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At least 37 records · Page 2Linked to original sources
PubMed1983

The effects of pentolinium on sympathetic activity in hypertensives and normotensive controls.

The effects of pentolinium tartrate 2.5 mg i.v. on blood pressure, heart rate and plasma noradrenaline and adrenaline concentrations were studied in 21 hypertensives and in 20 normal controls. Mean basal catecholamine concentrations and the extent of their suppression by pentolinium were similar in both groups. The reductions in both plasma catecholamine levels correlated with the prepentolinium values. Supine systolic blood pressure was significantly reduced and there was a small increase in heart rate. These data support the use of plasma noradrenaline as an index of sympathetic activity but are inconsistent with the hypothesis that essential hypertension is associated with hyperactivity of the sympathetic nervous system.

Adult↗
PubMed1979

Pentolinium for control of reflex hypertension in spinal cord injured patients.

Ganglioplegia was produced by intravenous infusion of pentolinium tartrate 5 mg to control reflex hypertension in 29 patients with chronic spinal cord injuries undergoing 32 elective surgical procedures. The patient group with lesions above the first thoracic segment (T1) demonstrated significant but moderate intraoperative elevation of both systolic and diastolic pressure whether pentolinium was given prior to or during surgical stimulation. Patients with lesions below T1 had no significant pressure elevations with either mode of therapy. Pentolinium ganglioplegia can safely maintain blood pressure within reasonable limits in these patients; some increase in dosage may be required in patients with lesions above T1.

Adolescent↗
PubMed1979

Neurogenic activity--angiotensin II interaction during the development and maintenance of renal hypertension in the rat.

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.

Angiotensin II↗
PubMed1989

Effect of ganglionic stimulating and blocking agents on the fast components of colonic myoelectrical activity in the rat.

The presence of two types of fast myoelectrical activities, medium fast activity and fast activity, has been demonstrated previously in the electromyogram of colon in normal children and in the rat by the authors. An absence of medium fast activity in Hirschsprung's disease and in experimental aganglionosis of colon in the rat has also been described. In the present study the fast components of colonic myoelectrical activity were analysed during the procedures affecting ganglionic transmission. It was observed that ganglionic stimulants, such as balloon inflation, and intra-arterial injections of acetylcholine and small amounts of nicotine, increased the spike activity and the frequency of medium fast activity without affecting fast activity. The intra-arterial injections of ganglionic blocking agents, such as nicotine in large amounts and pentolinium tartrate, completely abolished the medium fast activity. These observations suggest that the ganglionic activity is responsible for the genesis of medium fast activity and that the absence of cholinergic ganglionic transmission is the most important single factor for the reported altered electromyogram pattern in aganglionosis.

Acetylcholine↗
PubMed1989

Blood pressure elevation caused by inhibition of brain glutathione reductase.

The effect of brain glutathione reductase activity on blood pressure regulation was investigated. The intravenous administration of the glutathione reductase inhibitor, nitrofurantoin (0.1-0.3 mg/rat), to seven normotensive Wistar rats caused dose-dependent rises in blood pressure and the heart rate (delta mean blood pressure 17 +/- 1 mmHg; delta heart rate 89 +/- 7 beats/min for 0.3 mg). Rats treated with 0.3 mg nitrofurantoin showed a 50% decrease in glutathione reductase activity with a twofold increase in the ratio of glutathione disulphide to reduced glutathione in the hypothalamus and brainstem, and a 1.5-fold increase in plasma noradrenaline and plasma renin activity compared with controls. These nitrofurantoin-induced effects were totally abolished by pretreatment with a sympathetic ganglion blocker (4 mg pentolinium tartrate, administered subcutaneously) except for the increased ratio of glutathione disulphide to reduced glutathione and the decreased glutathione reductase activity in the brain. These results suggest that the blood pressure elevation caused by inhibition of brain glutathione reductase activity occurs through activation of the sympathetic nervous system and the renin-angiotensin system.

Animals↗
PubMed1977

Anaesthesia with profound hypotension for middle ear surgery.

To produce a blood-free field for middle ear surgery performed with the operating microscope, the arterial systolic pressure was reduced to less than 50 mm Hg in 700 patients by means of thiopentone-halothane-nitrous oxide in oxygen anaesthesia together with pentolinium tartrate. In 84% the results were excellent, in 12% moderately good and they were poor in 4%. There were more unsatisfactory results in males (22.8%) than in females (11.4%). In spite of the arterial pressure being reduced to very low values in many instances, there was no mortality or morbidity which could be ascribed to the technique.

