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PubMed1984

Pentagastrin-stimulated gastric acid secretion by the isolated perfused rat stomach.

The purpose of this present study was to develop a method for stimulation of acid secretion by the isolated perfused rat stomach. Rat stomachs were perfused in situ via the abdominal aorta and celiac axis with Krebs-Ringer bicarbonate buffer in the presence or absence of 10% ovine erythrocytes. The gastric lumen was perfused with distilled water and gastric contents were collected at frequent intervals through a catheter at the pylorus. Sixty minute gastric acid output in response to various concentrations of pentagastrin was determined by titration of gastric contents with 0.01 N NaOH to pH 7.0. During arterial perfusion with Krebs-Ringer bicarbonate buffer in the absence of ovine erythrocytes gastric acid output was 2.50 +/- 0.58 SEM microEq H+/h, which did not increase in response to perfusion with Krebs-Ringer bicarbonate buffer containing pentagastrin. However, inclusion of 10% ovine erythrocytes in the arterial perfusate resulted in substantial stimulation of gastric acid by pentagastrin: maximal acid output, achieved with a pentagastrin dose of 0.6 microgram/kg/h, was 23.5 +/- 3.73 microEq H+/h (p less than 0.01). The results of the present study demonstrate the capacity of the isolated vascularly perfused rat stomach to secrete acid and provide a model for studying interactions of gastrointestinal regulatory peptides and their physiologic roles in the regulation of gastric acid secretion.

Animals↗
PubMed2000

Exogenous neopterin causes cardiac contractile dysfunction in the isolated perfused rat heart.

Neopterin is known in humans as a sensitive marker for diseases associated with increased activity of the cellular immune system. Recent studies report neopterin also to exhibit distinct effects: neopterin induces inducible nitric oxide synthase expression in rat vascular smooth muscle cells and activates translocation of nuclear factor- kappa B. Neopterin may also induce oxidative stress causing apoptotic cell death, or superinduce tumor necrosis factor- alpha -mediated apoptosis. Observing these effects in cell cultures, we were interested in possible consequences of neopterin on cardiac function in the isolated perfused rat heart. The influence of neopterin in three different concentrations (10 micromol/l, 50 micromol/l, 100 micromol/l) on cardiac contractility parameters and coronary vascular resistance were studied in 67 male Sprague-Dawley rats using the temperature-controlled and pressure-constant Langendorff apparatus with retrograde perfusion of the aorta with a Krebs-Henseleit buffer. Treatment with 100 micromol/l neopterin resulted in a significant decrease in coronary flow and cardiac contractility. Coronary flow decreased from 15.2 to 9.5 ml/min (P=0.002), left ventricular pressure from 80 to 52 mmHg (P=0. 002), rate of pressure fall from 1605 to 923 mmHg/s (P=0.001) and rate of pressure rise from 2862 to 1709 mmHg/s (P=0.001). Concentrations lower than 100 micromol/l neopterin had no significant effect on cardiac function. Our study demonstrates a considerable influence of exogenous neopterin on cardiac performance in the Langendorff model of isolated perfused rat hearts. This has to be considered a potential pathogenic factor of cardiac disturbances in diseases in which high concentrations of neopterin are released due to immune activation. At present the exact mechanism remains unclear.

Animals↗
PubMed1997

Electrophysiology of the right anterior approach to the atrioventricular node: studies in vivo and in the isolated perfused dog heart.

INTRODUCTION: Previous reports have described electrophysiologic properties and rate-dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction. METHODS AND RESULTS: In five anesthetized dogs, the His-bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 +/- 14 msec. In ten isolated perfused canine hearts, a bipolar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 +/- 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 +/- 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 +/- 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 +/- 19 to 151 +/- 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2-mm spacing) was positioned along the anterior limbus of the fossa ovalis with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 +/- 25 vs 171 +/- 20 msec, P < 0.05), as did the 2:1 block between the two components (161 +/- 18 vs 150 +/- 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL. CONCLUSIONS: The transitional cell zone in the anterior interatrial septum exhibits a specific rate-dependent, spatial gradient of conduction block, which can be recorded in bipolar electrograms as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.

