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PubMed1977

Relationship between net 45calcium influx across a perfused isolated eel gill and the development of post-stanniectomy hypercalcemia.

The net 45calcium influx was measured in perfused isolated individual hemibranchs taken from Anguilla rostrata L. at various intervals following the surgical removal of the Corpuscles of Stannius. Total plasma calcium concentrations were recorded at the same time. A relationship between the development of post-stanniectomy hypercalcemia and the net rate of 45calcium uptake in the isolated gills is suggested. The net influx of 45calcium increased rapidly during the first week, peaked at two weeks and dropped back to control levels at three weeks. Plasma calcium levels followed the same trend over the first two weeks but continued to rise through the third week before dropping slightly during the fourth week. We conclude that the corpuscles of Stannius play some role in controlling the branchial uptake of calcium and that the gills are of primary importance in the appearance of post-stanniectomy hypercalcemia.

Animals↗
PubMed1989

The vasodilator action of parathyroid hormone fragments on isolated perfused rat kidney.

The renal vasodilator responses to various fragments of PTH were quantified on a model of isolated perfused rat kidney (IPK), under non-filtering conditions. The 1-34 fragment of bovine PTH, its Nle analogue and rat PTH, injected in sequential cumulative doses, caused concentration-dependent vasodilatation in the vasculature of the IPK which was preconstricted with prostaglandin F2 alpha. The EC50 of PTH for renal vasodilatation ranged from 1 to 2 nM for all PTH fragments and maximum vasodilatation ranged from 33 to 41% of the maximum vasodilatation induced by papaverine. Renal vasodilation was not related to prostaglandin release since similar vasodilatation occurred after the inhibition of prostaglandin synthesis with indomethacin. When PTH was administered in single bolus injections, using a separate kidney for each hormone concentration, rather than repeated injections into the same kidney, higher maximum vasodilatations were obtained (64%). These results most likely reflected tachyphylaxis of the renal vasculature to PTH occurring after repeated exposure of a single kidney to the hormone. The antagonist analogue [Nle8,18, Tyr34]-bPTH-(3-34)A shifted the concentration-related response curve to the right, indicating that the renal vasodilator response to rPTH-(1-34) involved specific vascular receptors.

Animals↗
PubMed1986

Increase in atrial pressure releases atrial natriuretic peptide from isolated perfused rat hearts.

To elucidate the mechanism involved in the release of atrial natriuretic peptide, we modified the isolated perfused rat heart preparation to permit a step-wise increase in right atrial tension. Perfusate was introduced into the right atrium through the superior vena cava and was collected via the pulmonary artery. Right atrial pressure was manipulated by changing the perfusion rate. Perfusate from the pulmonary artery was collected in 1-min-fractions, extracted, and assayed for atrial natriuretic peptide like immunoreactivity (ANP-li). The basal rate of ANP-li release at an atrial pressure of 1.41 +/- 0.31 mm Hg was 964 +/- 144 pg/min (n = 11). As right atrial pressure was increased (range 0.4-4.5 mm Hg), a linear correlation (r = 0.85, P less than 0.001) was observed between the change in ANP-li release and the change in atrial pressure. High pressure liquid chromatography revealed that the major fraction in the perfusate had the same elution time than alpha-rANP. This peak fraction, as well as synthetic atriopeptin III, caused a dose-dependent relaxation in rat aortic strips that had been subjected to contraction with norepinephrine. Further, it corresponded exactly to the material we previously identified in rat plasma. These results suggest that atrial distension is involved in the release of ANP. In addition, ANP is released per se, as the active peptide.

Animals↗
PubMed1984

Transport of L-cystine in isolated perfused proximal straight tubules.

