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Results for “Ganglionic Blockers”

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At least 19 recordsLinked to original sources
PubMed2002

[Ganglionic blockers in abdominal surgery: facts and hypotheses. 2.Clinical, pathophysiological and pharmacological aspects of ganglionic blocker use].

The authors discuss facts and hypotheses on the effects of benzohexonium upon the motor activity of the intestine and the significance of N-cholinolytics for prophylactics and treatment of postoperative pareses of the gastrointestinal tract. The ganglioblockers possess antistress effect, reduce the degree of pathological vegetative reactions and facilitate realization of the mechanisms of selfregulation of functions of the small and large intestine. Using benzohexonium during operation and in the first days after it makes the intestinal pareses less frequent. N-cholinolytics however do not have a considerable stimulating influence on the contracting activity of the gastrointestinal tract that accounts for their not high effectiveness in treatment of early functional motor evacuatory disorders. The points of action of gangliolytics, those at the level of the intestinal wall included, can not be considered to be completely established, as well as the mechanisms of their indirect effect. The ganglionic blockade should be considered as the basic method of prophylactics of the postoperative paresis of the intestine.

Abdomen↗
PubMed1996

Use of ganglionic blockers to assess neurogenic pressor activity in conscious rats.

The present study was conducted to develop a standardized ganglionic blockade protocol to assess neurogenic pressor activity in conscious rats. Rats were instrumented with arterial and venous catheters for measurement of arterial pressure and heart rate and for administration of three different ganglionic blockers (trimethaphan, hexamethonium, and chlorisondamine). To investigate the role of the pressor hormones angiotensin II (AII) and arginine vasopressin (AVP) in modulating the cardiovascular responses to ganglionic blockade, we also administered ganglionic blockers to rats pretreated with AVP and AII receptor antagonists. The peak depressor responses to trimethaphan (20 mg/kg; -45 +/- 2 mm Hg), hexamethonium (20 mg/kg; -44 +/- 2 mm Hg), and chlorisondamine (2.5 mg/kg; -47 +/- 3 mm Hg) were not different from each other. With trimethaphan, there was a significantly enhanced peak depressor response after blockade of AT1/V1 receptors (-45 +/- 2 vs -59 +/- 2 mm Hg). No significant differences were observed for hexamethonium or chlorisondamine after hormonal blockade (-44 +/- 2 vs. -46 +/- 3 and -47 +/- 3 vs -48 +/- 4 mm Hg, respectively). These observations suggest that, for hexamethonium and chlorisondamine, the peak depressor response to ganglionic blockade is a consistent measure of neurogenic pressor activity in the conscious rat. This response is not influenced by circulating AII or AVP. On the other hand, trimethaphan should be used carefully due to its complex interactions with other systems, particularly under conditions in which AVP or AII may be altered.

Analysis of Variance↗
PubMed2000

Non-effect of hexamethonium, a ganglionic blocker, on the response of ileal apolipoprotein A-IV mRNA following a massive small bowel resection in rats.

An intravenous infusion of hexamethonium, a ganglionic blocker, did not affect the increase in the apolipoprotein A-IV mRNA level in the residual ileum following a massive small bowel resection in unrestrained conscious rats. The result suggests that upregulation of the apolipoprotein A-IV gene in the residual ileum is not mediated by a neural pathway, including the nicotinic synapse route.

Animals↗
PubMed1997

Inhibitory effect of capsaicin on detrusor contractility: further study in the presence of ganglionic blocker and neurokinin receptor antagonist in the rat urinary bladder.

In order to understand the mechanisms by which capsaicin at high concentrations affects the micturition reflex and detrusor contractility, in vivo and in vitro whole bladder studies were conducted using ganglionic blockers and a neurokinin receptor antagonist. Thirty-eight adult rats were divided into control (normal saline cystometry) and experimental (1,000 microM capsaicin cystometry) groups. Both groups were subdivided to receive pretreatment with intravesical hexamethonium, perivesical hexamethonium, or intravesical spantide ([D-Arg1, D-Trp7,9, Leu11]-substance P). After in vivo cystometry, the bladders were removed and in vitro whole bladder contractility studies using electrical field stimulation as well as bethanechol and KCl stimulations were performed. In the bladders pretreated with perivesical hexamethonium, the amplitudes of contractions and in vitro detrusor contractility under electrical stimulation were decreased. Other bladder preparations showed no significant differences from the controls. However, when 1,000 microM capsaicin was infused into the bladders, both control and experimental bladders showed an initial excitation and a final inhibition with an elevated basal intravesical pressure and retention. Capsaicin at 100 microM did not have this effect. The results of this study conclude that blockage of perivesical ganglia or neurokinin receptors in the submucosa did not influence the depressant effects of 1,000 microM capsaicin on the micturition reflex and detrusor contractility in rats. Nonspecific toxic effects on detrusor muscle or nerves is likely when intravesical high-concentration capsaicin is administered.

Administration, Intravesical↗
PubMed1993

Chlorisondamine, a non-competitive ganglionic blocker, antagonizes the cardiovascular effects of cocaine in conscious squirrel monkeys.

Cocaine (0.3 mg/kg i.v.) produced prolonged pressor and tachycardiac responses in conscious squirrel monkeys. Peak pressor and tachycardiac responses following cocaine were 32.7 +/- 3.3 mm Hg and 78.8 +/- 7.4 beats/min, respectively. Pretreatment with 1 mg/kg chlorisondamine, a noncompetitive ganglionic blocker, attenuated the pressor (18.3 +/- 3.8 mm Hg) and tachycardiac (63.7 +/- 10 beats/min) effects of cocaine, while 5 mg/kg chlorisondamine completely prevented these effects of cocaine. This finding supports the conclusion that the cardiovascular effects of cocaine are centrally mediated.

Animals↗