Animals↗
PubMed1978

Handling of triamterene by the isolated perfused rat kidney.

Quantitative studies on the renal handling of [3H]triamterene were performed in an isolated perfused rat kidney with near normal function and in an isolated kidney with negligible filtration rate, but preserved perfusate flow rate. The excretory pattern for [3H]triamterene is compatible with that of other weak bases such as quinine and quinacrine. Tubular secretion of [3H]triamterene is strongly inhibited by anoxia and iodoacetate. Tubular reabsorption of [3H]triamterene becomes pronounced when the urine is alkaline. Clearances were reported with and without correction for perfusate albumin binding which is about 75%. Bidirectional transport processes are operative in that [3H]triamterene is secreted by the renal tubule and passively diffuses back across the tubular epithelium by a pH-dependent mechanism.

Animals↗
PubMed1992

Biologic activities of parathyroid hormone (1-34) and parathyroid hormone-related peptide (1-34) in isolated perfused rat femur.

Parathyroid hormone-related peptide (PTHrP) has substantial homology with both human and rat parathyroid hormone (66% and 73%, respectively) in the first 15 amino acids. PTHrP (1-34) stimulates cyclic adenosine monophosphate (cAMP) release in bone and kidney, and these effects are felt to occur through interaction with the parathyroid hormone (PTH) receptor. Differences in the biologic potency between rat PTH(1-34) and human PTH(1-34)--and between PTHrP and PTH--have been described in a variety of experimental systems. In this study, we compared the bioactivity of these three amino-terminal synthetic fragments on the stimulation of cAMP formation in an isolated perfused rat femur preparation. Dose-response experiments demonstrated that PTHrP(1-34) was more potent in stimulating cAMP release than human PTH(1-34), whereas PTHrP(1-34) and rat PTH(1-34) were equipotent. Despite the fact that the extraction of immunoreactive rat PTH(1-34) and human PTH(1-34) was the same, rat PTH(1-34) was more potent in stimulating adenylate cyclase activity than human PTH(1-34). These data show that the isolated perfused rat femur preparation is an effective method for evaluation of the effects of PTH and PTHrP. Despite significant structural differences in the binding domain between rat PTH(1-34) and PTHrP(1-34), the effects of rat PTH(1-34) and PTHrP(1-34) are similar. Because the structure of rat PTHrP(1-34) and human PTHrP(1-34) are identical, and because it is desirable to utilize homologous systems to study the potency and effects of test peptides, it would appear that rat PTH(1-34) is the most appropriate peptide for comparison with PTHrP in rat-based experimental systems.

Amino Acid Sequence↗
PubMed1994

Isolated perfusion of the limb with high-dose tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and melphalan for melanoma stage III. Results of a multi-centre pilot study.

We report an update of a multi-centre pilot study previously published. Fifty-three patients (42 women, 11 men) were accrued between October 1988 and May 1992: 34 had stage IIIA, 15 had stage IIIAB, and four had stage IV melanoma. Most of them had more than five in-transit metastases; 50% had been previously treated by regional chemotherapy. Protocol included 90-min isolation perfusion at 40 degrees C with 2-4 mg rTNF-alpha, 0.2 mg rIFN-gamma and 10/13 mg/l melphalan. We prevented severe TNF systemic side effects by administration of dopamine and fluid loading. There has been no toxic death and the toxicity remained acceptable, with only one multi-organ failure (MOF) and no prolonged shock. Response rates remained very high, with 90% complete remission, 10% partial response and no failure. With a median follow-up time of 26 months, there were 12 regional recurrences, 15 distant metastases and nine local and distant recurrences. The median overall survival has been 28 months. We conclude that high-dose rTNF-alpha associated with melphalan in isolation perfusion is the therapy of choice for in-transit melanoma metastases.

Adult↗
PubMed1990

[Characterization of surface fluorescence signals of isolated perfused rat kidney].

