SEARCH · PubMed Health

Results for “Ganglionic Blockers”

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 91 records · Page 5Linked to original sources

PubMed1987

Influence of neural blockages and proglumide on rat pancreatic enzyme secretion in response to intraluminal fatty acid.

Effects of neural blockages on pancreatic enzyme secretion in response to infusing fatty acid into the lumen were investigated using anesthetized rats, equipped with bile-pancreatic and duodenal cannulae, to evaluate the relative contribution of the neural and the hormonal mediations in the pancreatic response. Oleate (0.2 ml) was injected as a bolus into the rat duodenum, and the trypsin output in bile-pancreatic juice was monitored to determine the pancreatic enzyme secretion response with continuous return of bile-pancreatic juice to the intestine. When anticholinergic agents such as atropine sulfate and scopolamine were administrated, although basal level in pancreatic enzyme secretion fell, the increase of pancreatic enzyme secretion from basal level after stimulation by oleate was not significantly different from that of the control (no blockage). However, the ganglion blocker, hexamethonium, inhibited the pancreatic enzyme secretion in response to oleate by 94%. An adrenergic blocker, guanethidine, also led to as much of a decrease as the ganglion blocker-induced decrease. Adrenergic alpha- and beta-blockers partially, but not completely, inhibited the enzyme secretion. Adrenergic blockage also suppressed the basal level in pancreatic enzyme secretion. On the other hand, a specific CCK antagonist, proglumide, significantly inhibited pancreatic enzyme secretion induced by oleate in the presence of scopolamine. These observations suggest that pancreatic enzyme secretion in response to oleate is primarily mediated by CCK and that adrenergic modulation may play an important role in the CCK-mediated pancreatic enzyme secretion in response to oleate, although interpretation of these results may have some restriction related to anesthesia.

Adrenergic alpha-Antagonists↗

PubMed1987

Prescription patterns and costs of antihypertensive drugs in two outpatient clinics: Zürich (Switzerland) and Münster (FRG), 1975-1985.

In the present study the prescription patterns and cost of antihypertensive drugs in two outpatient clinics located in two different countries (Zürich, Switzerland, and Münster, FRG), were analyzed from 1975 till 1985 by using representative random samples of hypertensive outpatients. Throughout the observed period the leading positions were held by diuretics and beta-blockers, whereas central sympatholytics and ganglion blockers nearly disappeared. A rapid increase in the use of calcium antagonists occurred within the last 2 analyzed years. Drugs in fixed combination containing reserpin showed a constant decrease during the observed period, whereas beta-blocker-containing combination drugs increased in both clinics. The comparison between the two clinics revealed only minor differences in the prescription pattern of the various known classes of antihypertensive drugs. However, marked differences were observed within given classes between the preferred products. Both in Zürich and Münster the mean annual drug cost per patient doubled from 1975 to 1985. Especially during the last few years these changes took place with a remarkable rapidity, obviously the result of a more intense promotion of new antihypertensive drugs.

Adrenergic beta-Antagonists↗

PubMed2000

Intravenous infusion of hexamethonium and atropine but not propranolol diminishes apolipoprotein A-IV gene expression in rat ileum.

To clarify the role of neural factors in the regulation of apolipoprotein (apo) A-IV expression in the small intestine, we investigated the effect of neural blockers on mRNA levels of apo A-IV in rat small intestine. Either ganglionic blocker (hexamethonium), cholinergic blocker (atropine) or beta-adrenergic blocker (propranolol) was infused intravenously to unrestrained conscious rats for 8 h, and then total RNA was isolated from the small intestine and analyzed using Northern hybridization. Apo A-IV mRNA levels in the ileum were significantly lower in hexamethonium- or atropine-infused rats than in saline- (control) or propranolol-infused rats. Immunoblot analysis showed no difference in plasma apo A-IV concentrations between hexamethonium- and saline-infused groups. The lower mRNA levels of apo A-IV in the ileum of hexamethonium-infused rats were observed even in bile-drained rats, indicating that the lower expression was not due to any changes in bile availability. The ileal apo A-IV mRNA levels were significantly higher in rats infused with lipid emulsion into the ileum than in rats infused with glucose-saline, and the concomitant infusion of intravenous hexamethonium did not affect the higher levels of apo A-IV mRNA. These results suggest that the basal expression of the ileal A-IV gene is at least partially regulated in a site-specific manner by cholinergic neurons.

