Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ISOLATION PERFUSION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources

Sensitivity and specificity of isolated perfused guinea pig heart to test for drug-induced lengthening of QTc.

INTRODUCTION: The purpose of this study was to determine the sensitivity and specificity for predicting the liability of a compound to lengthen QTc using isolated, perfused guinea pig hearts (Langendorff preparation). METHODS: QTc (Fridericia correction) was calculated from bipolar transventricular electrograms. Hearts were exposed to escalating concentrations of 26 compounds thought to lengthen, and 13 compounds thought not to lengthen, QTc in humans. RESULTS: In this preparation, QTc was found to lengthen in 26 of 26 compounds thought to be positive (sensitivity 1.00) and not to lengthen or to lengthen insignificantly in 13 of 13 compounds thought to be negative (specificity 1.0) in man. Probucol and ontazolast could not be studied because of limited solubility. Successful experiments were conducted on over 98% of guinea pigs anesthetized. DISCUSSION: We believe that the isolated perfused guinea pig heart is an in vitro preparation that could be utilized early in preclinical testing for identifying a liability to lengthen QTc in humans, but we do not believe--as is true also for other in vitro methods--that the concentration at which the liability is demonstrated in vitro necessarily predicts the concentration at which a liability exists in man.

Animals↗

Nephrotoxicity of the glutathione conjugate of menadione (2-methyl-1, 4-naphthoquinone) in the isolated perfused rat kidney. Role of metabolism by gamma-glutamyltranspeptidase and probenecid-sensitive transport.

The renal processing of the glutathione conjugate of menadione, 2-methyl-3-S-glutathionyl-1,4-naphthoquinone (thiodione) was studied in the isolated perfused rat kidney. Thiodione at an initial concentration of 600 microM was eliminated rapidly from the perfusate (clearance = 6.0 ml/min). Renal disposition could be ascribed to metabolism and transport of the glutathione conjugate. Renal metabolism by gamma-glutamyltranspeptidase was inhibited by AT-125 [L-(alpha S,5S)-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid] (0.5 mM) resulting in a reduction of the thiodione clearance to 0.86 ml/min. Further reduction of the renal clearance of thiodione was achieved by a combination of AT-125 (0.5 mM) and probenecid (0.5 mM), resulting in a renal clearance of 0.58 ml/min which equalled glomerular filtration rate. Addition of thiodione to the perfusate caused loss of renal function and cellular damage, as reflected by a decreased glucose reabsorption and an increased urinary secretion of lactate dehydrogenase, respectively. Thiodione-induced nephrotoxicity was ameliorated by AT-125 and prevented completely by a combination of AT-125 and probenecid. Aminooxyacetic acid (0.5 mM), an inhibitor of beta-lyase, did not afford protection against the nephrotoxic action of thiodione. From our results it can be concluded that the thiodione-mediated toxicity in the isolated perfused rat kidney can be linked to cellular uptake by anionic transport systems and metabolism by gamma-glutamyltranspeptidase.

Animals↗

Relationship between activity of hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase and secretion of very-low-density-lipoprotein cholesterol by the isolated perfused liver and in the intact rat.

The hepatic output of triacylglycerol and cholesterol from very-low-density lipoprotein (VLD lipoprotein), and the activity of 3-hydroxy-3-methylglutaryl-coenzyme A reductase were compared in the isolated perfused rat-liver preparation and in the intact rat. The output of triacylglycerol and cholesterol from VLD lipoprotein by the perfused liver was stimulated by oleate concomitant with stimulation of hepatic microsomal hydroxymethylglutaryl-coenzyme A reductase activity. In the intact animal treated with Triton WR-1339, the magnitude of secretion of triacylglycerol and cholesterol from VLD lipoprotein coincided with the diurnal rhythm of hepatic hydroxymethylglutaryl-coenzyme A reductase activity, which was maximal at 24:00 h and minimal at 12:00 h. These observations suggest that the stimulation of the reductase and of the secretion of cholesterol from VLD lipoprotein by non-esterified fatty acids, as observed with the isolated perfused rat liver preparation in vitro, may also be an important physiological mechanism in vivo. Hepatic cholesterogenesis may be stimulated under conditions conductive to the secretion of the VLD lipoprotein, the primary transport form for triacylglycerol in the postabsorptive state.