The NAD(P)H- and flavoprotein fluorescence signals of the isolated perfused rat kidney were characterized by their electrochemical properties and by comparing them with those of isolated kidney cortex mitochondria. From titration experiments with lactate pyruvate under anoxic conditions it is concluded that about 25% of the NAD(P)H-fluorescence can be attributed to the cytosolic pyridine nucleotides. For this signal a midpoint potential of -268 mV was calculated. The major part of the NAD(P)H-fluorescence signal was of mitochondrial origin, showing a midpoint potential of -304 mV which was titrated with beta-hydroxybutyrate/acetoacetate. A comparable value (Em7.4 = -310 mV) was found for isolated kidney cortex mitochondria using the same redox couple. The flavoprotein fluorescence could be totally attributed to the mitochondrial compartment and was found to originate from the NAD-dependent alpha-lipoamide dehydrogenase and the electron transfer flavoprotein of beta-oxidation to approx. 60% and 40%, respectively. A midpoint potential of -285 mV was determined for the NAD-dependent part of the flavoprotein signal. On the basis of these results it can be concluded that the fluorescence changes which were caused by ouabain in the normoxically perfused rat kidney reflect an increase in reduction of the mitochondrial NAD-system.

3-Hydroxybutyric Acid↗
PubMed2005

Propofol attenuates oxidant-induced acute lung injury in an isolated perfused rabbit-lung model.

PURPOSE: Reactive oxygen species have been strongly implicated in the pathogenesis of acute lung injury (ALI). Some animal studies suggest that free radical scavengers inhibit the onset of oxidant-induced ALI. Propofol (2,6-diisopropylphenol) is chemically similar to phenol-based free radical scavengers such as the endogenous antioxidant vitamin E. Both in vivo and in vitro studies have suggested that propofol has antioxidant potential. We hypothesized that propofol may attenuate ALI by acting as a free-radical scavenger. METHODS: We investigated the effects of propofol on oxidant-induced ALI induced by purine and xanthine oxidase (XO), in isolated perfused rabbit lung, in two series of experiments. In series 1, we examined the relationship between the severity of ALI and the presence of hydrogen peroxide (H2O2). In series 2, we evaluated the effects of propofol on attenuating ALI and the dose dependence of these effects. The lungs were perfused for 90 min, and we evaluated the effects on the severity of ALI by monitoring the pulmonary capillary filtration coefficient (Kfc), pulmonary arterial pressure (Ppa), and the pulmonary capillary hydrostatic pressure (Ppc). RESULTS: In series 1, treatment with catalase (an H2O2 scavenger) prior to the addition of purine and XO resulted in complete prevention of ALI, suggesting that H2O2 may be involved closely in the pathogenesis of ALI. In series 2, pretreatment with propofol at concentrations in excess of 0.5 mM significantly inhibited the increases in the Kfc values, and that in excess of 0.75 mM significantly inhibited the increase in the Ppa values. CONCLUSION: Propofol attenuates oxidant-induced ALI in an isolated perfused rabbit lung model, probably due to its antioxidant action.

Animals↗
PubMed1989

Metabolic effects of acetaminophen. Studies in the isolated perfused rat liver.

The effects of acetaminophen on the metabolism of the isolated perfused rat liver were investigated. The following results were obtained: (1) Acetaminophen increased glucose release and glycolysis from endogenous glycogen (glycogenolysis). (2) Oxygen uptake, gluconeogenesis from either pyruvate or fructose and glycogen synthesis were inhibited. (3) In isolated rat liver mitochondria acetaminophen decreased state III and state IV respiration; it also decreased the ADP/O ratio and the respiratory control ratio. (4) The action of acetaminophen on glycogenolysis was not affected by N-acetylcysteine; this compound, however, increased glycogen synthesis. (5) The effects of acetaminophen are reversible. It was concluded that glycogen depletion by acetaminophen can be produced by two mechanisms. The first, as previously demonstrated by several workers, depends on irreversible binding of a reactive metabolite. The second, however, is reversible and depends primarily on an inhibition of mitochondrial energy metabolism.

Acetaminophen↗
PubMed1991

Evidence against a role of arachidonic acid metabolites in autoregulatory responses of the isolated perfused kidney of the rat.

