PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PENTOLINIUM TARTRATE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1991

Hyperperfusion and enhanced metabolic state of the brain during sudden lowering of the cutaneous temperature in rats.

Forty-eight anesthetized and artificially ventilated rats were pretreated with the ganglion blocking agent, pentolinium (5 mg/kg, i.v.), followed by continuous phenylephrine infusion for maintenance of normotension. The rats were subjected to mock treatment (16 rats), to sudden exposure to thermoneutral water (34-36 degrees C, 16 rats), or to cold water (16 degrees C, 16 rats). The latter treatment lowered the cutaneous temperature to 25-30 degrees C. Neither one of these treatments produced any significant changes in arterial pressure or heart rate. Exposure to cold elicited hyperperfusion (microsphere method) in each of the brain regions studied. The increase in cerebral cortical blood flow (by 59 +/- 8%, mean +/- SEM) was most significant. The cerebral cortical metabolic rate for oxygen was increased by 46 +/- 10%. During the cold exposure, excellent tight coupling between the metabolic rate and blood flow was observed in the cerebral cortex. Mock treatment and exposure to thermoneutral water resulted in only trivial increases in blood flow and in metabolic rate. Thus, during cold exposure, an enhanced metabolic state of the brain represented the primary determinant increasing the brain blood flow, provided that normotension was maintained.

Animals↗
PubMed1992

Chronic central administration of enalaprilat lowers blood pressure in stroke-prone spontaneously hypertensive rats.

Earlier studies on the cardiovascular effects of intracerebroventricular (i.c.v.) administration of angiotensin converting enzyme (ACE) inhibitors implicate angiotensin II (AII) present in the central nervous system in the pathogenesis of hypertension. We have now examined whether central AII contributes to the maintenance of established hypertension in adult stroke-prone spontaneously hypertensive rats (SHRSP). The ACE inhibitor, enalaprilat, was infused i.c.v. for two weeks at a rate of 5 micrograms/h via osmotic minipumps. Control rats were either untreated or infused with saline. Mean arterial pressure (MAP), measured via an indwelling catheter, fell within 24 h in the enalaprilat-treated rats and remained at least 30 mmHg lower than in controls. This difference persisted after intravenous (i.v.) administration of a vasopressin (AVP) antagonist but was eliminated by subsequent ganglion blockade with i.v. pentolinium. Without prior administration of the AVP antagonist, however, the reductions of MAP after pentolinium were smaller. The reduction was still attenuated in treated rats compared with controls but there was a significant difference in the residual MAP. Circulating catecholamine levels were reduced by central ACE inhibition. However, pressor responsiveness to i.v. phenylephrine was unaffected. The results suggest that, in SHRSP, central ACE inhibition lowers blood pressure by reducing sympathetic outflow, implying that central AII has a tonic sympathoexcitatory effect in this strain.

Animals↗
PubMedDate not supplied

Epicardial application of bradykinin elicits pressor effects and tachycardia in guinea pigs. Possible mechanisms.

Topical application of bradykinin (BK) to the surface of the left ventricle (epicardial application) of anesthetized guinea pigs elicited dose-dependent pressor effects and tachycardia. The pressor effect of epicardial BK was reduced by prior systemic treatment of animals with pentolinium or a combination of phentolamine and propranolol, but it was not affected by acute bilateral vagotomy or systemic administration of atropine, indomethacin, naloxone or a combination of mepyramine and cimetidine. The tachycardia caused by epicardial BK was not affected by any of the aforementioned drugs or by section of the vagi. Both the pressor effect and tachycardia evoked by epicardial BK were abolished by prior epicardial application of lidocaine, a local anesthetic, or by chronic systemic capsaicin treatment. These results suggest that the pressor effect of epicardial BK is partially reflex in nature and likely to result from the stimulation by BK of cardiac sympathetic, capsaicin-sensitive primary afferents, whereas the tachycardia caused by epicardial BK could be mediated by an intracardiac release of (a) cardioaccelerating substance(s) from cardiac, capsaicin-sensitive sensory nerve fibers and/or terminals.

Animals↗
PubMedDate not supplied

Local application of neurotensin to abdominal organs triggers cardiovascular reflexes in guinea pigs: possible mechanisms.

