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PubMed1992

Biosynthesis and excretion of gangliosides by the isolated perfused rat liver.

De novo synthesis and excretion into perfusate and bile fluid of hepatic gangliosides were studied in isolated perfused rat livers. Addition of N-acetyl-[6-3H(n)]D-mannosamine to the perfusate resulted in radioactive synthesis of at least eight gangliosides labeled in their sialic acid residues. About 10% of total de novo synthesized gangliosides were excreted into the perfusate, less than 1% into the bile fluid. Labeled gangliosides were tentatively identified by cochromatography with known standards. All of them are known to occur in rat liver and sera. The results indicate that most, if not all, normal serum gangliosides are synthesized in the liver; excretion with bile fluid is negligible. They explain previous observations, and indicate clinical implications, which are discussed.

Animals↗
PubMed1974

The effect of vasopressin upon the vasculature of the isolated perfused rat kidney.

The timed uptake of (131)I-labelled human serum albumin was used as an index of regional perfusion in the isolated rat kidney.1. Arginine vasopressin in doses of 1, 5 and 10 muu./ml. of perfusate decreased papillary perfusion. Total renal perfusion was decreased only by the 5 muu. dose.2. Ornithine-8-vasopressin in doses of 5 and 10 muu./ml. of perfusate decreased papillary perfusion. Total renal perfusion was decreased only by the 10 muu. dose.3. When the relative viscosity of the perfusate was increased to a value of 2.0 from the control value of 1.7, both papillary perfusion and total renal perfusion were reduced.4. Arginine vasopressin further reduced papillary flow in kidneys perfused with high viscosity artificial plasma.

Animals↗
PubMed2005

Voluntary exercise protects against acute doxorubicin cardiotoxicity in the isolated perfused rat heart.

The clinical use of doxorubicin (DOX) is limited by a dose-dependent cardiotoxicity. The purpose of this study was to determine whether voluntary exercise training would confer protection against DOX cardiotoxicity in the isolated perfused rat heart. Female Sprague-Dawley rats were randomly assigned to standard holding cages or cages with running wheels for 8 wk. Twenty-four hours after the sedentary (SED) or voluntary exercise (VEX) running period, rats were anesthetized with pentobarbital sodium, and hearts were isolated and perfused with oxygenated Krebs-Henseleit (KH) buffer at a constant flow of 15 ml/min. After a 20-min stabilization period, hearts were paced at 300 beats per minute and perfused with KH buffer containing 10 microM DOX for 60 min. A set of control hearts from SED and VEX rats were perfused under identical conditions without DOX for the same period. DOX perfusion led to significant decreases in left ventricular developed pressure, +dP/dt, and -dP/dt, and significant increases in LV lipid peroxidation in sedentary rats compared with non-DOX controls (P < 0.05). Prior voluntary exercise training attenuated these DOX-induced effects and was associated with a significant increase (78%, P < 0.05) in heat shock protein (HSP72), but not mitochondrial isoform of SOD (MnSOD) or CuZnSOD protein expression in the hearts of wheel-run animals. These data indicate that chronic physical activity may provide resistance against the cardiac dysfunction and oxidative damage associated with DOX exposure and provide novel evidence of HSP72 induction in the heart after voluntary exercise.

Animals↗
PubMed1985

Effects of nicotine on beta-endorphin, alpha MSH, and ACTH secretion by isolated perfused mouse brains and pituitary glands, in vitro.

The effects of nicotine on secretion of the pituitary peptides beta-endorphin, alpha MSH, and ACTH were studied using the isolated perfused mouse brain (IPMB) and isolated superfused pituitaries of C3H mice. Nicotine (6.1 microM) stimulated secretion of beta-endorphin immunoreactivity from C3H IPMB approximately twofold. Secretion of alpha MSH immunoreactivity was stimulated approximately two- and sixfold by 6.1 microM and 12.2 microM nicotine, respectively. However, nicotine (6.1 microM) had no direct effect on the secretion of beta-endorphin, alpha MSH, or ACTH immunoreactivities from the isolated superfused pituitaries. The data suggest nicotine acts in the brain to stimulate pituitary secretion of alpha MSH and beta-endorphin. Electrocorticographic (ECoG) activity of the IPMB was monitored. Nicotine induced characteristic ECoG changes including a reduction of input voltage, a biphasic response of rapid desynchronization followed by prolonged synchronization, and seizure at high doses (12.2 microM).