Animals↗

Activation of somatostatin receptor subtype 2 inhibits insulin secretion in the isolated perfused human pancreas.

OBJECTIVES: Five distinct somatostatin receptors (SSTRs) have been cloned, characterized, and designated SSTRs 1-5. The role of these receptors in B-cell signaling has not been well characterized. METHODS: In the current study, the isolated perfused human pancreas model was used to determine the specific effect of 4 different somatostatin receptor agonists on insulin secretion. CONCLUSION: We demonstrated that the SSTR 2 agonist and octreotide significantly suppressed insulin secretion. Furthermore, even during the immunoneutralization of endogenous intrapancreatic somatostatin, the SSTR 2 agonist was able to reverse the effect of somatostatin immunoneutralization by suppressing insulin secretion. These results demonstrate that activation of SSTR 2 suppresses insulin secretion in the isolated perfused human pancreas.

Adolescent↗

Hyporesponsiveness to inhaled nitric oxide in isolated, perfused lungs from endotoxin-challenged rats.

Inhaled nitric oxide (iNO) causes selective pulmonary vasodilation and improves oxygenation in patients with the adult respiratory distress syndrome (ARDS). Approximately 30% of ARDS patients fail to respond to iNO. Because sepsis syndrome often accompanies a decreased response to iNO, we investigated NO responsiveness in isolated, perfused lungs from rats exposed to lipopolysaccharide (LPS). Eighteen hours after intraperitoneal injection of 0.5 mg/kg LPS, rat lungs were isolated, perfused, and preconstricted with U-46619. Ventilation with 0.4, 4, and 40 parts per million by volume NO vasodilated LPS-pretreated lungs 75, 47, and 42% less than control lungs (P < 0.01 value differs at each concentration). The diminished vasodilatory response to iNO was associated with decreased NO-stimulated guanosine 3',5'-cyclic monophosphate (cGMP) release into the perfusate. Soluble guanylate cyclase activity did not differ in lung extracts from LPS-pretreated and control rats. LPS increased pulmonary cGMP-phosphodiesterase (PDE) activity by 40%. The PDE-sensitive cGMP analogue 8-bromoguanosine 3',5'-cyclic monophosphate vasodilated lungs from LPS-pretreated rats less than lungs from control rats. In contrast, the PDE-insensitive 8-para-chlorophenylthioguanosine 3',5'-cyclic monophosphate vasodilated lungs equally from both groups. After LPS challenge, the rat pulmonary vasculature becomes hyporesponsive to iNO. Hyporesponsiveness to iNO appears partly attributable to increased pulmonary cGMP-PDE activity.

Administration, Inhalation↗

Calcium ion dependence of myogenic renal plasma flow autoregulation: evidence from the isolated perfused rat kidney.

1. The independent roles of Ca2+ and glomerular filtration in the control of renal plasma flow autoregulation were examined in the isolated perfused rat kidney. Control kidneys autoregulated plasma flow between perfusion pressures of 120 and 160 mmHg. 2. Complete ischaemia, induced by clamping of the renal artery cannula for 1 h induced relative vasoconstriction and a loss of autoregulatory capacity. 3. The addition of either nifedipine (10(-7) M) or verapamil (10(-4) M) to the perfusion medium produced vasodilation and a loss of autoregulation. 4. Kidneys that were rendered non-filtering by raising the perfusate albumin concentration from 65 to 100 g/l appeared to shift autoregulatory capacity to a higher pressure range, whereas raising it to 150 g/l reduced autoregulation at all pressures studied. 5. The addition of ouabain (10(-3) M) restored autoregulation to the lower pressure range in non-filtering kidneys perfused with an albumin concentration of 100 g/l. Ouabain-treated non-filtering kidneys displayed a loss of autoregulation when perfused either with nifedipine or with reduced perfusate Ca2+. 6. Plasma flow was reduced in isolated kidneys perfused at pressures of 100 or 150 mmHg when ionized Ca2+ in the medium was raised from 0 to 1.8 mM. However, no decrement in flow was observed in kidneys perfused at 50 mmHg when ionized Ca2+ in the perfusate was raised to the same level. Thus the vasoconstrictive effect of raised ionized Ca2+ was pressure-dependent. 7. We conclude that renal plasma flow autoregulation occurs in the isolated kidney in the absence of glomerular filtration and is at least in part a myogenic phenomenon. Myogenic control of renal plasma flow autoregulation is regulated by smooth muscle permeability to Ca2+. Changes in smooth muscle Ca2+ permeability appear to be pressure-regulated.