Unidirectional fluxes of L-35S-cystine and intracellular 35S activity were measured in isolated perfused segments of rabbit proximal straight tubule. The absorptive (lumen-to-both) flux of L-35S-cysteine showed a tendency toward saturation within the concentration limits imposed by the low solubility of cystine (0.3 mmol . l-1). In contrast, for the bath-to-lumen fluxes, there was a linear relation between the bathing solution concentration of L-35S-cystine and the rate of 35S appearance in the lumen. Nonlinear fitting of both sets of unidirectional flux data gave a maximal cystine transport rate (Jmax) of 1.45 +/- 0.27 (SEM) pmol min-1 mm-1, a Michaelis constant (Km) of 0.20 +/- 0.07 mmol . l-1, and an apparent permeability coefficient of 0.27 +/- 0.11 pmol min-1 mm-1 (mmol . l-1)-1 (approximately 0.06 micrometer/s). The 35S concentration in the cell exceeded that in the lumen by almost 60-fold during the lumen-to-bath flux, and exceeded the bathing solution concentration by 4.7-fold during the bath-to-lumen flux. Thus cystine was accumulated by the cells across either membrane, but over 77% of the intracellular activity was in the form of cysteine. Although the presence of luminal L-lysine or cycloleucine inhibited the absorptive flux of cystine, neither amino acid affected the bath-to-lumen flux.

Animals↗
PubMed1986

Determination of reactivity of resistance blood vessels in the isolated perfused legs of animals with inflammation as exemplified in adjuvant arthritis.

Vasodepression was found ex vivo in the isolated perfused hind legs of rats, mice and guinea-pigs with paw inflammation using maximum pressure amplitude, EAm, pD2-value and intrinsic sensitivity (i.s.) as the test parameters of dose-response curves of vasopressor substances (noradrenaline, lys- and arg-vasopressin, angiotensin II, substance P, Na2-ATP). Vasodepression is strong in the anaphylactic and dextran paw edema, moderate in the carrageenin paw edema and adjuvant arthritis, but weak in the pertussis vaccine and kaolin paw edema. It is partly long-lasting, does not closely correlate with edema strength and can also be shown in the contralateral non-inflamed leg. Thus, a vasoreactivity depressing factor(s) must be liberated from the site of inflammation and reach the general circulation. Here, the method is described using the adjuvant arthritis as an example.

Animals↗
PubMed1988

High flow attenuates relaxation by acetylcholine in isolated perfused canine femoral arteries.

The effect of changes in flow on endothelial-dependent and -independent dilation of isolated perfused arteries was determined. Femoral arteries from ten dogs were excised and mounted in a vessel bath containing a physiological salt solution (PSS) at 37 degrees C, bubbled with 95% O2-5% CO2. The vessel outer diameter was measured using an ultrasonic crystal dimension system. Arteries were perfused with PSS at a steady flow of 1 ml/s at 90 mmHg. Tone was induced in the arteries by the addition of phenylephrine to the vessel bath. Acetylcholine (six dogs) and sodium nitroprusside (four dogs) were added to the perfusate in a cumulative fashion and changes in vessel diameter were recorded until maximum vasodilation was achieved. Dose-response relationships to the agents were determined with each vessel perfused at 1 and 4 ml/s. Sensitivity to each agent was measured as the ED50 value calculated from the respective dose-response relationships. Sensitivity to acetylcholine, but not sodium nitroprusside, was significantly decreased in arteries perfused at 4 ml/s versus 1 ml/s [acetylcholine ED50: 1 ml/s = (0.79 +/- 0.31) x 10(-8) mol/l, 4 ml/s = (1.55 +/- 0.60) x 10(-8) mol/l, P less than 0.05; sodium nitroprusside ED50: 1 ml/s = (2.57 +/- 0.12) x 10(-7) mol/l, 4 ml/s = (2.69 +/- 0.60) x 10(-7) mol/l, not significant]. We conclude that high flow decreases sensitivity to acetylcholine in canine femoral arteries and suggest that vascular reactivity to this agent may be modified by changes in shear on the vascular endothelium.

Acetylcholine↗
PubMed1987

Pharmacological analysis of 5-HT-induced vasoconstriction in isolated, perfused dog skeletal muscle arteries.