Adrenocorticotropic Hormone↗
PubMed1993

Bile salt inhibition of motility in the isolated perfused rabbit terminal ileum.

The effects of bile on small bowel motility were studied in isolated, perfused rabbit terminal ileum. It was proposed that bile delivery into the distal ileum would inhibit ileal motor activity, by peptide YY (PYY) release and therefore the effect of luminal bile on motor activity was examined and PYY release measured. Luminal bile and taurocheodeoxycholic acid (10 mmol) inhibited ileal motor activity. Arterial infusion of venous effluents from a bile inhibited ileum suppressed motor activity in a second isolated ileum. This shows the presence of a humoral inhibitor of ileal motor activity. Luminal bile increased venous PYY concentrations (42.5 (8.5) to 502 (46.2) pmol/l; p < 0.01) and increased bile salt values (1.7 (0.36) to 88.6 (5.6) 10 mumol/l/l; p < 0.005). Arterial infusion of taurocheodeoxycholic acid at concentrations found in the venous effluent (100 mumol/l/l) suppressed motility (p < 0.001) but infusion of PYY at concentrations in the venous effluent (500.0 pmol/l) failed to inhibit motility. Furthermore, PYY antagonist, PYX 1, failed to reverse the bile induced inhibition of motility. Luminal bile salts inhibit terminal ileal motility and this is independent of PYY release. By slowing motility, bile salts may participate in their own absorption by the 'ileal pump' and in the 'ileal brake' mechanism.

Animals↗
PubMed1984

Release of cyclic AMP and progesterone from the isolated perfused luteal ovary of the PMSG treated rat.

A model for in vitro perfusion of the isolated rat ovary was developed. In the luteinized ovaries of PMSG treated rats the relationship between perfusion flow and progesterone production was evaluated. A positive correlation was found indicating that a high blood flow rate may be necessary for an optimal secretion of progesterone from the fully developed corpus luteum in the rat. Also the effects of a continuous exposure of LH on ovarian cyclic AMP and progesterone release was studied. A rapid and sustained increase in both cyclic AMP and progesterone release was seen and this release tended to have episodic pattern with elevations occurring at intervals between 30 and 90 min following LH.

Animals↗
PubMed1995

The uptake and metabolism of cystamine and taurine by isolated perfused rat and rabbit lungs.

Cystamine has been reported to be taken up and metabolized to taurine by the rat lung slices. The objectives of the present study were to compare the uptake and metabolism of cystamine and taurine in isolated perfused lungs of rats and rabbits and examine the action of glutathione (GSH) on these processes. The uptake and metabolism of [14C]cystamine and [14C]taurine were studied at 20 microM concentrations each in isolated, ventilated, perfused rat and rabbit lungs. In some experiments, 1 microM GSH was included in the perfusate prior to the addition of cystamine. The perfusate and lung homogenate samples were analyzed for cystamine and its metabolites. [14C]cystamine uptake with and without GSH was 13 and 14% in rat lungs and 37 and 32% in rabbit lungs. [14C]taurine uptake was 10% in rat and 37% in rabbit lungs. The levels of radiolabeled cystamine and its metabolites were (nmol/g lung): 20.0 +/- 10.0 and 11.5 +/- 7.0 cystamine, 4.7 +/- 0.5 and 3.2 +/- 0.5 hypotaurine and 56.0 +/- 16.0 and 49.4 +/- 6.0 taurine, for rat and rabbit lungs, respectively, when perfused without GSH; and 18.0 +/- 1.0 and 2.5 +/- 0.5 cystamine, 6.6 +/- 0.5 and 18 +/- 10 hypotaurine and 60.0 +/- 12.0 and 33.6 +/- 9.0 taurine, when perfused with GSH, for rats and rabbit lungs, respectively. Taurine did not undergo any further metabolism in either of the lungs. These studies show that cystamine is taken up and metabolized to taurine via hypotaurine by both rat and rabbit lungs in a manner similar to that seen in rat lung slices. However, rat lungs have much greater capacity to metabolize cystamine to taurine than rabbit. Inclusion of GSH did not significantly alter the ability of lungs to sequester cystamine from the perfusate but the metabolism of hypotaurine to taurine was markedly decreased in rabbit lungs. Taurine was not metabolized any further. It is concluded that rat and rabbit lungs take up cystamine from the systemic circulation, metabolize it via hypotaurine to taurine, and effuse most of the latter in to the circulation.