Animals↗

[Pharmacokinetics of cyclophosphamide, adriamycin and adriamycin prodrug (HMR 1928) using an ex vivo isolated perfused human lung model (IHLP)].

BACKGROUND: Today knowledge about pharmacokinetics of anticancer drugs in human malignant tumors is poor. Data from in vivo studies are limited and difficult to obtain due to ethical aspects. An ex vivo isolated perfused and ventilated human lung model however allows pharmacological studies of human bronchial carcinoma inside their host organ, the lung, under physiological conditions without compromising the patient. METHODS: Following surgery for bronchial carcinoma human lung preparations were reperfused and ventilated extracorporally for 2-3 hours. During the reperfusion anticancer drugs are added to the perfusion solution and their uptake into tumor, normal lung tissue, and lymph nodes is studied. RESULTS: An initial study showed that lung reperfusion under physiological circumstances over a period of 2-3 hours did not interfere with histo-pathological diagnostics and staging; an important precondition for potential adjuvant treatment. Pharmacokinetics of cyclophosphamid, adriamycin, and a water soluble adriamycin prodrug (HMR 1826) were measured. Final tissue concentrations of adriamycin and cyclophosphamid in peripheral lung parenchyma turned out to be 10 times higher compared to tumor tissue. However, following perfusion with adriamycin prodrug final tissue concentrations of adriamycin were in the same range in lung and tumor. CONCLUSIONS: The ex-vivo isolated human lung perfusion model (IHLP) has proven to be an ideal scientific model for pharmacological investigations of human tumors as an intermediate step between cell culture and in-vivo situation without any disadvantage for the patient. The tumor-to-host interaction is completely saved in this model. However, first pass reactions of drugs in other organs must not play a role for the substances studied with the IHLP. The role and future applications of the isolated perfused human lung model for other indications is discussed.

Antineoplastic Agents↗

Effect of carbon monoxide on the cytochrome P-450-mediated metabolism of aniline and p-nitroanisole in the isolated perfused rabbit lung.

Carbon monoxide (CO), an environmental pollutant, inhibits the cytochrome P-450-mediated metabolism of xenobiotics in vitro. In recent years, the importance of the lung in the metabolic disposition of certain airborne and systemically administered xenobiotics has been demonstrated. The purpose of this investigation was to establish a threshold for the CO-induced inhibition of cytochrome P-450-mediated activities in the isolated perfused rabbit lung and to determine if these reactions are equally sensitive to this toxicant in this model. Neither the mixed-function oxidase-mediated hydroxylation nor the acetylation of aniline was altered by exposure to 7.5% CO/20% O2 for 2.5 h in the isolated perfused rabbit lung. p-Nitroanisole O-demethylation by isolated rabbit lungs ventilated with 7.5% CO/20% O2 was significantly decreased (approximately 37%) in comparison to controls. That these reactions are not similarly influenced by carbon monoxide may indicate that the constitutive isozymes of cytochrome P-450 in the rabbit lung are differentially sensitive to CO-induced inhibition.

Aniline Compounds↗

Dominant role of an endothelium-derived hyperpolarizing factor (EDHF)-like vasodilator in the ciliary vascular bed of the bovine isolated perfused eye.

