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At least 991 records · Page 55Linked to original sources
PubMed1990

Modification of the gluconeogenic/glycolytic balance in isolated perfused liver of myeloproliferative leukemia infected mice: a 13C NMR study.

1. Isolated perfused livers from starved mice inoculated with myeloproliferative leukemia virus exhibited similar rates of consumption of [3-13C]alanine and of synthesis of glutamine and glutamate labeled at the C-2 or C-3 positions as livers from uninfected mice. 2. Leukemic livers also formed glutamine and glutamate labeled at the C-4 position. This is related to their lower content of triglyceride as compared to that of control livers which do not produce these isotopomers. 3. The glucose synthesis rate was much lower in livers from leukemic mice. This is explained by the glycolytic properties of the leukemic infiltrating cells.

Alanine↗
PubMed1996

The isolated perfused "working" rat heart: a new method.

This paper presents a "working" isolated perfused rat heart. A special double cannula was designed consisting of an outer cannula that is inserted in the aorta and an inner cannula that is advanced into the left ventricle. The perfusion fluid flows through the inner cannula into the left ventricle, and is ejected from there into the aorta. If the outer cannula system is closed, the fluid perfuses the coronary vessels and drips off outside the heart. When the outer cannula is open and certain pressure resistance is applied, a fraction of the ejected fluid perfuses coronary vessels and the rest is expelled. Because the inner cannula can easily be retracted into the outer cannula, which is placed in the aorta, this preparation provides an opportunity to use the same heart as a "working" or "non-working" model for investigating functions of the heart. The effects of epinephrine and yohimbine were tested on this model. This preparation is simple, durable, and reliable.

Adrenergic alpha-Agonists↗
PubMed1996

The ex-vivo isolated, perfused human lung model: description and potential applications.

An ex-vivo isolated, perfused, and ventilated human lung (IPHL) model is well suited for many kinds of physiological, pharmacological, and surgical studies, when the physiological and biochemical conditions in the lung can be maintained near to those in vivo. The aim of this work was to develop such a model. The lung preparations used were available after resection because of bronchial carcinoma. Since the tumor remains intact in these anatomical preparations, this model is particularly suitable for investigation of the pharmacokinetics and effects of anticancer agents. Carrying out a series of 52 IPHL experiments (with 11 whole-lung preparations and 41 lobe preparations), we have established an IPHL model which allows extracorporeal perfusion and ventilation of the resected lungs in physiological conditions for 2-3 hours. The net weight gain during the experiment, wet-to-dry weight ratio for lung tissue, angiography of the pulmonary artery, pulmonary vascular resistance, color and fluorescence of the lung surface, and alveolar gas diffusion into the perfusate proved to be useful parameters to assess the stability of the preparations and the quality of the experiments. To confirm that an intraparenchymal tumor was perfused via the pulmonary artery, methods to detect avidin and dextran-biotin in tumor tissue after administration into the perfusion solution were employed. Histological examination of bronchial as well as tumor tissue, a computerized histoanalyzation, and a tumor grading program demonstrated that IPHL experiments did not interfere with the grading and staging of the tumors-an important ethical precondition for the use of human preparations in an extracorporeal perfusion model.

Carcinoma, Bronchogenic↗
PubMedDate not supplied

Nmda alters the development of hypoxic pulmonary vasoconstriction and nitric oxide synthetase activity in the isolated perfused rat lung.

Using an isolated salt-perfused rat lung model, the authors investigated whether N-methyl-D-aspartate (NMDA) (1 mM) in the pulmonary circulation effects the pulmonary vascular responses to an acute stimulus of hypoxic insult under baseline, nitric oxide synthetase (NOS)-blocked conditions (N-omega-nitro-L arginine methyl ester; L-NAME, 2 mM), and with an NMDA receptor blocker, MK-801 (0.3 microM) added. NOS activity at baseline, and in response to hypoxia, NMDA, L-NAME, and a combination of these stimuli were also assessed. NMDA did not in itself alter hypoxic pulmonary vasoconstriction (HPV), but did significantly attenuate HPV during VOS blockade. This effect of NMDA was erased by MK-801. Assessment of NOS activity showed that hypoxia alone caused a doubling of NO production within the lung. This effect was erased by the addition of L-NAME. NMDA alone caused a significant, 3-fold increase in NOS activity, which was not further affected by hypoxic chalenge. L-NAME did not depress NOS activity in the hypoxia + NMDA group. These data suggest that NMDA receptor activation results in increased NOS activity and presumably increased production of NO. The increased NOS activity induced by NMDA receptor stimulation is resistant to the blockade effect of L-NAME. The actions of NMDA receptor activation may represent a natural protective mechanism, at least within the pulmonary vasculature, in face of acute, abnormal stimuli such as hypoxia.