Adrenergic beta-Antagonists↗

PubMed1993

Depressor effect of intraventricular administration of calcium on spontaneously hypertensive rats.

The role of central Ca2+ in the regulation of blood pressure (BP) was investigated in conscious spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Ten microliters of a high Ca2+ solution (Ca2+: 32.6 mM) administered intracerebroventricularly (i.c.v.) decreased the mean arterial pressure (MAP) for more than 20 min in SHR (n = 7, P < 0.005), while no change of MAP was observed in the WKY (n = 6). This depressor response to Ca2+ i.c.v. was dose-dependent at Ca2+ concentrations between 16.3 and 65.2 mM. We also investigated the effect of high Ca2+ i.c.v. in SHR after pretreatment with Ca2+ channel blockers, diltiazem (60 micrograms/10 microliters) or nisoldipine (4, 8, 16 and 32 micrograms/10 microliters), administered i.c.v., the autonomic ganglion blocker, hexamethonium (50 mg/kg), administered i.v. and alpha-methyl-p-tyrosine (100 and 400 micrograms/10 microliters) delivered i.c.v. Pretreatment with i.c.v. diltiazem (n = 8) or nisoldipine (n = 5 for 8 micrograms, n = 6 for 4, 16, 32 micrograms) abolished and/or blunted the decrease of MAP due to high Ca2+. Hexamethonium administered i.v. (n = 6) also canceled the depressor action of i.c.v. Ca2+. Pretreatment with 100 micrograms of i.c.v. alpha-methyl-p-tyrosine could not prevent the depressor action of i.c.v. Ca2+; however, 400 micrograms of alpha-methyl-p-tyrosine administered i.c.v. abolished the effect of i.c.v. Ca2+. Furthermore Ca2+ channel blockers administered i.c.v. in themselves increased MAP in SHR (P < 0.05). These results suggest that central Ca2+ is involved in the central regulation of BP in SHR. This effect may be mediated through changes in sympathetic activity.

Animals↗

PubMed1992

Thermogenic, thermolytic and body temperature effects of fenfluramine, a 5-hydroxytryptamine agonist, in the domestic fowl (Gallus domesticus).

1. Intramuscular injection of the 5-HT agonist DL-fenfluramine increased the metabolic rate of mature cockerels by about 25% over the following 22 hr. The acute effect, over the 3 hr following injection, attained 40% at 10 degrees C, 35% at 20 degrees C and 25% at 32 degrees C. 2. Heat loss mechanisms (peripheral vasodilatation, postural change and panting) were also stimulated, to an extent which varied with ambient temperature. 3. Food intake, respiratory quotient and locomotor activity were significantly reduced by fenfluramine injection. 4. The opposing effects on heat production and heat loss had an influence on deep-body temperature which varied from a reduction of 0.5 degrees C at 10 degrees C ambient to an increase of about 0.5 degrees C at 32 degrees C. 5. The 5-HT blocker, methysergide, prevented the effects of fenfluramine on both heat production and heat loss for about 5 hr after injection. 6. The autonomic ganglion blocker, hexamethonium chloride, reduced the thermogenic but not the heat-loss effects of fenfluramine. 7. The results suggest that DL-fenfluramine has centrally-occurring but independent effects on heat production and a number of heat loss effectors, and that the heat production effect is mediated by the autonomic nervous system. The effect of fenfluramine on deep-body temperature appears to result from an altered equilibrium between heat production and heat loss.

Animals↗

PubMed2006

Increased sympathetic activity in rats submitted to chronic intermittent hypoxia.