1. The roles of the endothelium-derived nitric oxide, prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in mediating vasodilator responses to acetylcholine and bradykinin were assessed in the ciliary vascular bed of the bovine isolated perfused eye preparation. 2. Vasodilatation to acetylcholine or bradykinin was unaffected by the nitric oxide synthase inhibitor, L-NAME (100 microM), or the cyclo-oxygenase inhibitor, flurbiprofen (30 microM), but was virtually abolished following treatment with a high concentration of KCl (30 mM), or by damaging the endothelium with the detergent, CHAPS (0.3%, 2 min). 3. Acetylcholine-induced vasodilatation was unaffected by glibenclamide (10 microM), an inhibitor of ATP-sensitive K(+) channels (K(+)(ATP)), but was significantly attenuated by TEA (10 mM), a non-selective inhibitor of K(+) channels. 4. The small conductance calcium-sensitive K(+) channel (SK(+)(Ca)) inhibitor, apamin (100 nM), and the large conductance calcium-sensitive K(+) channel (BK(+)(Ca)) inhibitor, iberiotoxin (50 nM), had no significant effect on acetylcholine-induced vasodilatation. In contrast, the intermediate (IK(+)(Ca))/large conductance calcium-sensitive K(+) channel inhibitor, charybdotoxin (50 nM), powerfully blocked these vasodilator responses, and uncovered a vasoconstrictor response. 5. The combination of apamin (100 nM) with a sub-threshold concentration of charybdotoxin (10 nM) significantly attenuated acetylcholine-induced vasodilatation, but the combination of apamin (100 nM) with iberiotoxin (50 nM) had no effect. 6. In conclusion, blockade by a high concentration of KCl, by charybdotoxin, or by the combination of apamin with a sub-threshold concentration of charybdotoxin, strongly suggests that vasodilatation in the bovine isolated perfused eye is mediated by an EDHF.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Effect of three loop diuretics and prostaglandins E2 & I2 on the isolated perfused rat mesenteric vasculature.

Rat superior mesenteric vascular bed was isolated, perfused by the artery with Krebs solution and the perfusion pressure monitored. Dose-response curves to noradrenaline and KCl administered as bolus doses were obtained. A 1 hr continuous infusion of either piretanide (10 micrograms ml-1) frusemide (40 micrograms ml-1) or bumetanide (2 micrograms ml-1) decreased the sensitivity of the preparation to noradrenaline but not to KCl. This effect was antagonized by flurbiprofen (12 micrograms ml-1) pretreatment. A 1 hr continuous infusion of prostaglandin (PG)E2 increased the sensitivity of the preparation to both noradrenaline and KCl. PGI2 (5 ng bolus) or diuretic perfusion antagonized the responses to noradrenaline but not those to KCl. PGI2 and diuretics in combination further decreased the responsiveness of the preparation to noradrenaline. KCl responses were unaffected by either PGI2 or diuretics, alone or combined. The results suggest that the loop diuretics decrease the responsiveness of the isolated rat superior mesenteric vascular bed preparation to noradrenaline, possibly by increasing the level of PGI2, an effect which may be an important factor in the cardiovascular activity of the diuretics.

Animals↗

Improved survival rates of patients with acral lentiginous melanoma treated with hyperthermic isolation perfusion, wide excision, and regional lymphadenectomy.

Twenty-three patients with extremity malignant melanoma who fit the clinical and pathologic criteria for acral lentiginous melanoma were treated in a prospective, nonrandomized trial of wide local excision, regional lymphadenectomy, and hyperthermic isolation perfusion. There were 17 patients (73.9 percent) pathologically judged to be in stage I and 6 (26.1 percent) in stage II. Three patients entered the study with regional recurrence. Delay in diagnosis of the lesions averaged almost 3 1/2 years. Increasing awareness about the occurrence of acral lentiginous melanoma may result in earlier diagnosis, increased survival rates, and cure. Life table survival analysis revealed 5 and 10 year survival rates of 75 percent and 58 percent, respectively. This supports the findings of Krementz et al and suggests not only that a marked improvement in survival can be achieved through the use of hyperthermic isolation perfusion, but that the survival of patients with acral lentiginous melanoma is comparable with that of patients with other extremity malignant melanomas treated with aggressive multimodality therapy.

Actuarial Analysis↗

Enzymatic and histological alterations in the isolated perfused rat pancreas under conditions of oxidative stress.