Animals↗
PubMed1986

Effects of kallikrein (K), bradykinin (B) and insulin (I), on substrate metabolism in the isolated perfused rat heart.

In the isolated rat heart preparation, perfused at physiological glucose levels, effects of kallikrein (K), bradykinin (B) and insulin (I) on carbohydrate metabolism have been compared. A flow- and I-independent K-effect, obviously working via proteolytic kinin formation, was shown. While I elevated glucose-uptake into the heart preferably via accelerated transport across the membrane and increased rates of glycogen synthesis, B and K significantly activated PFK and reduced myocardial glucose uptake. The latter effect is probably due to an accelerated glycolytic flux leading to decreased G6P-levels and thereby stimulating glycogenolysis. Since aprotinin was able to abolish the K-effect, the latter may possibly be mediated via kinin release.

Animals↗
PubMedDate not supplied

Effect of ouabain on the responses to vasoconstrictor agents in isolated perfused rat tail arteries.

In isolated rat tail arteries perfused with Krebs-Henseleit solution, ouabain, in concentrations of less than 10(-5) M, caused a concentration-dependent, noncompetitive inhibition of the vasoconstrictor response to phenylephrine. Concentrations of 10(-8) and 10(-6) M caused 30 and 61% inhibition, respectively. The inhibition was gradual in onset, with a maximal effect at 45 min. In concentrations greater than 10(-5) M, ouabain caused a parallel shift to the left of the phenylephrine dose-response curve, indicating potentiation. The potentiation was rapid in onset (within 1 min), and was approximately 1.4-fold. The cutoff point between inhibition and potentiation of vasoconstrictors occurred at a ouabain concentration of 10(-5) M. Ouabain-induced potentiation was nonspecific in regard to the vasoconstrictor used. Phenylephrine, clonidine, and serotonin were each potentiated. Potentiation probably resulted from a reduction in the smooth muscle membrane potential as a consequence of inhibition of Na-K ATPase. The mechanism of the inhibitory effect of ouabain on vasoconstrictors was not resolved but may operate via stimulation of Na-K ATPase. The results are consistent with a "partial agonist" action of ouabain on Na-K ATPase.

Animals↗
PubMed1992

Dopamine and adrenaline, but not isoprenaline, are substrates for uptake and metabolism in isolated perfused lungs of rats.

The uptake and subsequent metabolism by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) of dopamine, adrenaline, isoprenaline and noradrenaline in isolated perfused lungs of rats has been examined. In lung preparations in which COMT and MAO were inhibited, the uptake of 3H-labelled dopamine, (-)-adrenaline and (-)-noradrenaline, but not (+/-)-isoprenaline, was reduced by cocaine (10 or 100 mumol/l). The rank order of the Km values of the amines that were substrates for uptake in the lungs were: dopamine (0.246 mumol/l) less than noradrenaline (0.967 mumol/l) less than adrenaline (3.32 mumol/l). These results are consistent with transport of catecholamines in rat lungs by Uptake1. In lung preparations with COMT and MAO intact, dopamine and noradrenaline were removed from the circulation (50% and 32%, respectively) and mainly metabolized. There was very little (3.0%) removal of isoprenaline by the lungs and adrenaline was not included in this part of the study. In lung preparations in which only MAO was inhibited, the rank order of COMT activity for O-methylation of the amines was dopamine much much greater than noradrenaline greater than or equal to adrenaline (kCOMT values: 4.98 min-1, 0.357 min-1 and 0.234 min-1, respectively). If dopamine or adrenaline are perfused through the pulmonary circulation in isolated lungs of the rat, they are taken up and then metabolized by COMT and MAO, as also occurs for noradrenaline. Isoprenaline is not a substrate for uptake in the lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

The effect of isolated perfusion on limb circulation in peripheral arterial occlusion.

The effects of isolated limb perfusion were studied in 12 patients suffering from peripheral arterial occlusion. The hemodynamic investigations show that the vascular resistance decreases considerably during isolated limb perfusion. After administration of a vasodilator cocktail, added to the perfusion, the vascular resistance continues to decrease. Angiographic records, made before, during and after the perfusion, suggest that the calibre of the collateral vessels increases significantly and besides new collaterals can also be observed. The mechanism of the effects of isolated hyperbaric limb perfusion and its clinical value are discussed.