Long-term exposure to intermittent hypoxia may lead to important cardiovascular dysfunctions, such as hypertension. Rodent models of chronic intermittent hypoxia (CIH) have been used to study the mechanisms underlying the increase in mean arterial pressure (MAP) observed after exposure to CIH. Several studies suggest that the hypertension of rats submitted to CIH is associated with an increase in sympathetic activity. However, there are no studies documenting the direct measurement of sympathetic activity in conscious freely moving rats exposed to CIH. Therefore, the present study aimed to evaluate whether or not the increase of MAP in rats exposed to CIH is associated with an increase in sympathetic activity. To reach this goal, we analysed the effect of ganglionic blockade on baseline MAP as well as the plasma levels of catecholamines. Rats submitted to CIH (fractional inspired O(2) of 6%, for 40 s in every 9 min, 8 h day(-1)) for 35 days (n = 31) exhibited a significant increase in MAP compared with control rats (n = 28) maintained under normoxia (112 +/- 2 versus 103 +/- 1 mmHg, P = 0.0003). The injection of the ganglionic blocker hexamethonium resulted in a similar fall in MAP in CIH and control groups (-46 +/- 2 versus -41 +/- 3 mmHg). However, hexamethonium after previous antagonism of the angiotensin II type 1 (AT(1)) receptors with losartan produced a larger decrease in MAP in the CIH than in the control group (-58 +/- 2 versus -50 +/- 2 mmHg, P = 0.0165). The injection of losartan itself produced no major changes in the baseline MAP in both groups. The measurement of plasma catecholamines showed an increase in plasma noradrenaline (10.12 +/- 0.90 versus 4.74 +/- 0.32 ng ml(-1), P = 0.0042) in rats exposed to CIH compared with control rats. These data provide strong evidence to support the concept that rats submitted to CIH exhibit an increase in sympathetic activity, which seems to be determinant in the maintenance of hypertension in this experimental model.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2006

Lack of involvement of the autonomic nervous system in early ventilatory and pulmonary vascular acclimatization to hypoxia in humans.

The activity within the autonomic nervous system may be altered following sustained exposure to hypoxia, and it is possible that this increase in activity underlies the early acclimatization of both ventilation and the pulmonary vasculature to hypoxia. To test this hypothesis, seven individuals were infused with the ganglionic blocker trimetaphan before and after an 8 h exposure to hypoxia. The short half-life of trimetaphan should ensure that the initial infusion does not affect acclimatization to the 8 h hypoxia exposure, and the use of a ganglion blocking agent should inhibit activity within all branches of the autonomic nervous system. During the infusions of trimetaphan, measurements of ventilation and echocardiographic assessments of pulmonary vascular tone (DeltaPmax) were made during euoxia and during a short period of isocapnic hypoxia. Subjects were also studied on two control days, when a saline infusion was substituted for trimetaphan. Trimetaphan had no effect on either euoxic ventilation or the sensitivity of ventilation to acute hypoxia. Trimetaphan significantly reduced DeltaPmax in euoxia (P<0.05), but had no significant effect on the sensitivity of DeltaPmax to acute hypoxia once changes in cardiac output had been controlled for. The 8 h period of hypoxia elevated euoxic ventilation (P<0.001) and DeltaPmax (P<0.001) and increased their sensitivities to acute hypoxia (P<0.001 for both), indicating that significant acclimatization had occurred. Trimetaphan had no effect on the acclimatization response of any of these variables. We conclude that altered autonomic activity following 8 h of hypoxia does not underlie the acclimatization observed in ventilation or pulmonary vascular tone.

Acclimatization↗

PubMed1994

Systemic hypertension induced by aortic cross-clamping: detrimental effects of direct smooth muscle relaxation compared with ganglionic blockade.

PURPOSE: Infrarenal aortic cross-clamping performed during vascular reconstructive procedures is often accompanied by systemic supraclamp hypertension. Much of the disease and death that attend aortic cross-clamping centers around hypertension. Many different strategies have been developed to attenuate intraoperative hypertension, and a host of pharmacologic agents are regularly used to lessen the heart-related, cerebral, and systemic effects of clamp-induced hypertension. This study was performed to evaluate two such strategies; the intravenous administration of either trimethaphan camsylate or nitroprusside. METHODS: We used a highly controllable and reproducible model of aortic cross-clamping in which we have previously shown the hypertension associated with clamping to be an active process mediated by means of a reflex arc. Ten dogs, five treated with nitroprusside (NP group) and five treated with trimethaphan camsylate (TC group), underwent 90 minutes of aortic cross-clamping. During this 90-minute period each group received 30 minutes of antihypertensive therapy. RESULTS: Control mean arterial pressure +/- SEM was 80 +/- 5 mm Hg for both groups and increased to 140 +/- 5 mm Hg with clamp application. With antihypertensive treatment the elevation in mean arterial pressure produced by cross-clamping was reduced to preclamp levels in the TC group and only partially (52%) in the NP group, despite very high doses of nitroprusside. Cardiac output (CO) increased in the NP group by 115% and decreased by 36% in the TC group. This increase in CO translates into a large (101%) increase in cardiac minute work for the NP group. CONCLUSIONS: The attenuation of clamp-induced hypertension by nitroprusside is associated with a dramatic increase in CO and cardiac work whereas the use of trimethaphan camsylate is not. The use of this ganglionic blocker may be more appropriate in this setting.