BACKGROUND: Oxidative stress is a relevant event in the pathogenesis of acute pancreatitis. Investigations in vivo are limited because of the complexity of the organism and the short half-life of free radicals. The isolated perfused rat pancreas could be useful for investigations in the early phase of acute pancreatitis especially under conditions of oxidative stress. METHODS: External perfusions of the pancreatic glands of Wistar rats were carried out using a modified Krebs-Ringer buffer including an additive of the detergents Triton X-100 and a perfusion including hydrogen peroxide (0.0012%) or tert-butylhydroperoxide (0.0042%) or xanthine oxidase (0.1 U/ml). Changes in amylase, lipase, LDH in the portal outflow fluid and for histological alterations were analyzed. RESULTS: Damage to pancreatic parenchyma using Triton X-100 was indicated by increased levels of pancreatic enzymes in the perfusion medium. During perfusion with hydrogen peroxide or tert-butylhydroperoxide we found no changes in pancreatic enzymes in the portal outflow. In contrast, perfusion with xanthine oxidase induced a significant elevation in lipase and amylase in the effusion fluid after 30 min. We found a significant increase in edema in the hydrogen peroxide and in the xanthine oxidase group. Focal necroses of the pancreatic parenchyma were detected in all groups of oxidative stress. CONCLUSIONS: The isolated perfused rat pancreas is a valuable experimental model for investigating the early phase of pathophysiology in acute pancreatitis, for instance, the effect of oxidative stress as an early event in acute pancreatitis. Using hydrogen peroxide tert-butylhydroperoxide or xanthine oxidase, only xanthine oxidase was able to induce a typical elevation in the pancreas enzymes in the effusion fluid.

Acute Disease↗

Characterization of bronchodilator effects and fate of S-nitrosothiols in the isolated perfused and ventilated guinea pig lung.

In this study the effects of S-nitrosothiols, in particular S-nitrosoglutathione (GSNO), were evaluated with regard to their bronchodilating properties, both after infusion via the pulmonary circulation and after inhalation, in the isolated perfused and ventilated guinea pig lung. Infused GSNO induced bronchorelaxation of lungs that were precontracted with methacholine. During a 15-min period of single-passage perfusion with GSNO (10 microM), maximally 10% was taken up and/or degraded by the lung. A spontaneous breakdown of GSNO in the perfusion buffer was also observed, which was partially accompanied by the formation of nitrite. Low levels of nitric oxide (NO) were detected in the perfusion buffer when GSNO was present. This was due to the presence of contaminating transition metals, because EDTA and 2,2'-dipyridyl largely reduced the formation of NO. The NO-scavenging agents oxyhemoglobin and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide abolished levels of NO in the buffer but did not abolish GSNO-induced bronchodilation. The effects of infused GSNO are therefore attributed to an action of the intact S-nitrosothiol and not to NO released from GSNO in the perfusion buffer. Similarly, perfusion with S-nitrosated glutathione isopropyl ester, cysteinyl glycine, N-acetyl-L-cysteine or N-acetyl-D,L-penicillamine, but not with nitrosated bovine serum albumin or sodium nitrite, was found to induce bronchodilation. Inhalation of nebulized GSNO induced bronchodilation of methacholine-precontracted lungs with a rapid onset of action, although it was a less potent bronchodilator than salbutamol. The results show that infused or inhaled S-nitrosothiols have bronchodilating properties in the isolated perfused and ventilated guinea pig lung.

Aerosols↗

DuP 753 is a potent nonpeptide antagonist of angiotensin II receptors in isolated perfused rat kidney and cultured renal cells.

In the present study we investigated the antagonist action of DuP 753 (2-n-butyl-4-chloro-5-hydroxy-methyl-1-[2'-(1H-tetrazol-5-yl)biphe nyl-4-yl) methyl]imidazole, potassium salt) on angiotensin II (AII) binding and vascular effects in the isolated perfused rat kidney. In addition, we determined binding of DuP 753 in cultured glomerular mesangial cells and renomedullary interstitial cells. In the isolated kidney, DuP 753 fully displaced AII from its specific binding sites with high affinity (IC50 = 200 nmol/L) and antagonized the vasoconstrictive effect of AII in a dose-related manner with an ED50 of 170 nmol/L. These effects of DuP 753 were qualitatively similar to those of saralasin and the antagonist effect of DuP 753 on AII-induced renal vasoconstriction was fully overcome by excess AII. DuP 753 had no effect on its own on renal vascular resistance. In cultured glomerular mesangial cells and renomedullary interstitial cells, DuP 753 fully inhibited the specific binding of [125I]-Sar-AII at 1 mumol/L with IC50s of 6.7 and 11 nmol/L for glomerular mesangial cells and renomedullary interstitial cells, respectively. The present results demonstrate that a novel imidazole derivative, DuP 753, is a powerful non-peptide antagonist of angiotensin II receptors in isolated perfused rat kidney and in cultured glomerular mesangial and renomedullary interstitial cells.

Angiotensin Receptor Antagonists↗

Evidence that mitochondrial phosphate is visible in 31P NMR spectra of isolated, perfused rat hearts.