Adult↗
PubMed1981

Effect of chemical sympathectomy and ganglion blockade on angiotensin-stimulated fluid absorption in the rat jejunum.

A study has been made of the effects of chemical sympathectomy and ganglion blockade on the responses of rat jejunum in vivo to intravenous doses of angiotension and noradrenaline capable of stimulating fluid transport. Pretreatment with 6-hydroxydopamine (chemical sympathectomy) or pentolinium tartrate (ganglion blockade) abolished the stimulatory actions of angiotensin II but left the responses to noradrenaline unimpaired. Dopamine, like noradrenaline, stimulated fluid transport but this response required very high dopamine infusion rates, was refractory to the dopamine antagonist sulpiride and was inhibited by the alpha- blocker phentolamine. The possible interaction between angiotensin and the intestinal sympathetics is discussed with reference to control in extracellular fluid volume.

Angiotensin II↗
PubMed1967

Cardiac sympathetic adrenergic pathways in which synaptic transmission is blocked by atropine sulfate.

1. Stimulation of the thoracic sympathetic nerve trunk caused a rise in arterial blood pressure and heart rate which was reduced but not abolished during the infusion of hexamethonium chloride, pentolinium tartrate, mecamylamine or tetraethylammonium chloride.2. Preganglionic stimulation no longer elicited a synchronous sC elevation in the post-ganglionic nerves. The persistent blood pressure and heart rate response was associated with an asynchronous discharge in these nerves.3. Both the persistent response and the asynchronous discharge were abolished by the intravenous injection of atropine sulphate in doses of 30 mug/kg.4. Atropine had no effect on spike amplitude or shape, conduction velocity or frequency response in either the pre- or post-ganglionic nerve trunks. Nor did it affect the rise in blood pressure and heart rate evoked by stimulation of the post-ganglionic cardiac sympathetic nerves.5. It is concluded that atropine partially blocked synaptic transmission in cardiac sympathetic adrenergic pathways.

Animals↗
PubMed1990

Ganglion-blocking agents enhance neurally mediated bronchoconstriction in the guinea-pig: possible role of sensory neuropeptides.

The effect of ganglion blockade by hexamethonium bromide (0.1-100 mumol.kg-1) and pentolinium tartrate (0.01-3 mumol.kg-1) on the bronchoconstriction induced by vagal nerve stimulation (15 Hz, 0.2 ms, 3 s, 7-20 V) was evaluated in the anaesthetized guinea-pig. Both ganglion-blocking agents potentiated this response dose dependently. When the neural bronchoconstriction was suppressed by atropine, hexamethonium restored this response dose dependently. Hexamethonium produced inhibitory effects on vagally induced bronchoconstriction in capsaicin-desensitized and in propranolol- or reserpine-pretreated guinea-pigs. Propranolol (0.03-3 mumol.kg-1) produced a marked dose-dependent increase of neural bronchoconstriction (which was markedly reduced, about 10 times) in capsaicin-desensitized animals. Our results show that ganglion-blocking agents potentiate neural bronchoconstriction in the guinea-pig and that sensory neuropeptides may have a role in this effect. Moreover, beta-adrenergic modulation of the release of neuropeptides from vagal sensory fibers is suggested.

Anesthesia↗
PubMed1986

[Effect of ganglionic blockade and subsequent i.v. infusion of catecholamines and angiotensin II on the formation and transport of lymph. Studies in anesthesized dogs and a review of the literature].

The effect of ganglionic blockade (GB) and subsequent i.v. infusion of adrenaline (AD), noradrenaline (NA), isoproterenol (IP), and angiotensin II (AII) on thoracic duct lymph flow (LF) and transcapillary escape rate of plasma proteins (FER) was studied in anaesthetized (Nembutal), paralyzed (pancuronium), and artificially ventilated dogs. The carotid artery, the external jugular vein, and the thoracic duct were cannulated. Following a control period, GB was performed by pentolinium tartrate and thereafter the other drugs were infused in a random sequence for 30-60 min with 1 h intervals. Mean arterial blood pressure was decreased from 125 to 90 mmHg by GB, it was increased by 36 mmHg by AD, 41 mmHg by NA, and 44 mmHg by AII, and was decreased by 27 mmHg by IP. LF was about 38 microliter/min/kg before GB and was not changed systematically by GB, because either the sympathetic tone was rather weak or the intrinsic contractions and the tone of lymphatics were reduced by GB. FER was not affected by GB. LF increased by 9 microliter/min/kg (control 36 microliter/min/kg) during AII infusion, probably due to increased lymph formation; the latter can be concluded from the 68% increase in FER. NA raised LF by 15 microliter/min/kg (control 44 microliter/min/kg) probably due to alpha-adrenergic stimulation of the intrinsic contractions of lymphatics; lymph formation seemed not to be affected because FER was not changed systematically. AD enhanced LF by 29 microliters/min/kg (control 39 microliters/min/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1980

Effect of converting enzyme inhibition on glucocorticoid hypertension in the rat.