Animals↗

PubMed1998

Active sleep in cold-exposed infant Norway rats and Syrian golden hamsters: the role of brown adipose tissue thermogenesis.

It was previously hypothesized that brown adipose tissue (BAT) thermogenesis helps to maintain high rates of myoclonic twitching during cold exposure in infant rats (M. S. Blumberg & M. A. Stolba, 1996). To test this hypothesis, the sensitivity of twitching to various levels of cold exposure was assessed in week-old rats that were untreated or whose BAT thermogenesis was inhibited using a ganglionic blocker. Because week-old golden hamsters do not exhibit BAT thermogenesis, their sleep behaviors during cold exposure also were examined. Additional investigations in infant rats were conducted in which supplemental heat was provided to the interscapular region using a thermode and in which BAT was activated pharmacologically in ganglionically blocked pups. The results support the hypothesis that myoclonic twitching is sensitive to the prevailing air temperature and the activation of BAT thermogenesis.

Adipose Tissue, Brown↗

PubMed1987

Role of the parasympathetic nervous system in airway hyperresponsiveness after ozone inhalation.

Airway hyperresponsiveness develops in dogs after ozone inhalation. This study examined the role of the parasympathetic nervous system in ozone-induced airway hyperresponsiveness in dogs. Dose-response curves to acetylcholine (n = 8) and histamine (n = 4) were measured before and after exposure to ozone (3 ppm for 30 min). The provocative concentration of each agonist was measured on two randomly assigned days separated by at least 1 wk. On one day a control experiment was performed, and on the other day the dogs were pretreated with the ganglionic blocker hexamethonium bromide in doses that block ganglionic transmission. The acetylcholine provocative concentration decreased on the control day from 5.5 mg/ml (%SE 1.8) before ozone to 0.5 mg/ml (%SE 2.0) after ozone (P less than 0.0001). After pretreatment with hexamethonium the acetylcholine provocative concentration decreased from 9.0 mg/ml (%SE 1.8) before ozone to 1.0 mg/ml (%SE 2.0) after ozone (P = 0.002). The results were similar when histamine was used as the agonist. Therefore, ganglionic blockade does not prevent airway hyperresponsiveness after ozone inhalation, and a parasympathetic reflex mechanism is not responsible for airway hyperresponsiveness after ozone inhalation in dogs.

Acetylcholine↗

PubMed2005

[An electrophysiological study on the artificial somato-autonomic pathway for inducing voiding].

OBJECTIVE: To investigate the possibility of regeneration of somatic motor nerve to replace splanchnic nerve and the electrophysiologic characters of the regenerated nerve. METHODS: An artificial somato-autonomic reflex pathway was established by intradural microanastomosis of L(4) ventral root (VR) to L(6)VR at the left side in 12 male Wistar rats. Then the L(4)VR proximal to the anastomosis was stimulated by silver electrode and the evoked potentials were recorded on the distal end to the anastomosis, pelvic nerve and postganlionic fibers of the major pelvic ganglia (MPG). Cystometrography was used to record the intravesical pressure. Hexamethonium, a cholinergic ganglion blocker, was given directly on the pelvic ganglion so as to observe the change of the intravesical pressure evoked by stimulation of the nerves. Another 12 rats were used as controls. RESULTS: (1) In the experimental group, stimulation of the L(4)VR proximal end to the anastomosis evoked potentials on the distal end, the pelvic nerve, and the postganglionic fibers of the MPG, and induced bladder contraction. Stimulation of the contralateral sciatic nerve failed to evoke change of intravesical pressure. In the control group stimulation of the L(4)VR or sciatic nerve failed to evoke potentials on the postganglionic fibers of pelvic nerve and change of intravesical pressure. (2) Stimulation of the ipsilateral sciatic nerve led to an increase of intravesical pressure. (3) After the use of hexamethonium stimulation of the ipsilateral sciatic nerve and proximal end of L(4)-L(6) anastomosis failed to evoke change of intravesical pressure. (4) The conduction velocity of the regenerated motor axons was 33.3 m/s +/- 6.9m/s, significantly higher than that of the control group (11.6 m/s +/- 1.6 m/s). CONCLUSION: Somatic motor axons can regenerate to the MPG and reinnervate the bladder and the impulses from the somatic motor neurons can initiate voiding.