The mechanism of the vasoconstriction caused by 5-HT was analysed pharmacologically in isolated, perfused skeletal muscle branches of the canine femoral artery. An intraluminal injection of serotonin (5-HT) produced a marked vasoconstriction and the dose-response curve was bell-shaped. The 5-HT-induced response was inhibited by methysergide and ketanserin but a larger dose of ketanserin (10-30 micrograms) reduced the maximal responses to 5-HT, indicating its general depressant action. Norepinephrine (NE) and KCl-induced constrictions were not significantly affected by methysergide. Ketanserin significantly suppressed the NE-induced response at a relatively large dose but not the KCl-induced one. 5-HT- and KCl-induced constrictions were not modified by a potent alpha 1-adrenoceptor antagonist, bunazosin. It is considered that 5-HT may mediate its contractile effect on these arteries via specific 5-HT2 receptors but not alpha-adrenoceptors. Diltiazem at a relatively large dose (30-100 micrograms) slightly but significantly depressed NE-induced constrictions, and KCl-induced responses were markedly depressed by diltiazem (10-100 micrograms). On the other hand, 5-HT-induced constrictions were not suppressed by diltiazem at any of the doses used. It was shown that cold storage (at 4 degrees C, for 3-7 days) did not significantly modify 5-HT-induced responses although the KCl-induced effects were suppressed. Thus, it is considered that the calcium channel in these vessels may be dominantly depressed by cold storage. It is concluded that 5-HT-induced constriction in skeletal muscle arteries may be independent of the influx of extracellular Ca ions.

Adrenergic alpha-Antagonists↗
PubMed1990

Taurocholate stimulates transcytotic vesicular pathways labeled by horseradish peroxidase in the isolated perfused rat liver.

The effect of taurocholate on transcytotic vesicular pathways labeled with horseradish peroxidase was assessed in isolated perfused rat liver preparations. Forty-five minutes after a horseradish peroxidase load in a recirculating system, continuous infusion of taurocholate but not taurodehydrocholate significantly increased horseradish peroxidase excretion in bile by 50% compared with controls. When horseradish peroxidase (25 mg) was pulse loaded for 1 minute in control perfusions, it appeared in bile in early (4-6 minutes) and late (20-25 minutes) peaks, the latter accounting for 90% of total horseradish peroxidase output. Taurocholate infusion significantly increased horseradish peroxidase output in both early and late peaks, whereas only a small increase in the early peak was observed with taurodehydrocholate. Colchicine pretreatment increased the early peak in bile but abolished the second peak. Electron micrographs from control livers revealed the accumulation of horseradish peroxidase-containing vesicles in pericanalicular regions at early (2 minutes) as well as late (18 minutes) periods. When a morphometric analysis of electron micrographs was performed from pericanalicular regions 2 minutes after a 1-minute pulse of horseradish peroxidase (500 mg), taurocholate but not taurodehydrocholate increased both the density and percent area of horseradish peroxidase-containing vesicles compared with controls. In contrast, colchicine pretreatment had no effect on the density of the early-appearing vesicles, although their individual sizes were reduced. Taurocholate but not taurodehydrocholate also increased the percent of tubular structures in the pericanalicular region. These findings indicate that taurocholate stimulates both early and late transcytotic vesicle pathways and therefore probably microtubule-independent vesicle pathway is present in hepatocytes that must be distinguished from paracellular routes.

Animals↗
PubMed1984

Reduced tolerance to digitalis-induced arrhythmias caused by coronary-flow alterations in isolated perfused heart of guinea pigs.

The ligation of a main branch of coronary vein elevates the sensitivity of isolated, perfused (Langendorff) preparations of guinea-pig heart to arrhythmogenic actions of digoxin. Retrograde perfusion studies indicate that the presence of an area with a high extracellular K+ concentration, adjacent to an area with normal K+ concentration and exposed to the glycoside, predisposes the heart to digitalis-induced toxicity. This model may be useful in studying the mechanism by which acute myocardial infarction decreases the therapeutic index of cardiac glycosides.