The renin-angiotensin system was evaluated by inhibition of converting enzyme (CEI) and by testing sensitivity to angiotensin II (AII) in sodium-depleted rats made hypertensive by methylprednisolone (MP), 20 mg/kg im. During a 2-wk period blood pressure rose 38 +/- 4 mmHg (P less than 0.001) in MP and 3 +/- 4 mmHg in controls. After pentobarbital anesthesia, intra-arterial pressure and dose-response curves to AII were determined, before and after SQ14225 (d-3-mercapto-2-methylpropranoyl-l-proline) (1 mg/kg iv). CEI reduced pressure significantly in both MP and controls, although the decrease was smaller in the former (P less than 0.05). Pressor responses to AII were nearly identical in MP and controls and were enhanced to a similar extent by CEI. Ganglionic blockade with pentolinium tartrate, given after CEI, did reduce the pressure in both groups to equal levels. Responses to AII after pentolinium were similar to those obtained after CEI alone. These results indicate that the renin component of glucocorticoid hypertension during sodium deficiency is smaller than that of the normotensive controls. No evidence of glucocorticoid-induced vascular hypersensitivity to AII was detected in this model of experimental hypertension.

Angiotensin II↗
PubMedDate not supplied

Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoceptors are not involved.

The effect of i.v. ergonovine tartrate infusions (0.05-20 micrograms/kg/min, 12 minutes duration) on coronary arteries was studied in 14 conscious dogs instrumented to continuously measure vascular diameter by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Ergonovine induced a biphasic coronary response: small, transient dilation during the first minutes of infusion, followed by slowly developing constriction reaching its maximum 5 to 15 minutes after the end of the infusion and persisting at this level for at least 10 minutes. The threshold dosage for significant constriction was 0.05 microgram/kg/min. A dosage of 5 micrograms/kg/min (cumulative 60 micrograms/kg, corresponding to 35 micrograms/kg ergonovine maleate) caused a decline in mean left circumflex artery diameter by 137 +/- 15 micrometers (= 4.6%) without significantly altering heart rate, plasma catecholamines or plasma renin activity. Coronary venous O2 saturation did not decline, indicating the absence of coronary resistance vessel constriction. The epicardial artery constriction was not attenuated by a vasopressin antagonist. Under adrenergic blockade (2 mg/kg phentolamine and 2 mg/kg nadolol) or under ganglionic blockade (5 mg/kg pentolinium tartrate), ergonovine (5 micrograms/kg /min) caused substantial elevation in mean arterial pressure, while the decline in coronary artery diameter was attenuated. When this increase in arterial pressure was prevented by appropriate bleeding, the ergonovine-induced coronary constriction was not diminished by adrenergic or ganglionic blockade. The serotonin antagonist methysergide (0.5 mg/kg) completely abolished the ergonovine-induced coronary artery vasomotion. It is concluded that ergonovine in dogs causes an epicardial coronary artery constriction comparable to the diffuse coronary artery narrowing in men not suffering from variant angina pectoris. These constrictions are not mediated by an adrenergic mechanism.

Adrenergic beta-Antagonists↗
PubMed1997

Basal forebrain and cerebral cortical muscarinic receptors mediate increase in cortical blood flow provoked by periaqueductal gray matter.

The midbrain periaqueductal gray matter has been identified as a reflex centre located uppermost in the central organization of diverse defensive reactions. We recently found that when activated, the caudal third of the lateral periaqueductal gray was also capable of provoking a marked increase in cortical blood flow. The response may be the combined outcome of a flow increase of nitrergic origin and that coupled to a possible concomitant cortical activation. In the present study, we attempted to clarify the neural substrates for mediation of the increase in flow (observed by laser-Doppler flowmetry), in 49 anaesthetized, artificially ventilated, and cervically cordotomized rats. The flow increase provoked by stimulation of the particular subdivision of the periaqueductal gray with N-methyl-D-aspartate (1 mM, 100 nl) was unaffected by i.v. pentolinium tartrate (10 mg/kg), suggesting little contribution by the cerebrovasodilator parasympathetic nervous system to the response. The response was abolished by i.v. or topical cortical administration of scopolamine hydrobromide (3.16 mg/kg or 1.0 mM, respectively). Placement of bilateral lesions in the basal forebrain with alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (15 mM) impaired the cortical choline acetyltransferase activity and attenuated the flow response. Overall, we suggest that the cholinergic corticopetal neurons of the nucleus basalis of Meynert and cortical muscarinic receptors may form a principal efferent arm of a central circuitry emanating from the subdivision of the periaqueductal gray, in the mediation of the increase in cortical blood flow and possible cortical activation.