Adult↗
PubMed1984

Metabolism of 2,4-dichlorophenol by isolated perfused rat liver.

The uptake and metabolism of 2,4-[14C]dichlorophenol (2,4-[14C]DCP) was studied in the isolated perfused rat liver. The uptake of radioactivity in liver increased 6.6% (25.3-31.9%) in the presence of adenosine 5'-triphosphate (ATP) and 14.9% (25.3-40.2%) in the presence of ATP and galactosamine. This increase in the uptake of radioactivity was indicative of maintaining the integrity of liver cells. The glucuronide conjugate of 2,4-DCP in bile was derivatized by permethylation and characterized by gas chromatography-mass spectrometry (GC-MS). Two unusual metabolites were isolated from the liver and perfusate by extracting with hexane. The gas chromatogram of these metabolites gave peaks at retention times 12.0 and 15.5 min, and were characterized by mass spectrometry. The fragmentation pattern of these metabolites confirmed their identity as dichloromethoxyphenols.

Adenosine Triphosphate↗
PubMed1987

The effect of dibutyryl cAMP on sodium uptake by isolated perfused gills of Callinectes sapidus.

Hemolymph, collected from 25 and 100% seawater acclimated Callinectes sapidus and perfused through the isolated gill, causes increases in Na+ uptake in the gill. Similarly, dibutyryl cAMP causes increases in Na+ uptake when perfused through the gill. Since pericardial organ (PO) extracts dopamine and octopamine are known to increase cAMP levels in the perfused gill, it is suggested that these substances from the PO may be the hemolymph factors which increase Na+ uptake via the mediation of cAMP as second messenger.

Animals↗
PubMed2006

Alteration of fexofenadine disposition in the rat isolated perfused liver following injection of bacterial lipopolysaccharide.

1. The aim of the present study was to examine the effect of bacterial lipopolysaccharide (LPS) on the disposition of an organic anion transporting polypeptide and P-glycoprotein substrate in the rat isolated perfused liver. 2. Male Sprague-Dawley rats were divided into four groups. Three of the groups received 1, 2.5 or 5 mg/kg, i.p., Escherichia coli LPS in sterile saline. The fourth group received an equivalent volume of sterile saline i.p. Twenty-four hours after treatment, rats were anaesthetized and the liver isolated and perfused with fexofenadine at an initial concentration of 2000 ng/mL in a recirculating system. Perfusate and bile samples were collected for 60 min and the liver was collected at the end of the perfusion. Fexofenadine concentrations were determined by HPLC. Fexofenadine pharmacokinetic parameters, the final liver : perfusate (L : P) and bile : liver (B : L) concentration ratios were determined. 3. Injection of LPS changed the hepatic disposition of fexofenadine. The changes were most marked in the 5 mg/kg LPS group. Notably, clearance from the perfusate (CL) and into the bile (CLB; 5.9 +/- 0.6 and 1.24 +/- 0.20 mL/min, respectively), L : P (44 +/- 11) and B : L (17 +/- 2) were all reduced (P < 0.05) in this group compared with control (CL 10.0 +/- 1.1 mL/min; CLB 2.7 +/- 0.5 mL/min; L : P 87 +/- 14; and B : L 30 +/- 4). 4. In conclusion CL and CLB were reduced following treatment with LPS in a manner consistent with downregulation of both canalicular and sinusoidal transport.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

[The characteristics of the action of a direct electric (galvanic) current on the ultrastructure of the normal perfused isolated heart and during its postischemic reperfusion].

The effect of direct electric current (DEC), 0.4 mA, on the ultrastructure of normal perfusing isolated heart and in the course of its postischemic reperfusion was studied on the model of isolated rat heart using Langedorf method. DEC was shown to exert a normalizing, membrane-stabilizing effect on the subcellular organization of isolated heart CMC in the course of its normothermic perfusion. The observed changes are considered to attest to the adaptive aspect of the current effect on the ultrastructure of the myocardium under these conditions. In ischemia-reperfusion, DEC also facilitated marked stabilization of cardiomyocytes membranes and stimulation of intracellular reparative processes of the affected cardiac muscle.

Animals↗
PubMed2001

The effects of norepinephrine and prostaglandin E1 on pharmacokinetics of lidocaine in isolated perfused rat liver.

