Preoperative Assessment of Body Fluid Disturbances in Patients with Obstructive Jaundice

Padillo, Francisco J.; Rodríguez, Marcela A.; Gallardo, J.M.; Andicoberry, B; Naranjo, Antonio; Martín‐Malo, Alejandro; Míño, G; Sitges‐Serra, Antonio; Pera-Madrazo, C

doi:10.1007/pl00012368

Cited by 18 publications

(24 citation statements)

References 30 publications

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“…Our study found a drop in sodium excretion, and the concentration of sodium in urine that was related to the increase in aldosterone concentration, which suggests a rise in sodium retention in the distal tubule. In this respect, results corroborate clinical studies run by our group, which showed that patients with OJ suffered a depletion of extracellular volume that is directly related to biliary obstruction (16), and had renin and aldosterone levels in the upper range of normality (5). ET-1 is a peptide with a powerful vasoconstrictor action that is involved in the genesis of several diseases, mainly in the hepato-biliary area.…”

Section: Discussionsupporting

confidence: 88%

Alteration of the renal regulatory hormonal pattern during experimental obstructive jaundice

Padillo

Cruz

Espejo

et al. 2009

Rev. esp. enferm. dig.

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Objective: the alteration of hormones regulating sodium and water status is related to renal failure in obstructive jaundice (OJ).Experimental design: OJ was induced by common bile duct ligation. Samples were obtained from the control (SO) and OJ groups at 24 and 72 hours, and at 7 days. Different parameters related to biliary obstruction, liver and renal injury, and vasoactive mediators such as renin, aldosterone, endothelin-1 (ET-1) and prostaglandin E 2 (PGE 2 ) were studied.Results: bile duct ligation caused an increase in total bilirubin (p < 0.001) and alkaline phosphatase (AP) (p < 0.001). The SO and OJ groups had the same values for diuresis, renin, and creatinine clearance at 24 h. However, animals with OJ had a lower sodium concentration in urine than SO animals (p < 0.01), as well as an increase in aldosterone levels (p < 0.03). ANP levels were moderately increased during OJ but did not reach statistical significance when compared to the SO group. In contrast, OJ animals showed a rise in serum ET-1 concentration (p < 0.001) and increased PGE 2 in urine (p < 0.001).Conclusions: biliary obstruction induced an increase in ET-1 release and PGE 2 urine excretion. These hormones might play a role during the renal complications associated with renal disturbances that occur during OJ. INTRODUCTIONCholestasis is a clinical and biochemical syndrome caused by the impaired bile flow often associated with extrahepatic complications (1). Acute renal failure is a major complication of obstructive jaundice (OJ), with 8% incidence in several series (2). Biliary obstruction was first linked to renal failure in the early study carried out by Clairmont and von Haberer (1910) (3). Several hypotheses have sought to explain the pathogenesis of renal dysfunction in OJ. The depletion of the extracellular compartment (4), myocardial dysfunction, and altered hemodynamic status (5) have been linked to renal failure in biliary obstruction. In addition, severe oxidative stress has been implicated in the renal dysfunction associated to experimental OJ (6,7) as well as other liver diseases (8). Other lines of research have looked at the involvement of vasoactive mediators such as endothelin-1 (ET-1). ET-1 is a powerful paracrine vasoconstrictor that acts by means of specific type-A and type-B receptors. In biochemical terms, it is a 21-amino acid peptide derived from what is known as big ET-1 by the action of the endothelin-converter enzyme. It is synthesized mainly by endothelial cells and to a lesser degree by stellate cells in the liver and biliary epithelium (9,10). ET-1 changes have been related to different human diseases (11). ET-1 both acts on the mesangial cells and causes vasoconstriction in the renal microcirculation, which may contribute -along- Enferm Dig 2009; 101: 408-412.

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Section: Discussionsupporting

confidence: 88%

Alteration of the renal regulatory hormonal pattern during experimental obstructive jaundice

Padillo

Cruz

Espejo

et al. 2009

Rev. esp. enferm. dig.