The role of arachidonic acid metabolites in renal autoregulatory responses to changes in pressure was examined in rat isolated perfused kidneys. We also studied the influence of diabetes, a condition associated with hyperfiltration and altered renal eicosanoid production, on autoregulatory responses. The perfused rat kidney demonstrated autoregulation of flow within a pressure range of 100-150 mm Hg, with no differences between diabetic and control rat kidneys. Nifedipine resulted in vasodilatation and loss of autoregulation. Inhibition of the cyclooxygenase pathway of arachidonic acid metabolism with indomethacin failed to alter autoregulatory capacity. Similarly, inhibition of lipoxygenase with BW755C or NDGA, or inhibition of cytochrome P450-dependent enzymes with NDGA, clotrimazole or 7-ethoxyresorufin were without effect on autoregulatory responses. In vivo treatment with stannous chloride to deplete renal cytochrome P450-dependent enzymes also failed to modify autoregulatory responses. These results argue against a role of arachidonic acid metabolites in autoregulation of perfusate flow in the isolated kidney.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1983

Biliary protein output by isolated perfused rat livers. Effects of bile salts.

The output of proteins into bile was studied by using isolated perfused rat livers. Replacement of rat blood with defined perfusion media deprived the liver of rat serum proteins (albumin, immunoglobulin A) and resulted in a rapid decline in the amounts of these proteins in bile. When bovine serum albumin was incorporated into the perfusion medium it appeared in bile within 20 min and the amount in the bile was determined by the concentration of the protein in the perfusion medium. The use of a defined perfusion medium also deprived the livers of bile salts and the amounts of these, and of plasma-membrane enzymes [5'-nucleotidase (EC 3.1.3.5) and phosphodiesterase I], in bile declined rapidly. Introduction of micelle-forming bile salts (taurocholate or glycodeoxycholate) to the perfusion medium 80 min after liver isolation markedly increased the output of plasma-membrane enzymes but had no effect on the other proteins. The magnitude of this response was dependent on the bile salt used and its concentration in bile; there was little effect on plasma-membrane enzyme output until the critical micellar concentration of the bile salt had been exceeded in the bile. A bile salt analogue, taurodehydrocholate, which does not form micelles, did not produce the enhanced output of plasma-membrane enzymes. This work supports the view that the output of plasma-membrane enzymes in bile is a consequence of bile salt output and also provides evidence for mechanisms by which serum proteins enter the bile.

5'-Nucleotidase↗
PubMed1990

[Hyperthermic-antiblastic isolation perfusion for advanced melanoma of the limbs. The technic, immediate results and a review of the literature].

Hyperthermic antiblastic isolated perfusion is a method largely used for the treatment of locally advanced limb melanoma. The method requires vascular isolation and hyperthermic perfusion of the limb using an extracorporeal circuit and administering the melphalan as antiblastic drug. Twenty-six patients with primary or recurrent melanoma of the limbs have undergone this treatment at our Institute. There were no cases of operative mortality and systemic toxicity was negligible. The local complications were transitory and no patient showed symptoms of nervous toxicity or permanent functional damage. Two cases of deep thrombophlebitis and two of lymphocele were documented a few months after treatment. Four clinically complete responses, 3 partial and 2 cases of stable disease were observed in the 9 patients treated with unexcised lesions. Our data like the totality of the present experience points to the safety of this method in the therapy of locally advanced limb melanoma. Nevertheless further controlled studies are required to define its role in order to improve survival.

Adult↗
PubMed1999

Vascular kinin B(1) and B(2) receptor-mediated effects in the rat isolated perfused kidney - differential regulations.