Intraabdominal (IAB) injections or topical application of neurotensin (NT) to the serosal surface of the ileum or stomach evoked dose-dependent increases of blood pressure and of heart rate in anesthetized guinea pigs. These effects were markedly reduced by prior animal treatment with a ganglion blocker, alpha and beta adrenoceptor blockers, as well as by exposure of the abdominal organs to lidocaine, a local anesthetic. The blood pressure and heart rate responses to IAB injections or topical application of NT to the ileum or stomach were both inhibited by animal pretreatment with capsaicin. Cervical vagotomy or atropine pretreatment did not prevent or alter the cardiovascular responses to IAB injections of NT. These results suggest the presence in some organs and/or tissues of the abdominal cavity of sympathetic, capsaicin-sensitive sensory nerve fibers which, upon stimulation by NT, produce reflex increases of blood pressure and of heart rate.

Administration, Topical↗
PubMedDate not supplied

Capsaicin-sensitive primary afferents are involved in the hypotensive effect of neurotensin in ganglion-blocked guinea pigs.

The mechanism of the blood pressure (BP)-lowering effect of neurotensin (NT) in the anesthetized, ganglion-blocked guinea pigs was further examined using animals in which the basal BP was artificially raised by an IV infusion of noradrenaline (NA) to overcome the BP-lowering effect of the anesthesia as well as of the ganglion blocker. The animals were also vagotomized and given atropine at the beginning of the experiments to prevent potential baroreceptor-mediated vagal reflexes and/or activation of muscarinic receptors by endogenous acetylcholine. Under these experimental conditions, the IV bolus injections of NT as well as of capsaicin (a reference drug) produced dose-dependent hypotensive effects and variable levels of tachycardia. Omitting the ganglion blocker from the animal drug regimen attenuated but did not abolish the BP-lowering effect of NT and of capsaicin. Neither the hypotensive nor the tachycardic effects of NT and of capsaicin in ganglion-blocked guinea pigs were affected by prior animal treatment with propranolol (a beta adrenoceptor blocker), antihistaminics (mepyramine, cimetidine) or indomethacin (a cyclooxygenase inhibitor). Morphine was found to slightly reduced the hypotensive effect of NT without altering its slight tachycardic effect. Both the hypotensive and tachycardic effects of NT and of capsaicin, in contrast to those elicited by substance P (SP) and calcitonin gene-related peptide (CGRP), were inhibited in ganglion-blocked guinea pigs pretreated four days previously with capsaicin.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1986

Neonatal treatment with capsaicin influences hormonal regulation of blood pressure in adult, water-deprived Long-Evans but not Brattleboro rats.

Conscious, adult, water-deprived Brattleboro rats treated neonatally with capsaicin or vehicle showed similar hypotensive responses to sequential inhibition of the renin-angiotensin system (with captopril) and antagonism of ganglionic transmission (with pentolinium). Following a comparable experimental protocol, Long-Evans rats treated neonatally with capsaicin showed a more marked hypotensive response to captopril administration than did vehicle-injected animals. Furthermore, following administration of captopril and pentolinium, the capsaicin-treated animals showed marked impairment of the vasopressin-dependent recovery of blood pressure. These results indicate that the greater hypotensive response to captopril in water-deprived. Long-Evans rats treated neonatally with capsaicin may be due to less effective compensation for inhibition of the renin-angiotensin system when vasopressin release is impaired.

Animals↗
PubMed2003

The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure.

We investigated the role of renal sympathetic nervous system in the progression of ischemia/reperfusion-induced acute renal failure in rats. Acute renal failure was induced by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after the contralateral nephrectomy. Renal venous plasma norepinephrine concentrations markedly and significantly increased immediately after reperfusion, thereafter, the increased level declined but remained higher even at 24 h after reperfusion. Renal sympathetic nerve activity was significantly augmented during the renal ischemia. Renal denervation or the administration of pentolinium, a ganglion blocking agent, (5 mg/kg i.v.) at 5 min before ischemia attenuated the ischemia/reperfusion-induced renal dysfunction and histological damage, such as proteinaceous casts in tubuli and tubular necrosis. The elevation of renal venous norepinephrine levels after reperfusion was suppressed by renal denervation or pentolinium treatment. Thus, a surgical or pharmacological blockade of renal sympathetic nerve prevents the progression of ischemia/reperfusion-induced acute renal failure, thereby suggesting that renal sympathetic nervous system plays an important role in the development of the ischemic acute renal failure.

Acute Kidney Injury↗
PubMed2004

Fenfluramine-induced hypothermia is associated with cutaneous dilation in conscious rats.