Animals↗
PubMed1988

Dopamine 4-sulfate: effects on isolated perfused rat heart and role of atria.

We studied the effects of sulfate conjugate of dopamine on the isolated perfused rat heart (Langendorff preparation). In the experimental group, we removed atria from half number of the hearts. In the hearts with intact atria, dopamine 4-sulfate significantly improved the DT (developed tension), +dT/dt max (maximal rate of contraction), -dT/dt max (maximum rate of relaxation) over baseline values. But when atria were removed, dopamine 4-sulfate had no effect on the mechanical functions of heart. We analysed the effluent perfusate for the free and conjugated catecholamines. In the control group (no drug), and when atria were excised, the free catecholamine levels were negligible. But when the atria were kept intact, the effluent contained significant amount of free dopamine (DA), and norepinephrine (NE). These data suggested that dopamine sulfate had no direct effect on the ventricular muscle of rat heart, but was converted within the atrial tissues into free catecholamines which might be responsible for the positive inotropic actions.

Animals↗
PubMed1991

Effects of synthetic ANF (rANF(3-28)) on sympathetic neurotransmission in the isolated perfused rat kidney.

The effects of synthetic atrial natriuretic factor (rANF(3-28)) on sympathetic neurotransmission in the isolated perfused rat kidney was examined. ANF (10(-10)-10(-7) M) had no significant effect on stimulus-induced (1 Hz, 2 min) overflow of endogenous norepinephrine (NE) from the rat kidney. ANF also failed to affect stimulus-induced overflow which was markedly enhanced as a result of prejunctional beta-adrenoceptor activation with isoproterenol (10(-6)M). However, over the same concentration range ANF markedly attenuated the vasoconstrictor response to nerve stimulation. In addition, ANF significantly reduced the renal vasoconstrictor responses to intra-arterial injections of NE and angiotensin II. These results suggest that, while ANF potently inhibits renal sympathetic neurotransmission by inhibition of vascular responsiveness to vasoconstrictor stimuli, ANF does not appear to have a prejunctional effect to alter NE release from renal sympathetic nerves.

Animals↗
PubMed1993

Vasoactive intestinal peptide (VIP) stimulates androstenedione release in isolated perfused pig adrenals.

The effect of the vasoactive intestinal peptide (VIP) on adrenal androstenedione release was investigated in isolated perfused pig adrenals. Our system allowed a direct comparison with the effect of ACTH, gonadotropins and proopiomelanocortin 79-96, which has been suggested to be the specific cortical androgen stimulating hormone (CASH). VIP 10(-8) M provoked a threefold increase of androstenedione release which was similar to the effect of ACTH at a physiological concentration of 10(-10) M. Gonadotropins at a perfusate concentration of 0.5 I.U. weakly but significantly increased androstenedione output, the response amounting to 32% of that elicited by ACTH or VIP. Perfusion of the adrenals with CASH at concentrations of 10(-11) to 10(-8) M did not affect the release of adrenal androstenedione. VIP appears to be a modulator of adrenal androgen release which might be involved in a local neuroendocrine control of adrenal androgen secretion.

Adrenal Glands↗
PubMedDate not supplied

Transfer of acipimox across the isolated perfused human placenta.

The placental transfer of the new lipid-lowering agent, acipimox was investigated in the isolated perfused human placenta. Placentas obtained at caesarean section were perfused for 120 min, with both maternal and fetal circuits in closed recycling mode. Acipimox was added to either the maternal circuit alone (five experiments) or to both maternal and fetal circuits simultaneously (five experiments) to achieve initial concentrations of 5 micrograms/ml. Antipyrine (20 micrograms/ml) and l-(14C)-leucine (250 microM) were added in like fashion as reference compounds. Two hours after addition to the maternal circuit alone antipyrine was close to equilibrium across the placenta, but equilibration of acipimox was incomplete (fetal/maternal ratio = 0.58 +/- 0.11). Maternal to fetal placental clearance of acipimox (0.80 +/- 0.18 ml/min) was 25 per cent of antipyrine clearance. After simultaneous administration to both maternal and fetal circuits the l-(14C)-leucine fetal/maternal ratio was 1.44 +/- 0.13 at 120 min, whereas maternal and fetal concentrations of acipimox and antipyrine were at equilibrium for the duration of the experiment (fetal/maternal ratio of acipimox at 120 min = 1.10 +/- 0.06). This study shows that acipimox is transferred across the human placenta by diffusion at a slow rate. The low permeability of the placenta may afford some protection to the fetus from acipimox administered to the mother in vivo.