1. Bradydykinin (BK) and analogs acting preferentially at kinin B(1) or B(2) receptors were tested on the rat isolated perfused kidney. Kidneys were perfused in an open circuit with Tyrode's solution. Kidneys preconstricted with prostaglandin F(2alpha) were used for the analysis of vasodilator responses. 2. BK induced a concentration-dependent renal relaxation (pD(2)=8.9+/-0.4); this vasodilator response was reproduced by a selective B(2) receptor agonist, Tyr(Me)(8)-BK (pD(2)=9.0+/-0.1) with a higher maximum effect (E(max)=78.9+/-6.6 and 55.8+/-4.3% of ACh-induced relaxation respectively, n=6 and 19, P<0.02). Icatibant (10 nM), a selective B(2) receptor antagonist, abolished BK-elicited relaxation. Tachyphylaxis of kinin B(2) receptors appeared when repeatedly stimulated at 10 min intervals. 3. Des-Arg(9)-BK, a selective B(1) receptor agonist, induced concentration-dependent vasoconstriction at micromolar concentration. Maximum response was enhanced in the presence of lisinopril (1 microM) and inhibited by R 715 (8 microM), a selective B(1) receptor antagonist. Des-Arg(9)-[Leu(8)]-BK behaved as an agonist. 4. A contractile response to des-Arg(9)-BK occurred after 1 of perfusion and increased with time by a factor of about three over a 3 h perfusion. This post-isolation sensitization to des-Arg(9)-BK was abolished by dexamethasone (DEX, 30 mg kg(-1) i.p., 3 h before the start of the experiment and 10 microM in perfusate) and actinomycin D (2 microM). Acute exposure to DEX (10 microM) had no effect on sensitized des-Arg(9)-BK response, in contrast to indomethacin (30 microM) that abolished it. DEX pretreatment however had no effect on BK-induced renal vasodilation. 5. Present results indicate that the main renal vascular response to BK consists of relaxation linked to the activation of kinin B(2) receptors which rapidly desensitize. Renal B(1) receptors are also present and are time-dependently sensitized during the in vitro perfusion of the rat kidneys.

Animals↗
PubMed1979

Instantaneous measurement of glomerular filtration rate in the isolated perfused rat kidney.

In perfusion studies on the isolated cellfree perfused rat kidney, the glomerular filtration rate (GFR) can be controlled if the GFR can be measured instantaneously. This paper reports on a GFR meter which opens this possibility. Vitamin B12 is used as a marker for the GFR. A bubble flow meter determines urine flow rates ranging from 10 up to 200 microliter-min-1. A fiberoptic colorimeter measures vitamin B12 concentrations in the urine up to 400 mg-l-1. The flow meter and the colorimeter are described in detail. The reliability of vitamin B12 as a marker for the GFR is demonstrated and, moreover, the identity of GFR values obtained with the GFR meter and those from B12 spectrophotometry is demonstrated.

Animals↗
PubMed1996

Effect of alpha-KG in lumen on PAH transport by isolated perfused rabbit renal proximal tubules.

To determine whether dicarboxylate taken up at the luminal membrane could function in the p-aminohippurate (PAH) countertransport at the basolateral membrane, we examined the effect of adding alpha-ketoglutarate (alpha-KG) or glutarate (a nonmetabolized dicarboxylate that is countertransported for PAH at the basolateral membrane) to the luminal perfusate on net secretion of radiolabeled PAH in isolated perfused S2 segments of rabbit proximal tubules. Addition of 100 microM alpha-KG or glutarate to the luminal perfusate in tubules perfused and bathed with HEPES-buffered medium (in the absence of bicarbonate, glycine, lactate, malate, and citrate) produced a reversible twofold stimulation of net PAH transepithelial secretion. Addition of 4 mM LiCl (an inhibitor of Na-dicarboxylate transport that does not directly affect PAH transport) to the luminal perfusate along with alpha-KG eliminated stimulation of net PAH secretion. Addition of 100 microM or 1 mM alpha-KG or glutarate to the luminal perfusate in tubules perfused and bathed with bicarbonate-buffered medium containing glycine, lactate, malate, and citrate had no effect on net PAH transport from bath to lumen. These data indicate that alpha-KG (or glutarate) that enters the tubule cells via the luminal Na-dicarboxylate cotransporter can stimulate net PAH secretion, apparently via countertransport at the basolateral membrane, but only when tubules are not in an optimal metabolic state to produce intracellular alpha-KG.

Animals↗
PubMed1980

Potassium and hydrogen ion interaction in the vasculature of the isolated, perfused guinea pig heart.