Animals↗
PubMed1983

Cell surface changes and enzyme release during hypoxia and reoxygenation in the isolated, perfused rat liver.

We examined the effects of hypoxia and reoxygenation in isolated, perfused rat livers. Hypoxia induced by a low rate of perfusion led to near anoxia confined to centrilobular regions of the liver lobule. Periportal regions remained normoxic. Within 15 min, anoxic centrilobular hepatocytes developed surface blebs that projected into sinusoids through endothelial fenestrations. Periportal hepatocytes were unaffected. Both scanning and transmission electron microscopy suggested that blebs developed by transformation of preexisting microvilli. Upon reoxygenation by restoration of a high rate of perfusion, blebs disappeared. Other changes included marked shrinkage of hepatocytes, enlargement of sinusoids, and dilation of sinusoidal fenestrations. There was also an abrupt increase in the release of lactate dehydrogenase and protein after reoxygenation, and cytoplasmic fragments corresponding in size and shape to blebs were recovered by filtration of the effluent perfusate. We also studied phalloidin and cytochalasin D, agents that disrupt the cytoskeleton. Both substances at micromolar concentrations caused rapid and profound alterations of cell surface topography. We conclude that hepatic tissue is quite vulnerable to hypoxic injury. The morphological expression of hypoxic injury seems mediated by changes in the cortical cytoskeleton. Reoxygenation causes disappearance of blebs and paradoxically causes disruption of cellular volume control and release of blebs as cytoplasmic fragments. Such cytoplasmic shedding provides a mechanism for selective release of hepatic enzymes by injured liver tissue.

Animals↗
PubMed1975

Ventricular fibrillation threshold and vulnerable period in the isolated perfused rat heart.

Ventricular fibrillation threshold (VFT) measurements were obtained in the isolated perfused rat heart. Detailed morphology of the vulnerable period (VP) could be described by stimulating repeatedly at increasing levels of stimulus energy. Addition of lignocaine to the system caused an elevation of VGT, but also led to a delay of the VP to the end of the QT interval. The implications of these findings for the understanding of VFT measurements are discussed.

Animals↗
PubMed1985

Differences in pulmonary metabolism of benzo(a)pyrene in inbred mouse strains, using the isolated perfused lung.

The metabolism of benzo(a)pyrene (BaP) was studied in isolated perfused and ventilated lungs from two inbred strains of mice. C57BL/6 and DBA/2 mice were treated with beta-naphthoflavone (BNF) or corn oil alone in order to reveal strain differences in inducibility of the microsomal enzymes responsible for BaP oxidation. BaP metabolism was quantified by the rate of appearance of free and conjugated 14C-metabolites released into the perfusion medium, and the production of nonextractable metabolites covalently bound to lung macromolecules. In both strains, lungs from mice pretreated with BNF released BaP metabolites at a rate somewhat greater than vehicle-treated controls, without a distinct change in the profile of metabolites. However, the amount of BaP covalently bound to lung macromolecules was increased by BNF pretreatment in C57BL/6 mice only. Thus, release of BaP metabolites into the perfusion medium was not a predictor of the rate of production of reactive metabolites.

Animals↗
PubMed1990

The chronotropic effect of acetylcholine in the presence of vecuronium and atracurium. A study in the isolated perfused rabbit heart.

The bradycardia produced by 1 microgram acetylcholine in the isolated perfused rabbit heart, in the presence of vecuronium and atracurium, was studied and compared with control. Vecuronium at a concentration of 2.5 micrograms/litre and atracurium 6 micrograms/litre did not enhance the negative chronotropic effect of acetylcholine. Atracurium produced a statistically significant inhibition of the negative chronotropic effect of acetylcholine.

Acetylcholine↗
PubMed1994

Moment analysis of hepatic local disposition of allopurinol and oxipurinol: metabolism kinetics from allopurinol to oxipurinol in the rat isolated perfused liver.

Drug metabolism in the liver was examined by the rat isolated perfused liver using the single-pass bolus-input technique. The test compounds, allopurinol and its metabolite oxipurinol, were independently introduced into the liver from the portal vein, and the concentration profiles in the venous outflow were monitored and kinetically analysed by moment theory. The recovery ratios of allopurinol and oxipurinol after the individual administration of each drug were estimated to be 0.17 (+/- 0.08 s.d.) and 1.03 (+/- 0.02 s.d.), respectively. The outflow recovery ratio of oxipurinol as the metabolite after allopurinol administration was estimated to be 0.80 (+/- 0.07 s.d.). These results indicate that the combined outflow recovery of the precursor and the metabolite after allopurinol administration is almost 100% in the rat liver.

Allopurinol↗
PubMed1977

Renin stimulation by isoproterenol and theophylline in the isolated perfused kidney.