Anastomosis, Surgical↗

PubMed1996

Contribution of the sympathetic nervous system to hypertensive response to insulin excess in spontaneously hypertensive rats.

Our previous studies demonstrate that chronic insulin administration exacerbates hypertension in spontaneously hypertensive rats (SHR). In the present study, we tested the hypothesis that the pressor effect of insulin in SHR is medicated by sympathetic nervous system overactivity. Male SHR (7 weeks old) were given daily subcutaneous injection of insulin or vehicle for 3 days, after which each rat received an intravenous infusion of the peripheral ganglionic blocker hexamethonium. Two days later, in a second experiment, the infusion protocol was repeated with the alpha 2-adrenoceptor agonist clonidine, which more selectively inhibits sympathetic (as compared with parasympathetic) nervous system activity. Insulin treatment for 3 days caused a significant increase in mean arterial pressure (MAP; 164 +/- 2 mm Hg vs. saline control 148 +/- 3 mm Hg), but ganglionic blockade with hexamethonium eliminated the difference in blood pressure (BP) between the insulin-treated and control SHR. Infusion of clonidine significantly reduced MAP in the insulin-treated group to the level of the untreated control SHR, but the infusion did not reduce MAP in the latter group. In a second group of rats, acute administration of prazosin also eliminated the difference in MAP between insulin-treated and control SHR. We conclude that in SHR the sympathetic nervous system contributes importantly to the pressor effect of insulin administration and that this effect may be mediated by the central nervous system.

Adrenergic alpha-Agonists↗

PubMed1997

Metformin inhibits ganglionic neurotransmission in renal nerves.

Intravenous administration of the antihyperglycemic agent metformin decreases arterial pressure and sympathetic nerve activity (SNA). To test the hypothesis that metformin inhibits SNA by interrupting ganglionic neurotransmission, we compared the actions of intravenous administration of metformin and the ganglionic blocker trimethaphan on postganglionic renal and preganglionic adrenal sympathetic nerves in pentobarbital-anesthetized male Sprague-Dawley rats. Intravenous metformin elicited dose-dependent decreases in postganglionic renal SNA (1 mg/kg: 0 +/- 0%; 10 mg/kg: -20 +/- 4%; 100 mg/kg: -92 +/- 3%; n = 7). Conversely, only the maximal dose of metformin affected preganglionic adrenal SNA (100 mg/kg: delta adrenal SNA = -14 +/- 6%; n = 8). Ganglionic blockade with intravenous trimethaphan (5 mg/kg) produced a differential sympathoinhibitory response similar to the response observed after high-dose metformin (delta renal SNA = -100 +/- 3%; delta adrenal SNA = -17 +/- 7%; P < .001). Preganglionic renal neurons were electrically stimulated in the spinal cord, before and during the peak of the sympathoinhibitory response to intravenous metformin, and the magnitude of the stimulus-evoked increases in postganglionic renal SNA were compared. Metformin dose-dependently attenuated the magnitude of the increase in postganglionic renal SNA elicited by stimulation of the spinal cord (30 mg/kg: -23 +/- 8%; 90 mg/kg: -65 +/- 11%; 270 mg/kg: -91 +/- 8%; n = 6 per dose). We conclude that high-dose intravenous metformin interrupts ganglionic neurotransmission in renal nerves.

Animals↗

PubMed2004

Central but not the peripheral action of cholinergic compounds suppresses the immune system.