Animals↗
PubMed1987

Sensitivity of intestinal resistance vessels to vasopressin after ganglionic blockade in the conscious cat.

Superior mesenteric arterial flow, arterial pressure, and heart rate were recorded, and plasma arginine-vasopressin (AVP) concentration was measured, during intravenous infusions of AVP (0.1-8.1 mU X kg-1 X min-1) in conscious unrestrained cats under two experimental situations--when autonomic function remained intact and, on other days, when it had been impaired by pretreatment of the animals with the ganglionic blocking agent pentolinium tartrate (2.5 mg X kg-1 and 0.125 mg X kg-1 X min-1). The dose-related increases in the plasma concentrations of AVP attained during the infusions of the peptide were similar under the two experimental situations. The curve expressing the relationship between the dose of AVP and the decrease in superior mesenteric arterial conductance (ml X min-1 X kg-1 X mm Hg-1) for when ganglia were blocked was similar to the curve for when autonomic function remained intact. Elevations in the circulating levels of the peptide within the physiological range (less than 30 fmol X ml-1) were associated with significant decreases in conductance, both when ganglia were blocked and when they were intact. In contrast to conductance, the curve expressing the relationship between the dose of AVP and the increase in arterial pressure for when ganglia were blocked was displaced markedly to the left when compared with the curve for when reflexes remained intact, even though the effect of ganglion blockade on pressor responses did not reach statistical significance with the two lowest doses of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of morphine, H-Tyr-D-Arg-Phe-Lys-NH2 (DALDA) and B-HT920 on non-cholinergic nerve-mediated bronchoconstriction in pithed guinea-pigs.

1. Electrical stimulation (1 ms, 5 Hz, 80 V) for 5 or 15 s at the level of C4-T1 in the spinal canal of artificially respired pithed guinea-pigs (which had received intravenously (i.v.) (+)-tubocurarine chloride 2 mg kg-1, atropine sulphate 2 mg kg-1 and pentolinium tartrate 5 mg kg-1) caused constriction of airways, indicated by increased insufflation pressure. 2. This non-cholinergic constriction was inhibited by morphine (1-3 mg kg-1, i.v.), the peripherally acting mu-receptor agonist, H-Tyr-D-Arg-Phe-Lys-NH2 (DALDA, 0.1-1 mg kg-1, i.v.) or the alpha 2-adrenoceptor agonist B-HT920 (1-3 mg kg-1, i.v.). 3. The effects of either morphine (3 mg kg-1, i.v.) or DALDA (1 mg kg-1, i.v.) were inhibited by naloxone (3 mg kg-1, i.v.). Idazoxan (3 mg kg-1, i.v.) inhibited the anti-constrictor effect of B-HT920 (3 mg kg-1, i.v.), but not that of DALDA (0.1 mg kg-1, i.v.). 4. Thus activation of peripheral mu-opioid receptors or alpha 2-adrenoceptors inhibits airways constriction induced by non-cholinergic nerve stimulation in the pithed guinea-pig. This preparation therefore provides a further method for the in vivo examination of the effects of drugs on non-cholinergic tracheobronchial constrictor nerve function.

Adrenergic alpha-Agonists↗
PubMed1989

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses.

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Adrenocorticotropic Hormone↗
PubMed1979

Controlled hypotension and moderate haemodilution in major hip surgery.

This study presents a series of 38 patients in whom total hip replacement was performed by using a hypotensive anaesthetic technique with moderate haemodilution. 17 patients operated on during normotension without haemodilution served as controls. Halothane, d-tubocurarine and pentolinium tartrate were the agents used. During the operation circulation was monitored carefully. Hypotension with haemodilution decreased the amount of the transfused blood to 1/3, compared with the normotensive group. The bloodless field during the hypotension also shortened the duration of the operations. No complications attributable to the hypotensive technique occurred. The results suggest that the hypotensive anaesthetic technique with haemodilution reduces the need for blood transfusion in major surgery. However, only patients in good cardiovascular status are suitable for this technique, and careful monitoring of the circulation is mandatory during the anaesthesia.

Aged↗