The intrarenal mechanisms of renin release were studied in the isolated perfused rabbit kidney during stimulation by isoproterenol, 0.01 mug/kg per min, and by theophylline, 0.87 mg/kg per min. In the absence of urinary flow during the early stages of perfusion, isoproterenol caused a 17% increase of renal vein serum renin concentration (RVSRC) (P less than 0.001) without changing renal blood flow, renal vascular resistance, or serum potassium. dl-Propranolol, 2.0 mg/kg per min. abolished this isoproterenol-induced renin release. A moderate reduction in perfusion pressure prior to the infusion of isoproterenol resulted in a marked additional stimulation of renin release. Studies during and following ureteral occlusion demonstrated that theophylline stimulates renin release by decreasing renal vascular resistance, whereas the concomitant increase in sodium transport to the macula densa exerted an opposite effect. dl-Propranolol did not affect theophylline-induced renin secretion. It is concluded that single exogenous stimuli may activate more than one intrarenal mechanism simultaneously. Isoproterenol has a direct renin-stimulatory effect on intrarenal beta-adrenergic receptors that may be reinforced by baroreceptor stimulation. Theophylline stimulates renin via a baroreceptor mechanism, with simultaneous renin suppression via a sodium-macula densa effect.

Animals↗
PubMed1989

Protective effect of nicorandil on postischemic function and tissue adenine nucleotides following a brief period of low-flow global ischemia in the isolated perfused rat heart.

A new antianginal agent, nicorandil, was tested in an isolated perfused rat heart model. Hearts were subjected to 30 min of low-flow, global ischemia followed by 30 min of reperfusion in the presence or absence of nicorandil. Nicorandil (1,500 micrograms/l) significantly improved isovolumic left ventricular minute-work during reperfusion compared to untreated hearts. Nicorandil also prevented the rebound in cardiac phosphocreatine levels and the loss of total adenine nucleotides as a result of ischemia and reperfusion. The salient effect of nicorandil was independent of any alterations in the release of endogenous prostacyclin. These results suggest that nicorandil may possess a unique cytoprotective effect on the ischemic-reperfused myocardium.

Adenine Nucleotides↗
PubMed1985

Production and excretion of dopamine by the isolated perfused rat kidney.

Renal catecholamine concentrations and urinary dopamine excretion from the isolated perfused kidney were measured in intact and peripherally sympathectomized rats. Urinary dopamine excretion was not diminished by sympathectomy, was increased by l-dopa (but not tyrosine or dopamine 4-O-sulphate) in the perfusate and was virtually abolished by prior treatment with the dopa decarboxylase inhibitor, carbidopa. These results confirm the importance of renal extraneuronal dopamine production, from circulating l-dopa, as a contributor to urinary dopamine excretion.

Animals↗
PubMed1991

Effect of nitric oxide generators on ischemia-reperfusion injury and histamine release in isolated perfused guinea pig heart.

In an ischemia-reperfusion model obtained in isolated perfused guinea pig heart by means of a double ligature of the left anterior descending coronary artery, the reperfusion of the ischemic myocardium leads to a release of lactate dehydrogenase and histamine, related to a decrease in the microdensitometry of cardiac mast cells and to a tissue calcium overload. The perfusion of the heart with L-arginine and with nitric oxide donors significantly reduces the release of histamine, the loss of mast cell metachromasia and calcium overload. These effects were potentiated by superoxide dismutase.

Animals↗
PubMed1987

Stimulation of phosphatidylinositol metabolism in the isolated, perfused rat heart.

Receptor-stimulated phosphatidylinositol turnover has been studied in isolated, perfused, [3H]inositol-labelled rat hearts by measuring accumulation of inositol phosphates in the presence of lithium chloride. Inositol phosphate accumulation was stimulated by norepinephrine (3 X 10(-5) M) and carbachol (10(-3) M), the increases averaging from 931 +/- 59 (n = 6, mean +/- SEM, cpm/g heart) to 4,165 +/- 609 (n = 6, p less than 0.01) for norepinephrine and to 1,853 +/- 354 (n = 6, p less than 0.05) for carbachol. The norepinephrine stimulation was antagonized by prazosin (10(-7) M) but not by propranolol (10(-7) M), indicating mediation via alpha 1-adrenoceptors. The carbachol stimulation was antagonized by atropine (10(-7) M). The stimulation by norepinephrine was significantly higher in right atria (837 +/- 151 to 6,614 +/- 1,210, n = 6, cpm/g tissue) than in other regions of the heart. Both norepinephrine and carbachol stimulated the formation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate with norepinephrine stimulation being detected as early as 15 seconds. Furthermore, the inositol trisphosphate was identified as the -1,4,5 isomer by anion exchange high-performance liquid chromatography. These data are consistent with the hydrolysis of phosphatidylinositol-(4,5)-bisphosphate yielding inositol-(1,4,5)-trisphosphate. Inositol-(1,3,4)-trisphosphate was not detected in heart preparations, suggesting unusual metabolism of inositol-(1,4,5)-trisphosphate in heart tissue.

