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PubMed1999

Does aprotinin modify the effects of ischaemia-reperfusion on the myocardial performance of a blood perfused isolated rabbit heart?

Aprotinin has been reported to influence positively or negatively the process of ischaemia-reperfusion. However, it is a complex drug acting on platelets, neutrophils and coagulation, which may also have a direct effect by inhibiting intracellular proteases and free radical generation. The goal of this study was to determine the direct effects of aprotinin on the myocardial performances of an isolated blood perfused rabbit heart preparation after normothermic global ischaemia. Two groups of 10 hearts were studied. The control group (ischaemia) underwent 30 min of global normothermic ischaemia. In the aprotinin group, (aprotinin) 200 KUI mL-1 of aprotinin was added to the perfusate before ischaemia. Measurements were obtained at base-line, 10, 30 and 60 min after reperfusion. Normothermic ischaemia significantly decreased myocardial performance in both groups. After 60 min reperfusion, myocardial contractility significantly recovered in the aprotinin group compared with the ischaemia group. Aprotinin contributes significantly by limiting the consequences of ischaemia on myocardial performances. This effect may be due to a direct action of the drug because leucocytes and plasma proteins were removed in this preparation.

Animals↗
PubMed1985

The effects of naloxone on glucose uptake and metabolism in the isolated perfused hindlimb of the rat.

Naloxone, an opiate antagonist, is reported to reverse hypotension and to improve survival in hemorrhaged and septic animals. We have found recently that naloxone also blunts the hyperglycemic response to hemorrhage. This could result from a naloxone-induced diminution of the hypotensive stimulus to hyperglycemia, from a naloxone-induced diminution of hormonal secretion or action, from a naloxone-mediated decrease in glucose production, or from a direct action of naloxone on glucose uptake in skeletal muscle and other peripheral tissues. In order to examine the direct effect of naloxone on glucose uptake in skeletal muscle, male Sprague-Dawley rats were perfused in a standardized isolated perfused hindlimb system with or without naloxone (0.5 microgram/ml of perfusate). No insulin was added to the perfusate. Glucose uptake in animals treated with naloxone was 30.2% greater than that of control animals (p less than 0.05). This increase was not dependent on insulin. Although no significant differences were noted in the individual products of glucose utilization, the total tissue glucose that could be accounted for by these intermediates was increased in naloxone-treated hindlimbs (p less than 0.05). Thus the increase in glucose uptake by skeletal muscle noted in these experiments may explain, in part, the blunted hyperglycemic response to hemorrhage that occurs after naloxone administration. These results also suggest the possibility that endogenous opiates may be important in regulating glucose metabolism after hemorrhage.

Animals↗
PubMed1999

Urinary excretion of urodilatin is increased during pressure natriuresis in the isolated perfused rat kidney.

The findings about mechanisms regulating production and excretion of urodilatin [ANP-(95-126)], a member of the atrial natriuretic peptide (ANP) family, are controversial. To elucidate a possible relationship between arterial blood pressure and renal urodilatin excretion, we studied the effects of different perfusion pressures on urine flow (UV), urinary sodium (U(Na)V), urinary potassium (U(K)V), and urodilatin excretion (U(URO)V), and the concentration of urodilatin in the perfusate (P(URO)) of isolated perfused rat kidneys. Kidneys were perfused for 180 min with constant perfusion pressures (80 and 120 mmHg, respectively; each, n = 4) in a closed circuit system. Samples of urine and perfusate were taken every 30 min. Mean UV, U(Na)V, U(K)V, and U(URO)V values were significantly higher with a perfusion pressure of 120 mmHg than with 80 mmHg, whereas P(URO) did not change significantly. Serial measurements revealed no direct relation of U(URO)V with either U(Na)V or UV. This suggests that renal perfusion pressure is a determinant of U(URO)V and that urinary and venous effluent concentrations of urodilatin (probably production) are not coupled directly and that U(URO)V and U(Na)V may dissociate during acute variations of sodium excretion and UV.

Animals↗
PubMed2001

[Protective effect of berberine on isolated perfused heart in heart failure].