Antipyrine↗
PubMed1990

Influence of ethanol on glutathione-S-transferase activity and glutathione content in the isolated perfused rabbit lung.

The induction of pulmonary glutathione-S-transferase (GST) by ethanol was investigated using the isolated perfused rabbit lung (IPRL) preparation with particular attention paid to the duration and route of ethanol administration. For perfusion with buffer containing 0.2% ethanol or acute ethanol treatment (4 g/kg by gastric intubation) 4 h before the IPRL preparation, there were no differences in the rate of glutathione (GSH) conjugation with 1-chloro-2,4-dinitrobenzene (CDNB) at low substrate concentrations (100-400 microM) but a decrease was observed in the rate at high substrate concentrations (500-1000 microM). Lungs from rabbits treated acutely showed the lowest maximal rate of GSH conjugation in the IPRL. Prolonged treatment with ethanol (10% in drinking water for 3 weeks) increased GSH conjugation (CDNB concentration of 300-750 microM). None of these ethanol treatments altered GSH conjugation with 1,2-epoxy(p-nitrophenoxy)propane (ENP). Upon termination of perfusion, there were no differences in pulmonary GSH concentration between control and ethanol-treated groups. Therefore, the effect of altered GSH level as a co-substrate on GST activity in lung might be excluded as an explanation for the effects of ethanol. These data suggest that ethanol has differential effects on GST activity depending upon the substrate and duration of ethanol administration.

Animals↗
PubMed2006

Naproxen-induced oxidative stress in the isolated perfused rat liver.

We previously showed that naproxen induced the oxidative stress in the liver microsomes and the isolated hepatocytes of rats. In this study, the in situ effect of naproxen on the rat liver tissue was investigated, using the isolated perfused liver from the view-point of the naproxen-induced hepatotoxicity. The leakage of glutamic-oxaloacetic transaminase (GOT) from the perfused liver and appearance of thiobarbituric acid reactive substances (TBARS) in the perfusate increased with the progress of perfusion after a lag time of about 1h. The naproxen-perfusion of the liver decreased the biliary excretion of glutathione (GSH) and oxidized glutathione, glutathione disulfide (GSSG) prior to TBARS production and GOT leakage. GSSG content in the naproxen-perfused liver was significantly higher than in the control. TBARS appeared in the perfusate of the naproxen-perfused liver for 30 min, but not in the control. The biliary excretion clearance (CL(bile)) of indocyanine green (ICG), a reagent for testing the liver function, in the liver perfused with naproxen decreased to a half of that in the liver perfused without naproxen. Thus, the naproxen-induced oxidative stress in the liver was shown to affect the physiological function of liver through the impairment of biliary excretion, which is recognized as a detoxification system.

Animals↗
PubMed1999

Changes in hepatic nitrogen metabolism in isolated perfused liver during the development of thioacetamide-induced cirrhosis in rats.