Animals↗
PubMed1979

The handling of immunoreactive vasopressin by the isolated perfused rat kidney.

Using the isolated rat kidney perfused with an artificial medium containing glucose as the sole fuel, we studied the renal handling of immunoreactive arginine vasopressin (AVP) and determined the effect of various factors on the ability of the kidney to remove AVP. In control kidneys perfused with AVP at concentrations below 116 muU/ml, the organ clearance of AVP (OC(AVP)) was 1,145+/-47 (SE) mul/min, whereas glomerular filtration rate (GFR) averaged 515+/-37 mul/min. Filtration could thus account for up to 45% of the OC(AVP), the balance presumably being cleared from the peritubular circulation. Of the AVP filtered, only 38% could be recovered in the urine (urinary clearance AVP averaged 205+/-12 mul/min) suggesting that the balance was taken up by the tubular epithelium and degraded. Fractional excretion of filtered AVP rose significantly in the presence of anoxia and cold (10 degrees C) to 49 and 59%, respectively, but was not affected by ouabain or high levels of AVP (458+/-58 muU/ml). The OC(AVP) was not significantly altered by the absence of glucose in the perfusate, anoxia, or ureteral ligation, maneuvers that were associated with significant reductions in GFR. In these and the control experiments, there was a significant inverse correlation between GFR and peritubular clearance emphasizing the importance of the latter (r = -0.749; P < 0.001). Cold, ouabain, and high concentrations of AVP reduced the clearance of AVP by the kidneys. On the basis of these studies we conclude that the kidney clears AVP from the circulation via two pathways, glomerular clearance and peritubular clearance. This exposes both the luminal and contraluminal surfaces of the tubular cells to the hormone, allowing these cells to remove AVP from the filtrate and the peritubular compartment. Noteworthy is the observation that under several conditions when GFR falls reducing the glomerular clearance of AVP, peritubular clearance increases and the total clearance of AVP by the kidney remains constant.

Albumins↗
PubMed1984

Effect of ethanol on uptake of trichloroethylene in isolated perfused rat liver.

The effect of ethanol on uptake of trichloroethylene in isolated perfused rat liver was investigated. The uptake of trichloroethylene was measured in both phenobarbital (PB) non-treated and PB treated rat livers. Furthermore, for PB treated rat livers, the fluorescence of reduced pyridine nucleotides, oxygen consumption, and scanning reflectance spectrum were measured in the liver, perfused with Krebs-Henseleit buffer saturated with a 92%O2-5%CO2-3%CO gas mixture. The uptake of trichloroethylene was decreased by 6.0% in the PB non-treated rat liver and 10.6% in the PB treated rat liver following the addition of ethanol. This uptake decrease was thought to arise mainly from the inhibitory effect of ethanol on mixed-function oxidation in the liver because of the corresponding decrease in oxygen consumption and absorbance difference delta A450-490nm. The inhibition was considered to be due to interference with electron transfer to the complex of substrate and cytochrome P-450. Increase in intracellular NADH might also affect the formation of trichloroacetic acid since the reduction of NADH in the cytosol attained a maximum with 20 mM ethanol.

Animals↗
PubMed1982

Tolbutamide stimulates gastric somatostatin release from isolated perfused rat stomach.

The effect of tolbutamide on somatostatin release from the isolated perfused stomach was investigated in both normal and streptozotocin-diabetic rats. Tolbutamide (10, 100, and 1000 microgram/ml) evoked a significant and dose-dependent increase in gastric somatostatin release. The tolbutamide (100 microgram/ml)-induced gastric somatostatin secretion was not influenced by differences in glucose concentration (1.5, 5.5, and 16.5 mM) throughout the perfusion period. Tolbutamide (100 microgram/ml)-induced gastric somatostatin release in streptozotocin-diabetic rats was significantly higher than in normal rats. Thus, tolbutamide is a potent secretagogue for gastric somatostatin secretion, and this effect is more prominent in diabetic animals.

Animals↗
PubMed1987

The metabolic sulphation of polyethyleneglycols by isolated perfused rat and guinea-pig livers.

1. It is shown that isolated perfused rat and guinea-pig livers can sulphate polyethyleneglycol 200 at rates of about 5 and 10 nmol/g per min, respectively. 2. In the guinea-pig about equal amounts of sulphated polyethyleneglycol 200 appear in the bile and in the perfusate, while in the rat about 99% appears in the latter. 3. Polyethyleneglycols 400 and 1000 are also sulphated in perfused guinea-pig liver but polyethyleneglycol 6000 is not. 4. Polyethyleneglycols are therefore not suitable solvents for xenobiotics which may undergo sulphation because of the likelihood of competition for sulphate.

Animals↗