heart rate (HR) under basal conditions, this alteration being associated with mildly elevated blood pressure (BP) levels and ultimately with the development of cardiomyopathy. The goal of the present study was to determine whether genetic disruption of the B2-receptor alters autonomic cardiovascular reflexes to acute or chronic changes in BP. The direct mean BP and HR levels of unrestrained B2 knockout mice (B2-/-) were higher than those of wild type (B2+/+) controls (131 +/- 2 vs. 105 +/- 2 mm Hg and 480 +/- 5 vs. 414 +/- 8 beats/min, P < 0.01 for both comparisons). The difference in HR observed between groups under basal conditions was nullified by the acute administration of propranolol and atropine as well as by hexamethonium; it was attenuated by long-term blockade of angiotensin AT1 receptors. In B2-/- mice, the presence of an alteration in baroreceptor regulation of HR was supported by a reduced gain in the HR responses to acute nitroprusside-induced hypotension or phenylephrine-induced hypertension (slope of the regression line: 0.82 +/- 0.07 vs. 5.58 +/- 0.08 beats/min per mmHg in B2+/+, P < 0.01), as well as by an exaggerated tachycardic response to chronic hypertension induced by clipping of the left renal artery (60 +/- 3 vs. 15 +/- 3 beats/min in B2+/+, P < 0.01). Our findings indicate that disruption of the bradykinin B2-receptor gene is associated with an impaired baroreflex control of HR. The combination of chronically elevated resting HR and impaired baroreflex control could contribute to the development of cardiomyopathy in these animals.

Anesthetics↗
PubMed2000

Compensatory vasoconstrictor effects of sodium pentobarbital on the hindquarters of conscious normotensive control and lumbar-sympathectomized Wistar rats.

The aim of this study was to compare the vasoconstrictor effect of sodium pentobarbital on the hindquarter resistance of intact control Wistar rats with the effect on lumbar-sympathectomized rats. For this purpose, mean arterial pressure (MAP) and hindquarter (supplied terminal aorta) flow (HQF) were simultaneously measured in these conscious rats with an arterial in dwelling cannula and electromagnetic flow probe implanted around the terminal aorta. Hindquarter resistance (HQR) was calculated as MAP divided by HQF. In the intact control conscious rats, subsequent pentobarbital anesthesia (30 mg/kg, i.v.) caused an increase in HQR (+43.5 +/- 7.4%, mean +/- S.E.M.) and a decrease in MAP (-17.0 +/- 3.2%). After pentobarbital anesthesia, subsequent ganglionic blockade with hexamethonium bromide (C6; 25 mg, i.v.) induced a significant decrease in HQR (-30.9 +/- 3.0%) with a further lowering of MAP (-20.9 +/- 1.6%). However, in rats not anesthetized with sodium pentobarbital, C6 alone induced almost no change in HQR (-3.4 +/- 5.3%), even when MAP was lowered (-24.2 +/- 2.5%). In the lumbar-sympathectomized rats, pentobarbital anesthesia produced almost no change in HQR (-11.7 +/- 4.4%), although MAP decreased significantly (-24.3 +/- 2.2%). These findings suggest that: (1) sodium pentobarbital anesthesia newly generates a compensatory vasoconstrictor tone in the hindquarters acting against the depressor effect, and (2) the vasocompensator tone is controlled by the efferent fibers, including those in the lumbar sympathetic nerves.

Anesthesia↗
PubMed1997

Effect of byakko-ka-ninjin-to on the efferent activity of the autonomic nerve fibers innervating the sublingual gland of the rat.

The effect of intraduodenal infusion of Byakko-ka-ninjin-to (BN) on the efferent activity of the autonomic outflow to the sublingual gland was observed in the anesthetized rat. Intraduodenal infusion of BN (50-200 mg/kg) resulted in a dose-related increase in efferent activity. The enhancement of the nerve activity following administration of 200 mg/kg BN lasted longer than three hours. It was observed that the suppressive effect on efferent activity due to i.v. administration of hypertonic saline was antagonized by intraduodenal infusion of BN. From these observations it is suggested that Byakko-ka-ninjin-to acts as a facilitatory agent on salivary secretion.

Adrenergic alpha-Agonists↗
PubMed1997

In vitro characterisation of intramural neural pathways between the duodenum and the sphincter of Oddi of the brush-tailed possum.

The aims of this study were to determine if neural pathways between the duodenum and sphincter of Oddi are intramural, activated by duodenal electrical field stimulation (EFS) in vitro, and contain capsaicin-sensitive primary afferents. The possible involvement of cholinergic (muscarinic and/or nicotinic) and adrenergic receptors in these pathways were also investigated. Duodenal EFS (5-60 Hz, 70 V, 0.5 ms duration, 10 s train) at sites 2 cm oral and 2 cm anal to the sphincter of Oddi-duodenal junction produced frequency-dependent excitatory responses in the sphincter of Oddi, measured by manometry (n = 3). Excitatory responses from duodenal circular muscle were also evident. Tetrodotoxin (1 microM; n = 7) pretreatment abolished both sphincter of Oddi and duodenal responses to duodenal EFS. Crushing the duodenum between the site of stimulation and the sphincter of Oddi-duodenal junction also abolished sphincter of Oddi response. The sphincter of Oddi responses to duodenal EFS at the oral and anal sites were reduced by pretreatment with (i) atropine (100 nM: n = 7) to 19 +/- 6% (P < 0.05) and 22 +/- 8% (P < 0.05) of control respectively. (ii) hexamethonium (100 microM: n = 9) to 10 +/- 2% (P < 0.01) and 6.0 + 2.5% (P < 0.01) of control respectively and (iii) guanethidine (1 microM; n = 6) to 75 +/- 6% (P < 0.05) and 78 +/- 10% (P < 0.05) of control, respectively. Combined pretreatment with phentolamine and propranolol (both 1 microM; n = 7) was without effect, as was capsaicin (1 microM; n = 12) pretreatment. Excitatory intramural pathways between the sphincter of Oddi and the duodenum are primarily cholinergic in nature and contain an adrenergic component. Capsaicin-sensitive primary afferents are not involved.

Adrenergic Agents↗