OBJECTIVE: To examine the protective action of berberine against the development of heart failure. METHODS: Wister rats were divided into two groups. The Langendorff perfusion of isolated heart was performed and Verapamil was used to bring about acute heart failure. The experiment group was given berberine (10(-6) mol/L) before the use of Verapamil, but the control group was not given the berberine. A comparison was made on the degree of heart failure between the two group. RESULTS: The degree of heart failure in the experiment group was significantly less severe than that in the control group (P < 0.001). CONCLUSION: Berberine has the protective action against to the development of heart failure.

Animals↗
PubMed1988

Discrimination between alpha 1- and alpha 2-adrenergic receptors in the isolated perfused ileum.

Adrenergic control over intestinal homeostasis has been associated with changes in intestinal vascular resistance, motility, and transport. With the use of selective alpha-adrenergic agents, this study was designed to discriminate between the vascular and transport effects. Rabbit 20 cm ileal segments (n = 31) were vascularly perfused at a rate of 1.5 ml/min by means of a modified Krebs solution containing 15% to 20% red cells. The intestinal lumen was perfused with an isotonic solution containing carbon 14-polyethylene glycol as a nonabsorbable marker. Net fluxes of water and electrolytes were calculated during 20-minute basal, experimental, and recovery periods. Norepinephrine (mixed alpha 1- and alpha 2-agonist) significantly increased intestinal absorption and vascular resistance. Phenylephrine (alpha 1-agonist) significantly increased vascular resistance without altering transport. Clonidine (alpha 2-agonist) stimulated intestinal absorption without changing vascular perfusion pressure. Yohimbine (alpha 2-antagonist) prevented norepinephrine-induced absorption but had no effect on norepinephrine-induced increases in perfusion pressure. In this isolated perfused whole gut model, alpha 1-adrenergic stimulation was responsible for increases in vascular resistance, and alpha 2-adrenergic stimulation was responsible for increases in the absorption of water and electrolytes. The ability to discriminate between alpha 1- and alpha 2-effects has potential therapeutic implications in patients with malabsorption and diarrhea.

Adrenergic alpha-Agonists↗
PubMed1977

[Comparison in genetically obese and normal rats of the uptake and incorporation of labelled lauric acid, oleic acid, and glycerol by the isolated perfused liver].

Lauric acid, labelled oleic acid and glycerol are perfused in isolated liver of fafa Rats and Wistar Rats previously subjected to fasting. They synthesize TG and PL de novo, though in long time experiments with the normal Rat, the most important method of synthesis is an exchange of AG of the endogenous glycerolipids. However PL are not synthesized with lauric acid. In the livers of fafa Rats the synthesis of TG with oleic acid and glycerol is higher than in livers of Wistar Rats: 16:0 18 : 1 18: 1, 16:0 18: 1 18: 2, 18 : 1 18 :1 18:1, 16 : 0 16 :0 18 : 1 (this TG is not present in liver of Wistar Rat). The hepatic synthesis of PL by the fafa Rat, is less important after 15 min while it is important with Wistar Rats. The synthesized TG with lauric acid (only the TG 12 : 0 12 : 0 12 : 0 with the fafa Rat) are more rapidly oxidized by liver of obese Rat than by liver of normal Rat.

Animals↗
PubMed1982

Alteration by kallikrein and bradykinin of the conversion of angiotensin I to angiotensin II in the isolated perfused rat lung.

Pure kallikrein and bradykinin, when added to the perfusion medium of the isolated perfused rat lung, produced an equal inhibition in the conversion of angiotensin I to angiotensin II as measured in the venous return superfused over the rabbit aortic strips. Acetylsalicylic acid (ASA) prevented the inhibitory effect of kallikrein and bradykinin. Aprotinin, however, prevented the inhibitory effect of kallikrein without altering that of bradykinin. The recovery brought about by ASA of the bradykinin-produced inhibition of angiotensin I conversion was also prevented by prior addition of prostaglandin E2 (PGE2) into the perfusion medium. Neither kallikrein and bradykinin nor ASA altered the myotropic activity of angiotensin II. 5-Oxo-L-prolyl L-tryptophyl-L-prolyl-L-arginyl-L-prolyl-L-glutaminyl-L-isoleucyl-L-prolyl-L- proline (SQ 20 881), when added to the medium, greatly reduced the responses to angiotensin I but potentiated those of angiotensin II. The possible mechanisms of the inhibitory effects of kallikrein and bradykinin are discussed.

Angiotensin I↗
PubMed1981

Phospholipid synthesis in isolated perfused lungs of rats made tolerant to 100% oxygen.