Cholinergic compounds modulate the immune system; however, the mechanism of cholinergic immunotoxicity is largely unknown. Lewis rats were exposed chronically to cholinergic compounds via subcutaneous or intracerebroventricular routes. Compounds that crossed the blood-brain barrier (BBB) inhibited the antibody response when given by either route, however, poorly permeable compounds, unless given in high doses, inhibited the antibody response only by intracerebroventricular administration. Intracerebroventricular administration of cholinergic agents also reduced serum corticosterone levels, which along with the antibody response was attenuated by pretreatment with the ganglionic blocker chlorisondamine. Thus, cholinergic agents affect the neuroimmune communication and inhibit glucocorticoid production; the latter may be a biomarker for cholinergic toxicity.

Animals↗

PubMed2000

Parasympathetic reflex vasodilatation in rat submandibular gland.

The present study was designed to investigate 1) whether parasympathetic reflex vasodilatation occurs in the submandibular gland (SMG) in deeply urethan-anesthetized, cervically vagotomized, and sympathectomized rats when the central cut end of the lingual nerve (LN) is electrically stimulated and 2) to what extent the neural mechanisms underlying such responses are the same as those involved in the response to direct stimulation of the chorda-LN (CLN). Stimulation of each nerve separately elicited a marked blood flow increase in SMG. Section of the chorda tympani abolished the SMG blood flow response but had no effect on the lip blood flow increase evoked by LN stimulation. Section of the CLN abolished the SMG blood flow increases evoked by stimulation of either nerve. The SMG blood flow increases (regardless of whether they were evoked by LN or CLN stimulation) were markedly reduced by the autonomic cholinergic ganglion blocker hexamethonium. The present study demonstrates that a parasympathetic reflex vasodilator mechanism is present in the rat SMG and that it can express its effects under deep general anesthesia.

Afferent Pathways↗

PubMed1992

Calcitonin gene-related peptide is a venous dilator in conscious rats.

The effect of calcitonin gene-related peptide (CGRP) on body venous tone is not known. This study examines the dose-response effects of rat alpha CGRP on mean circulatory filling pressure (MCFP), an index of body venous tone, in conscious rats. Dose-response curves of CGRP were constructed in three groups of rats, namely, (I) intact, (III) rats pretreated with the ganglionic blocker hexamethonium and (V) rats pretreated with noradrenaline to raise mean arterial pressure (MAP) and MCFP. Three additional groups, (II), (IV) and (VI), served as time controls and were treated similarly to (I), (III) and (V), respectively, except that they were given saline (0.9% NaCl) in place of CGRP. The infusion of CGRP in intact rats dose dependently decreased MAP, increased heart rate (HR) and slightly reduced MCFP. In ganglionic-blocked rats, CGRP caused similar depressor responses but less tachycardia than in intact rats, however, it also slightly reduced MCFP. In rats given noradrenaline, CGRP dose dependently decreased MAP, MCFP and increased HR. The results show that CGRP has venodilator activities; its venous effect is best revealed at elevated venous tone.

Analysis of Variance↗

PubMed1997

Nitric oxide derived from sympathetic nerves regulates airway responsiveness to histamine in guinea pigs.

Nitric oxide (NO), which can be derived from the nervous system or the epithelium of the airway, may modulate airway responsiveness. We investigated how NO derived from the airway nervous system would affect the airway responsiveness to histamine and acetylcholine in mechanically ventilated guinea pigs. An NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (1 mmol/kg i.p.) significantly enhanced airway responsiveness to histamine but not to acetylcholine. Its enantiomer D-NAME (1 mmol/kg i.p.), in contrast, had no effect. The L-NAME-induced airway hyperresponsiveness was still observed in animals pretreated with propranolol (1 mg/kg i.v.) and atropine (1 mg/kg i.v.). Pretreatment with the ganglionic blocker hexamethonium (2 mg/kg i.v.) completely abolished enhancing effect of L-NAME on airway responsiveness. Bilateral cervical vagotomy did not alter the L-NAME-induced airway hyperresponsiveness, whereas sympathetic stellatectomy completely abolished it. Results suggest that NO that was presumably derived from the sympathetic nervous system regulates airway responsiveness to histamine in guinea pigs.

Airway Resistance↗

PubMed1995

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat.

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