Changes in hepatic nitrogen metabolism in isolated perfused liver were studied during the induction of experimental cirrhosis by thioacetamide in female Sprague-Dawley rats. Cirrhosis of the micronodular type developed during 12-week administration of thioacetamide. Despite an increase in food consumption for 4 weeks after the end of administration, the physiological changes characteristic of cirrhosis were maintained. The rate of urea excretion per unit liver weight was significantly decreased compared with pair-fed control rats both during and after thioacetamide treatment. During 4 weeks of thioacetamide treatment, the rate of urea production in perfused liver from a combination of 0.25 mM NH4Cl and 1 mM glutamine decreased slightly, without a decrease in the maximum rate of urea production from 10 mM NH4Cl. In cirrhotic rats, the rate of urea production in perfused liver from NH4Cl and/or glutamine decreased, with a decrease in the maximum rate of urea production. The Km of ureagenesis for NH3 was unchanged in cirrhotic livers. During 4 weeks of thioacetamide treatment, glutamate dehydrogenase activity decreased, but the thioacetamide-induced cirrhotic state had no effect on glutamate dehydrogenase or glutaminase activity. Glutamine synthetase activity was decreased in rats treated with thioacetamide for 4 or 12 weeks. These results are consistent with the hypothesis that the capacity for urea production from NH3 and amino acids is decreased in the development of cirrhosis.

Alanine Transaminase↗
PubMed1989

Reduction volume dependence of immunoreactive atrial natriuretic peptide secretion in isolated perfused rabbit atria.

A new technique to permit gradual changes in atrial distension has been developed in an isolated perfused rabbit atrium preparation. Graded volume reduction in the atrium was induced by changing the elevation of the outflow catheter tip. Pressure reduction from 6 cm H2O atrial distension resulted in a decrease in atrial distension volume. Atrial distension by 6 cmH2O did not change the release of immunoreactive atrial natriuretic peptide (irANP). The graded reduction in atrial distension from 0.11 +/- 0.03 (1.5 cm H2O) to 1.36 +/- 0.19 microliters/mg wet weight (6.0 cm H2O) resulted in 1.7 (6.76 +/- 2.05 versus 3.83 +/- 1.18 pg/mg per min, n = 9, P less than 0.025) to 40.1-fold (77.66 +/- 17.82 versus 3.0 +/- 1.14 pg/mg per min, n = 11, P less than 0.025) increases in irANP release. IrANP release in response to the reduction of atrial distension was volume dependent. The relation of percentage increase in irANP release with the percentage reduction of atrial distension was exponential. The data suggest that the atrial muscle shortening, but not stretch per se, may be a potent direct stimulus for the regulation of irANP secretion.

Animals↗
PubMed1991

Influence of hypoxia on the myocardial uptake and pharmacodynamics of quinidine in isolated perfused rabbit hearts.

The effects of hypoxia on the myocardial uptake and pharmacodynamics of quinidine were studied in isolated perfused rabbit hearts. Hearts were perfused with a modified Krebs-Henseleit buffer that was equilibrated with either 95% O2-5% CO2 (normoxia) or 95% N2-5% CO2 (hypoxia). The myocardial quinidine accumulation was determined from concentration differences in aortic perfusate and coronary sinus effluent. Under hypoxic conditions, the myocardial concentration of quinidine (12.0 +/- 3.6 micrograms/g) was significantly reduced compared to normoxic conditions (24.8 +/- 8.5 micrograms/g, p less than 0.01). Greater increases in QRS complex duration were observed during hypoxia (10.0 +/- 1.0 ms) compared to normoxia (7.5 +/- 1.3 ms; p less than 0.05). Greater increases in MAP duration were also observed during hypoxia (64 +/- 14 ms) compared to normoxia (37 +/- 14 ms; p less than 0.01). The myocardial concentration-effect relationships describing changes in QRS complex duration, QT interval, MAP duration, and ventricular effective refractory periods were linear in both groups. The curves of the concentration-effect relationships observed during hypoxia were shifted to the left compared to those observed during normoxia and the slopes of these relationships were also significantly greater (p less than 0.05). These pharmacokinetic and pharmacodynamic interactions may be explained by the development of acidosis during hypoxia since the pH of the coronary sinus effluent decreased significantly during hypoxia (7.10 +/- 0.04) compared to the normoxic group (7.25 +/- 0.04, p less than 0.001). Thus, although hypoxia reduces the myocardial accumulation of quinidine, greater electrophysiologic effects are observed compared to normoxic conditions. These observations likely relate to a change in responsiveness of acidotic tissue to quinidine.

Action Potentials↗