We hypothesized that depression of liver function by norepinephrine can be improved by prostaglandin E1. Isolated perfused rat liver was selected as an experimental model, since the flow rate can be regulated in it. Twenty-one rats were randomly allocated to three groups: control, norepinephrine, and norepinephrine and prostaglandin E1 groups. The liver was perfused in a recirculating system at a constant flow rate of 20 ml/min. After administration of two milligrams of lidocaine in each group, lidocaine and monoethylglycinexylidide concentrations in the recirculating system were measured. Lidocaine pharmacokinetics were analyzed using the SAAM II program, including metabolic rate from lidocaine to monoethylglycinexylidide using time-concentration curves. Norepinephrine significantly increased perfusion pressure and the area under the time-concentration curve for lidocaine. Norepinephrine decreased the clearance and the elimination rate constant of lidocaine compared with those in the control group. Although administration of prostaglandin E1 after infusion of norepinephrine did not significantly change perfusion pressure, it significantly (p < 0.05) improved metabolic rate, clearance and the elimination rate constant of lidocaine in the isolated rat liver model.

Alprostadil↗
PubMed1976

Survival and regional disease control after isolation-perfusion for invasive stage I melanoma of the extremities.

Excision of the primary and isolation-perfusion with 1-phenylalanine mustard was the treatment in 199 patients with invasive Stage I melanoma of the extremities with the goal of improving regional disease control and long-term survival. The determinant survival in patients followed 5-15 years was 83%; Berkson-Gage survivals were 98% at 2 years, 88% at 5 years, and 84% at 10 years. The site of first recurrence was determined in all 49 (25%) patients who failed treatment: three (2%) developed local recurrence, six (3%) developed intransit recurrence, 24 (13%) developed positive regional lymph nodes, 15 (8%) developed systemic metastases, and one developed local recurrence plus positive regional nodes. Of these 49 patients failing treatment, 15 (31%) are currently surviving with no evidence of disease after retreatment of the recurrence. These data are compared to historical controls in the literature. It is concluded that regional control rates are improved by perfusion and that survival has probably been improved. In 14 patients treated by perfusion without local excision, regional control and survival was poor. Single drug (L-PAM) perfusion with the techniques employed is effective in controlling regional subclinical disease, but the primary should be widely excised.

Adolescent↗
PubMed1995

Relationship between glutathione concentration and metabolism of the pyrrolizidine alkaloid, monocrotaline, in the isolated, perfused liver.

The influence of GSH concentration on metabolism of monocrotaline was examined in the isolated, perfused rat liver. Chloroethanol (0.37 mmol/kg), diethyl maleate (5.6 mmol/kg), and buthionine sulfoximine (72.9 mmol/kg) given in vivo reduced hepatic GSH from 3.7 mumol/g wet weight to 1.5, 0.6 and 0.9 mumol/g, respectively. Livers were then perfused in vitro for 1 hr with monocrotaline (0.5 mM). GSH depletion had no effect on the total release of pyrrolic metabolites of monocrotaline. Depletion, however, markedly affected the pattern of pyrrole release. Biliary release of 7-glutathionyl-6,7-dihydro-1-hydroxy-methyl-5H-pyrrolizine (GSDHP) was reduced by up to 72%. Pretreatment with diethyl maleate or buthionine sulfoximine increased the level of protein-bound pyrroles in the liver by 107 and 84%, respectively. Such pyrroles are probably responsible for liver toxicity. GSH depletion also led to a doubling of dehydromonocrotaline release into the perfusate. This metabolite is probably responsible for the extrahepatic toxicity of monocrotaline. Release into perfusate of the relatively nontoxic metabolite, 6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP) was correspondingly decreased. Hepatic GSH content was increased to 4.4 mumol/g by pretreatment with oxo-4-thiazolidine carboxylate (4.76 mmol/kg). This agent increased total pyrrolic metabolites by 54%. Biliary release of GSDHP and perfusate release of dehydromonocrotaline and DHP were all increased. Thus, hepatic GSH levels regulate the metabolism of monocrotaline and dehydromonocrotaline and, consequently, the hepatic and extrahepatic toxicity of monocrotaline. GSH depletion leads to a switch from the biliary release of the midly toxic GSDHP to the perfusate release of the highly toxic dehydromonocrotaline. GSH depletion also permits more dehydromonocrotaline in the liver to become available for macromolecular alkylation. These findings suggest that nutritional intake of sulfur-containing amino acids can influence the severity of pyrrolizidine poisoning.

Analysis of Variance↗