Potassium and hydrogen ion interactions have been reported in the pial vessels of the cerebral vasculature. Adenosine and hydrogen ion interactions were also found in the coronary circulation. We now report an interaction of perfusate pH and potassium in the coronary vasculature. Isolated, perfused guinea pig hearts were used to investigate the possible influence of perfusate pH on hyperkalemic vasodilatation and on ouabain blockade of the coronary response to hyperkalemia. At perfusate pH 7.45, potassium infusion increased coronary diastolic flow 18%. At pH 7.21, the same concentration of potassium increased flow 35% above control. The coronary vascular response to potassium was modestly diminished at pH 7.65. The duration of the transient vasodilatory response to potassium at low pH was more than doubled relative to pH 7.45. The presence of ouabain in the perfusate significantly (p < 0.05) reduced the dilating action of potassium at pH 7.01 and 7.65. We conclude that the effect of hyperkalemia on coronary flow is pH sensitive but that ouabain blockade of the potassium response is not effected by changes in pH.

Animals↗
PubMed1999

Evidence of a nonendothelial source of nitric oxide in the isolated perfused hindlimb vasculature of the pregnant rat.

OBJECTIVE: This study was undertaken to further elucidate the roles of the vascular endothelium and nitric oxide (NO) in the regulation of vascular tone and constrictor responsiveness in pregnancy. METHODS: The perfusion pressure-flow relationship was measured in isolated, perfused, norepinephrine-constricted (1) endothelium-intact, (2) endothelium-denuded, and (3) N omega-nitro-L-arginine methyl ester (L-NAME)-treated hindlimbs from nonpregnant and term-pregnant rates. RESULTS: Baseline perfusion pressure at a flow rate of 2 mL/min was similar (approximately 20 min Hg) in all hindlimbs. Norepinephrine (0.5 muM) increased perfusion pressure in both nonpregnant (+21.6 +/- 2.4 mm Hg) and pregnant (+13.6 +/- 0.9 mm Hg) endothelium-intact rat hindlimbs. In nonpregnant rat hindlimbs, endothelium removal and L-NAME increased norepinephrine vasoconstriction similarly (+44.3 +/- 4.0 mm Hg and +46.4 +/- 8.6 mm Hg, respectively). In pregnant-rat hindlimbs, L-NAME increased norepinephrine vasoconstriction by 43.5 +/- 10.8 mm Hg, similar to that in nonpregnant-rat hindlimbs, but endothelium removal only increased norepinephrine vasoconstriction by 28.0 +/- 2.2 mm Hg. Perfusion pressure increased linearly as the flow rate was increased from 2 to 4 mL/min, and the slope of the regression line of the endothelium-intact pregnant-rat hindlimbs (7.0 +/- 0.6) was slightly, but not significantly, lower than that of the nonpregnant-rat hindlimbs (9.6 +/- 0.9). Endothelium removal increased the slopes of the regression lines, but that of pregnant-rat hindlimbs (12.8 +/- 1.6) was significantly lower (p < or = 0.05) than that of the nonpregnant-rat hindlimbs (23.8 +/- 1.8). L-NAME caused a similar increase in the pressure-flow slopes of nonpregnant-rat (36.5 +/- 3.4) and pregnant-rat (32.1 +/- 5.3) hindlimbs. CONCLUSIONS: These results suggest that nonendothelial nitric oxide production may be increased in the hindlimb resistance vasculature of the pregnant rat, which may play a role in the normal pregnancy blunting of constrictor responsiveness and reduction of vascular resistance.

Acetylcholine↗
PubMed1988

Triacylglycerol output by the isolated perfused liver of endotoxin-treated rats.

Liver perfusion experiments were performed to further investigate the origin of hypertriacylglycerolemia associated with endotoxemia in rats. For this purpose male rats were treated with E. coli endotoxin in a dose of 0.5 mg/100 g b.w. intravenously, deprived of food (with free access to water), and used 18 h later for liver perfusion experiments. Livers were isolated and perfused for 4 h with a medium consisting of Krebs-Ringer bicarbonate buffer containing bovine serum albumin (4%, w/v), glucose, 5 mM, oleate, 0.7-0.8 mM, and aged human erythrocytes, 20% (v/v). The rates of triacylglycerol (TAG) output, oleate uptake, and ketogenesis were measured. Endotoxin treatment did not induce changes of the rate of either TAG output or ketogenesis in the perfused liver. The data give further support to the contention that hypertriacylglycerolemia associated with endotoxicosis is unlikely to originate in an overproduction of TAG by the liver.

Animals↗