Tolerance to 100% oxygen is readily induced in the rat by prior exposure to 80% oxygen for 7 days. In order to determine whether the rate of synthesis, or te alveolar content, of pulmonary phospholipids is altered in the tolerant rat, we perfused the isolated lung with medium containing 20 muM [14C]methyl choline chloride for 30 min at 10 ml/min, and then we measured the incorporation of carbon-14 into tissue phospholipids. We also measured the phospholipids in the lavage. There was no difference in the rate of incorporation in the tolerant rats (201 +/- 11 nmol/g dry lung, n = 8, mean +/- SEM) compared to control rats (210 +/- 9 nmol/g dry lung, n = 4) that had been exposed to air for 7 days under identical conditions. Whereas the induction of tolerance did not alter the total amount of phospholipid lavaged from the lung (tolerant: 251 +/- 31 microgram lipid phosphorus/g dry lung, n = 10; control: 228 +/- 9, n = 5) or the amount that was disaturated (tolerant: 44.7 +/- 4.2%, n = 5; control 45.0 +/- 2.1%, n = 4), there were marked increases in the relative amounts of phosphatidylcholine and phosphatidylethanolamine in the lavage from tolerant rats. Static compliance measurements revealed that the pressure required to maintain the tolerant lungs at 50% of total lung capacity was half that required in the control rats. At this stage it is not possible to say what role, if any, these changes have in the induction of tolerance to 100% oxygen.

Animals↗
PubMed2002

Benzene metabolism by the isolated perfused lung.

Benzene is an occupational hazard and environmental toxicant whose toxic effects are dependent on its metabolism by cytochrome P-450. Most physiologically based pharmacokinetic models assume that benzene is metabolized only in the liver. They may not be completely accurate in predicting metabolism, especially following inhalation exposure, if metabolism by the lung is important. In the current study, the metabolizing capability of the lung was examined in an in vivo simulation using the isolated perfused lung. Lungs from the rabbit, rat, and mouse were used to mimic benzene metabolism following exposure via the pulmonary vasculature. With the isolated perfused mouse lung, three concentrations (55 microM, 120 microM, and 200 microM) were used to evaluate concentration dependence. To evaluate the ability of the lung to metabolize inhaled benzene, the isolated perfused mouse lung was exposed to benzene (approximately 175 ppm) via the trachea. Benzene was metabolized in all species, with phenol being the major metabolite. Phenylsulfate was also detected in perfusate from rabbits and mice but at much lower levels. Benzene metabolism was concentration dependent in mice. The ability of the lung to metabolize benzene during inhalation exposure was demonstrated in the isolated perfused mouse lung. These results demonstrate that the lung can metabolize benzene in an in vivo simulation when exposed via the pulmonary vasculature or via inhalation.

Air Pollutants, Occupational↗
PubMedDate not supplied

Effects of energy and protein restriction on acetylcholine sensitivity of rat isolated perfused heart.

Responses to acetylcholine of isolated perfused hearts obtained from rats which were acutely starved, chronically half-starved or protein-restricted were compared with those of paired control groups. Isolated hearts of totally starved rats showed no significant change in the responses elicited by 10 and 20 micrograms doses of acetylcholine as compared with paired controls. With 40 micrograms acetylcholine a significantly greater reduction (P less than 0.001) in heart rate and coronary flow was seen and the duration of the negative chronotropic action was significantly increased (P less than 0.05), as compared with controls. Isolated hearts of half-starved and protein-restricted rats responded to 10, 20 and 40 micrograms doses of acetylcholine with significantly greater reduction (P less than 0.001) in heart rate, coronary flow and increase in duration of negative chronotropic action (P less than 0.001) as compared to controls.

Acetylcholine↗
PubMed1983

Mutagenicity of benzo(a)pyrene metabolites generated on the isolated perfused lung following particulate exposure.