The antiobesity agent, fenfluramine, produces hypothermia in rodents by an, as yet, uncharacterized mechanism. The present study was conducted in conscious rats to determine if fenfluramine-induced hypothermia was associated with cutaneous dilation. In animals maintained at 16 degrees C, core body temperature (T(CORE)) was measured telemetrically, and tail surface temperature was monitored with thermocouples fixed to the tail (T(TAIL)). D-Fenfluramine (10 mg/kg ip) produced a rapid increase in T(TAIL) of 7.7+/-0.4 degrees C (P<.001) and a decline in T(CORE) of 4+/-0.3 degrees C (P<.001). Two findings indicate that the increase in T(TAIL) was due to the withdrawal of a sympathetic vasoconstrictor tone. First, pretreatment with the ganglionic blocker, pentolinium, prevented fenfluramine-induced changes in T(TAIL). Second, when sympathetic tone to the tail was physiologically withdrawn by increasing the environmental temperature to 28 degrees C, fenfluramine treatment produced no increase in T(TAIL). Moreover, the effects of fenfluramine on T(TAIL) and T(CORE) depended on the uptake of fenfluramine into serotonergic neurons because these effects were markedly attenuated by pretreatment with the selective serotonin re-uptake inhibitor, fluoxetine. The hypothermic effect of fenfluramine occurred despite the fact that total body oxygen consumption increased by 20%. The results suggest that heat loss due to the dilation of the cutaneous circulation contributes to fenfluramine-induced hypothermia.

Animals↗
PubMed1976

Pentolinium in the management of autonomic hyperreflexia.

Patients with high spinal cord injuries frequently will develop a syndrome of autonomic hyperreflexia when stimulated by urological instrumentation. Severe sustained hypertension is the most hazardous component encountered during this reaction. Herein we report a series of patients exhibiting this condition who were managed safely and successfully by the use of the ganglionic blocking agent, pentolinium.

Adolescent↗
PubMed1988

Demonstration of a depressor substance in serum from CCl4 treated rats.

Previous studies have shown that blood pressure was reduced in rat experimental hypertension following a series of carbon tetrachloride (CCl4) injections. To define this effect more precisely the presently reported experiments were done. Serum from rats treated with CCl4 was injected into various recipients. The mean systolic blood pressure of renal hypertensive recipients decreased significantly at 60 minutes by -15 mm Hg. In normotensive and spontaneous hypertensive rat recipients the pressure did not fall. It is concluded that a vasodepressor substance appears in the serum of CCl4 treated rats which affects only renal hypertensive recipients.

Animals↗
PubMed2002

Sympathetic activation by fenfluramine depletes brown adipose tissue norepinephrine content in rats.

The antiobesity agent fenfluramine (FEN) has been reported to produce an activation of sympathetic neurons to brown adipose tissue (BAT) resulting in thermogenesis. The present study was conducted to determine if FEN-induced activation of BAT is affected by the ambient temperature at which animals are maintained. Body temperature was determined in conscious male Sprague-Dawley rats using implanted temperature transmitters, and sympathetic activation of BAT was determined by measuring norepinephrine (NE) content. Animals maintained at 22 and 4 degrees C incurred a significant decline in core body temperature following FEN administration. FEN produced a significant depletion of BAT NE content, and the magnitude of BAT NE depletion was related to the dose of FEN (-57.4% at 3 mg/kg dose and -75.9% at 10 mg/kg dose). However, the extent of BAT NE depletion was equal at 22 and 4 degrees C. BAT NE depletion by FEN appears to depend on activation of sympathetic neurons because it was prevented by pretreatment with the ganglionic blocker pentolinium (10 mg/kg ip). Furthermore, NE depletion by FEN could be blocked with fluoxetine (10 mg/kg ip) pretreatment, indicating that the action of FEN is mediated through the release of serotonin.

Adipose Tissue↗
PubMed1981

Increased sensitivity and accuracy of phaeochromocytoma diagnosis achieved by use of plasma-adrenaline estimations and a pentolinium-suppression test.

26 patients with suspected phaeochromocytoma underwent selective venous sampling: a tumour was identified and removed in 18.4 of these patients did not have sustained hypertension, and the only persistent abnormality was an elevated plasma-adrenaline level. The increased plasma-catecholamine concentrations in the tumour patients were not suppressed by pentolinium 2.5 mg i.v., whereas the levels in the 8 non-tumour patients were lowered to the normal range. Calculations based on the arteriovenous differences of adrenaline and noradrenaline suggest that adrenal medullary secretion contributed less than 2% of circulating noradrenaline in the non-tumour patients. Plasma-adrenaline, however, is derived almost entirely from the adrenal gland, and its estimation appears superior to that of noradrenaline in the detection of a small adrenal phaeochromocytoma.

Adrenal Gland Neoplasms↗