We have previously found (P. B. Garlick, T. R. Brown, R. H. Sullivan and K. Ugurbil, J. Mol. Cell Cardiol. 15, 855-858 (1983)) that two peaks could be observed in the phosphate region of NMR spectra of isolated, perfused rat hearts. Upon valinomycin treatment, an increase in the peak at 2.8 ppm in the phosphate region (phosphocreatine set at -2.52 ppm) had been observed. We have now confirmed our hypothesis that this peak originates from the mitochondrial phosphate by: (i) determination of myocardial mitochondrial phosphate contents using density gradient centrifugation in non-aqueous solvents; and (ii) quantitative electron microscopy of the heart tissue. Thus, we conclude that mitochondrial and cytosolic phosphate can be distinguished from each other in 31P NMR spectra of isolated, perfused rat hearts.

Adenosine Triphosphate↗

Isolated perfused liver technology for studying metabolic and toxicological problems.

The isolated perfused liver system is a versatile model for investigating the effects and mechanisms of action of hepatotoxins and the metabolism of endogenous and exogenous compounds. The interpretation of metabolic data and apparent toxic events is dependent upon the viability and reproducibility of the model. In this study, a new approach has been undertaken to assess the viability of isolated liver preparations. This has involved the continuous monitoring of multistage processes namely, the synthesis and secretion of radiolabelled proteins, glycoproteins and lipoproteins on the one hand and the uptake of macromolecules by receptor-mediated endocytosis on the other. The consistency of these complex integrated processes from one liver to another and in particular the steady-state rate of production of radiolabelled macromolecules over 6h perfusion periods suggests that this model can be used with confidence for metabolic/toxicological investigations. The selectivity of the responses to chemical challenge(s) shows that this system can be exploited for (a) screening potential hepatotoxins; (b) identifying areas of metabolism which are affected and (c) advancing basic knowledge of liver biochemistry.

Animals↗

Effect of potassium concentration and ouabain on the renal adaptation to potassium depletion in isolated perfused rat kidney.

Renal adaptation for potassium (K) conservation has been demonstrated in isolated perfused kidneys from rats within 3 days of K depletion and appears to be independent of aldosterone and sodium excretion. This study was designed to investigate whether the renal adaptation for K conservation is independent of ambient [K] and renal tissue levels of K and whether ouabain may have effects on K excretion, which are in contrast to the effects on K excretion in normal animals. In the first study, rats K depleted for 3 days received 2500 mu equiv. KCI intraperitoneally, while other K-depleted rats and a group of control diet animals received intraperitoneal H2O alone to determine whether simple restoration of K deficits would reverse the renal adaptation for K conservation. Intraperitoneal KCI increased plasma [K] and kidney tissue K significantly within 3 h in the K-repleted group compared with the K-depleted rats. Isolated Kidneys were perfused from the three groups of rats 3 h after intraperitoneal injection. Despite K repletion in vivo, perfused kidneys from the K-repleted group still had significantly decreased K excretion (1.28 +/- 0.085 mu equiv./min) compared with controls (2.05 +/- 0.291 mu equiv./min), and K excretion was still not different from the K-depleted group (0.57 +/- 0.134 mu equiv./min). However, fractional K excretion by the kidneys from K-repleted rats was increased above K-depleted kidneys (0.48 +/- 0.051 vs. 0.18 +/- 0.034, p less than 0.01). Despite the increased renal tissue K in K-repleted kidneys at the start of perfusion (285 +/- 5.1 vs. 257 +/- 5.4 mu equiv./g), by the end of the perfusion tissue K in perfused kidneys was identical in all three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Haemodynamic effects of water-soluble contrast media on the isolated perfused rat kidney.

The precise mechanism underlying the nephrotoxicity of radiocontrast media remains ill defined. In this study we have examined the direct effect of a wide range of low- and high-osmolar water-soluble contrast media (WSCM) on the vascular resistance of the isolated perfused rat kidney (IPRK). Water-soluble contrast media led to a significant fall in the renal perfusate flow and an increase in the renal vascular resistance (RVR). The magnitude of these haemodynamic changes was independent of the osmolality of the tested agents. This study shows a direct effect of WSCM on the vascular resistance of the isolated perfused rat kidney.

Animals↗