The isolated perfused rabbit lung (IPL) is being used to study the effects of particulate exposure on the pulmonary metabolism of benzo(a)pyrene (BaP). Pasturealla-free New Zealand white rabbits were treated intraperitoneally with BaP prior to kill. The isolated lungs were then administered either 14C-labeled BaP alone or BaP plus Fe2O3 or fly ash by intratracheal injection. Rates of appearance of BaP metabolites in the perfusing blood were determined. The extent of metabolism, distribution of metabolites, and types of metabolites produced were quantified for various lung tissue types by high-performance liquid chromatography and liquid scintillation spectrometry. Procedures were developed to apply the Salmonella/microsome test in the assay of mutagenicity of lung tissue and blood extracts as an indicator of their biologic activity. With few exceptions, blood extracts from IPL receiving BaP only were not mutagenic. Lung, trachea-bronchi, and macrophage extracts, by contrast, were mutagenic. A part of this activity could be attributed to BaP metabolites rather than to parent compound remaining in extracts. When lungs were exposed to Fe2O3 or to fly ash, only macrophage extracts were consistently mutagenic. This activity was due to significant amounts of unmetabolized BaP.

Animals↗
PubMed1991

Flow-dependent extraction of 1-naphthol by the rat isolated perfused kidney.

The influence of variation of perfusion flow rate on the renal clearance of p-aminohippuric acid and 1-naphthol was studied with an isolated perfused rat kidney preparation. Kidney functions were well maintained at low perfusion flow rates by the use of a fluorocarbon emulsion to increase the oxygen capacity of the perfusion buffer. Renal extraction of p-aminohippuric acid decreased with increasing perfusion flow. Our data show that at high perfusion flow rates maximal extractable perfusion flow forms only a small part of the total perfusion flow. 1-Naphthol is rapidly metabolized to its glucuronide and sulfate conjugate in the isolated perfused rat kidney. Using PAH as a marker for the maximal extractable perfusion flow, 1-naphthol could be regarded as a high-extraction compound even at high perfusion flow rates. Our results suggest that p-aminohippuric acid clearance, rather than total perfusion flow rate, should be used as the measure of maximal extractable blood flow for the estimation of extraction ratio in the isolated perfused kidney of compounds excreted or metabolized by the proximal tubules.

Animals↗
PubMed1980

Influence of dietary lipid on the metabolism of hexobarbital by the isolated, perfused rat liver.

Isolated livers from rats fed a diet containing corn oil (10% W/W) perfused with a blood-free, modified Krebs-Henseleit solution cleared hexobarbital at a rate significantly faster than livers from rats fed a similar diet devoid of corn oil. The half-lives of hexobarbital in these experiments were 22.4 +/- 1.8 min for livers from rats fed corn oil and 30.0 +/- 1.2 min for those from rats fed the fat-free diet. This represented a metabolic rate of 54 microgram hexobarbital/g liver/min in fat-fed animals and 36 microgram hexobarbital/g liver/min in those fed a rat-free diet.

Animals↗
PubMed1978

The role of cyclic adenosine monophosphate in adrenergic effects on ventricular vulnerability to fibrillation in the isolated perfused rat heart.

The relation between myocardial tissue cyclic AMP (cAMP) and the vulnerability to ventricular fibrillation was assessed in the isolated perfused rat heart by measurement of ventricular fibrillation threshold (VFT) and vulnerable period duration (VP). Exogenous dibutyryl cyclic AMP (DBcAMP) reduced VFT and increased VP by a concentration-related action whereas exogenous cAMP did not. Theophylline (1.0 mmol/liter) increased the tissue content of cAMP by 58% (P < 0.001) and caused a leftward shift in the concentration-response curve to DBcAMP. An effect of cAMP on VFT and VP could be shown in the presence of phosphodiesterase inhibition by theophylline. beta-1-Adrenergic receptor blockade with atenolol did not alter the concentration-response curve for VFT when DBcAMP was administered. Epinephrine (100 nmol/liter to 1 mumol/liter) also increased vulnerability to VF; this effect was accompanied by a concentration-related increase in tissue cAMP, but inconsistent changes in tissue ATP, phosphocreatine and potassium. The concentration-response curve of VFT to epinephrine was shifted leftward by theophylline and rightward by atenolol. The increases in vulnerability to fibrillation in the isolated perfused rat heart, in response to DBcAMP, theophylline or epinephrine, could be related more closely to changes of tissue cAMP than to effects on tissue high energy phosphates or potassium. The effect of epinephrine and theophylline on vulnerability to ventricular fibrillation is mediated via alterations in the intracellular level of cAMP in the isolated perfused rat heart.

Adenosine Triphosphate↗
PubMed1993

Effects of endogenous and exogenous lysophosphatidylcholine in isolated perfused rat hearts.