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“…In our in vivo experiments, increased LVSEP, +dP/dt max and -dP/dt max , were associated with myocardial contractility, suggesting up regulation of the sympathetic nervous system. In addition, LVEDP which directly relates to the cardiac preload might remain unchanged possibly not owing to the depletion of body fluid in obstructive jaundice [30,31]. However, the lower heart rate may be caused in part by accumulated bile acids, which impair cardiac function by affecting calcium uptake from the sarcoplasmic reticulum [32,33].…”

Section: Discussionmentioning

confidence: 99%

In vivo and ex vivo effects of propofol on myocardial performance in rats with obstructive jaundice

et al. 2011

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BackgroundResponsiveness of the "jaundiced heart" to propofol is not completely understood. The purpose of this study was to evaluate the effect of propofol on myocardial performance in rats with obstructive jaundice.MethodsMale Sprague-Dawley rats (n = 40) were randomly allocated into two groups, twenty underwent bile duct ligation (BDL), and 20 underwent a sham operation. Seven days after the surgery, propofol was administered in vivo and ex vivo (Langendorff preparations). Heart rate, left ventricular end-systolic pressure (LVESP) left ventricular end-diastolic pressure (LVEDP), and maximal rate for left ventricular pressure rise and decline (± dP/dtmax ) were measured to determine the influence of propofol on the cardiac function of rats.ResultsImpaired basal cardiac function was observed in the isolated BDL hearts, whereas in vivo indices of basal cardiac function (LVESP and ± dP/dt) in vivo were significantly higher in rats that underwent BDL compared with controls. With low or intermediate concentrations of propofol, these indices of cardiac function were within the normal physiologic range in both groups, and responsiveness to propofol was unaffected by BDL. When the highest concentration of propofol was administrated, a significant decline in cardiac function was observed in the BDL group.ConclusionsIn rats that underwent BDL, basal cardiac performance was better in vivo and worse ex vivo compared with controls. Low and intermediate concentrations of propofol did not appear to impair cardiac function in rats with obstructive jaundice.

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“…Decrease in the glomerular filtration rate and acute renal failure (ARF) are observed in 60-75 and 4-18% of the patients respectively. The mortality of patients with renal failure varies between 32 and 100% [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

Küçük¹,

Sözüer²,

Ikizceli³

et al. 2003

Eur Surg Res

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Obstructive jaundice is associated with high morbidity and mortality. Major complications such as pulmonary dysfunction, renal failure and sepsis are frequently encountered. Recent studies and observations suggest that the free oxygen radicals (FORs) produced in obstructive jaundice may play a significant role in the etiopathogenesis of acute renal failure (ARF). Thirty rats were divided into three groups, as sham, control and treatment groups containing 10 rats each. Laparatomy was performed on each animal in the control and treatment groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection was begun on the first day of surgical procedure and repeated once a day during the following 5 days. The same procedure was performed with oxygen radical scavenger dimethyl sulfoxide (1.5 mg/kg/day i.p.) instead of saline in the treatment group. The rats were sacrificed on the 7th postoperative day. On the 7th postoperative day, the bilirubin, urea and creatinine levels of the control and treatment groups were significantly higher in comparison with the sham group (p < 0.01). Although there was no statistically significant difference between the bilirubin levels of the control and treatment groups (p > 0.05), the urea and creatinine levels in the treatment group were significantly lower (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and treatment groups were significantly lower than those of the sham group (p < 0.01), whereas renal and erythrocyte malondialdehyde (MDA) levels were significantly higher (p < 0.01). Although SOD and GSH-Px levels did not differ significantly between the treatment and control groups (p > 0.05), renal and erythrocyte MDA levels of the treatment group were significantly lower than those of the control group (p < 0.01). The histopathological scores were significantly higher in the control and treatment groups (p < 0.01); there was no significant difference between the control and treatment groups (p > 0.05). FORs seem to play a significant role in the etiopathogenesis of renal failure in obstructive jaundice. Antioxidant treatment may decrease oxidative damage due to FORs and may prevent renal failure.

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Preoperative Assessment of Body Fluid Disturbances in Patients with Obstructive Jaundice

Cited by 18 publications

References 30 publications

Alteration of the renal regulatory hormonal pattern during experimental obstructive jaundice

Alteration of the renal regulatory hormonal pattern during experimental obstructive jaundice

In vivo and ex vivo effects of propofol on myocardial performance in rats with obstructive jaundice

Role of Oxygen Free Radical Scavengers in Acute Renal Failure Complicating Obstructive Jaundice

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