In isolated Langendorff perfused rat hearts, treatment with exogenous palmitoyl-lysophosphatidylcholine (P-LPC; 3-50 microM) under normoxic conditions, resulted in reduced heart rate (HR), coronary flow (CF) and contractile function. After 30 min Krebs perfusion, following P-LPC infusion, HR and CF remained reduced and contractile function continued to deteriorate. End diastolic pressure (EDP) and lactate dehydrogenase (LDH) release in LPC treated hearts were significantly increased from controls. Myocardial lysophosphatidylcholine (LPC) levels after 25 min global ischemia were significantly higher than controls (463 +/- 10 for control vs 550 +/- 15 nmol/g dry wt for ischemia). Following 30 min reperfusion an increase from control was still observed (475 +/- 11 for control vs. 594 +/- 17 for ischemia+reperfusion). Analysis of molecular species of LPC demonstrated that palmitoyl, oleoyl and stearoyl were increased after 25 min ischemia. After 30 min of reperfusion only palmitoyl and stearoyl were significantly increased. After 25 min treatment with 3 microM P-LPC and 30 min normoxic perfusion, myocardial LPC was three-fold higher than after 25 min ischemia. Treatment with 0.2 microM exogenous P-LPC resulted in myocardial tissue LPC levels (562 +/- 23) equivalent to those seen after 25 min ischemia (550 +/- 15). Compared to time matched controls hearts perfused with 0.2 microM P-LPC displayed no significant reductions in contractile function nor increase in LDH release. Thus, in isolated rat hearts, the increase in LPC seen after 25 min of global ischemia may not solely mediate the contractile dysfunction and LDH release observed.

Animals↗
PubMed1987

Effects of chlorothiazide, furosemide and PTH on Na+ and Ca2+ handling in isolated perfused kidneys of the spontaneously hypertensive rat.

The role of the kidney in a disturbed calcium metabolism in spontaneously hypertensive rats (SHR) was investigated. The hemodynamics of isolated perfused SHR kidneys were not basically altered compared to Wistar-Kyoto (WKY) control kidneys. Renal calcium handling by isolated perfused WKY and SHR kidneys at 12 weeks of age was not significantly different. In addition, the effects of chlorothiazide and furosemide on renal calcium handling were studied in isolated perfused kidneys from both rat strains. Both diuretics increased glomerular filtration rate, diuresis and excretion of sodium and calcium. However, both diuretics stimulated diuresis and calcium excretion significantly less in SHR than in WKY kidneys. The calciuric action of chlorothiazide was completely abolished by administration of human-parathyroidhormone (hPTH), while the natriuric effect was unchanged by hPTH. This observation suggests that a hypocalciuric action of chlorothiazide 'in vivo' is possibly mediated by PTH. Our study suggests that the kidney is not responsible for the disturbance in calcium metabolism in SHR. A surprising finding is that the SHR kidney was less responsive to the diuretics furosemide and chlorothiazide than the kidney of the WKY control.

Animals↗
PubMed1989

Uptake, production and metabolism of cysteinyl leukotrienes in the isolated perfused rat liver. Inhibition of leukotriene uptake by cyclosporine.

1. The isolated perfused rat liver efficiently takes up cysteinyl leukotrienes (LTs) C4, D4, E4 and N-acetyl-LTE4 from circulation. More than 70% of these cysteinyl LTs are excreted from liver into bile within 1 h of onset of a 5 min infusion, while about 5% remain in the liver. About 20% of infused N-acetyl-LTE4 escapes hepatic first-pass extraction under our conditions. 2. Metabolites of LTC4 appearing in bile within 20 min of the onset of infusion include mainly LTD4 and N-acetyl-LTE4, but also omega-hydroxy-N-acetyl-LTE4 and omega-carboxy-N-acetyl-LTE4. Metabolites generated from omega-carboxy-N-acetyl-LTE4 by beta-oxidation from the omega-end represent the major biliary LTs secreted at later times. 3. Stimulation of the isolated perfused liver by the combined infusion of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and the Ca2+ ionophore A23187 results in a transient increase of endogenous cysteinyl LT production, which is independent of extrahepatic cells. 4. The immunosuppressive drug cyclosporine causes a dose-dependent inhibition of hepatobiliary cysteinyl LT excretion, probably by interference with the sinusoidal uptake system for cysteinyl LTs.

Animals↗