[Appendectomy and Crohn's disease]. / Apendicectomía y enfermedad de Crohn.

UNLABELLED: We analyzed the relationship between Crohn's disease and appendectomy in paediatric age. METHOD AND MATERIAL: We studied the patients diagnosed with Crohn's disease and appendectomy (under 20) between 1999 and 2011. We retrieved their previous medical histories and carried out an histological re evaluation of those appendix. RESULTS: 11 patients out of 137 (8,02%) had an appendectomy before the development of Crohn's disease. An average age in which the appendectomy took place and the development of Crohn's disease was diagnosed 14 (5-20 years), having 90% of the patients diagnosed in the early post-surgical stages. A patient did not develop any symptoms until a year later. There were no more appendectomies carried out in comparison with the adult population. The initial anatomopathologic diagnosis and the histological re evaluation agreed in just one case, compatible with Crohn's disease. CONCLUSION: The majority of appendectomies carried out in paediatric patients that later develop Crohn's disease are realized by a bias diagnosis of acute appendicitis and the relation between the two of them can be explained as the not yet developed Crohn's disease at the moment of the appendectomy. Appendectomies at a paediatric age are not associated with a potential development of Crohn's disease. There is no evidence of histological changes compatible with Crohn's disease in the first episode.

[Hepatopulmonary syndrome]. / Le syndrome hépatopulmonaire.

Hepatopulmonary syndrome is characterized by the presence of portal hypertension with or without cirrhosis, an increased alveolar-arterial oxygen partial pressure difference greater than or equal to 15 mm Hg, and dilated pulmonary capillaries. Hepatopulmonary syndrome is found in up to 20% of patients with cirrhosis and should be considered in any patient who develops dyspnea or hypoxemia. Contrast echocardiography is enough to make the diagnosis of hepatopulmonary syndrome. The exact pathophysiology of hepatopulmonary syndrome remains unknown but nitric oxide is an important factor underlying hepatopulmonary syndrome. Hypoxemia progressively deteriorates and worsens the prognosis of cirrhotic patients. Hypoxemic patients must be controlled regularly to optimise the timing of liver transplantation. Indeed, a preoperative PaO(2) of less than or equal to 50 mm Hg alone or in combination with an isotopic shunt fraction greater than or equal to 20% are the strongest predictors of postoperative mortality. There are currently no effective medical therapies for hepatopulmonary syndrome but garlic powder and iloprost inhalation demonstrate clinical improvements in the pre- and in the post-transplant period.

Laparoscopic colon surgery: unreliability of end-tidal CO2 monitoring.

BACKGROUND: The relatively good haemodynamic and respiratory tolerance to abdominal CO(2) insufflation has mostly been observed in healthy patients during short-lasting laparoscopic procedures. End-tidal CO(2) pressure (PetCO(2)) has been shown to be a reliable method to assess arterial CO(2) (PaCO(2)) in the absence of cardio-respiratory disease in this setting. However, no study has investigated whether PetCO(2) is accurately related to PaCO(2) during laparoscopic colon surgery. Indeed, these procedures last longer, prolonging the pneumoperitoneum and requiring a Trendelenburg position. The aim of the present study was to measure the PaCO(2)-PetCO(2) difference over time in patients undergoing laparoscopic colon surgery and to determine whether PaCO(2) is reliably assessed by PetCO(2). METHODS: Forty consecutive patients (ASA I and II) scheduled for laparoscopic colon surgery were anaesthetized and ventilated to obtain a PetCO(2) between 4.0 and 5.5 kPa. After initiation of CO(2) insufflation, PaCO(2) and PetCO(2) were recorded every 30 min during surgery. RESULTS: No complication was observed during anaesthesia. The mean arterial pressure increased significantly after CO(2) insufflation and remained steady up to the end of pneumoperitoneum. The heart rate remained stable over time. The relation between PaCO(2) and PetCO(2) was not constant among patients and increased over time within the same patients. The R(2) values fluctuated and did not show a constant correlation between PaCO(2) and PetCO(2). CONCLUSION: The correlation between PaCO(2) and PetCO(2) during laparoscopic colon surgery is inconsistent mainly due to inter- and intra-individual variability.

The role of junctional adhesion molecule C (JAM-C) in acute pancreatitis.

The recruitment of inflammatory cells contributes significantly to tissue injury in acute pancreatitis. This process implies several molecular interactions between circulating and endothelial cells. The adhesion molecule junctional adhesion molecule C (JAM-C) is involved in leukocyte transendothelial migration and it can form homophilic (JAM-C/JAM-C) and heterophilic interactions with the leukocyte integrin alpha(M)beta(2). In this study, the effect of early administration of monoclonal antibodies directed against JAM-C in cerulein-induced acute pancreatitis was assessed. This reagent significantly blocked influx of leukocytes, release of serum amylase, secretion of inflammatory cytokines, and acinar cell necrosis. These effects were rapid and protected against tissue injury throughout the duration of the model. Conversely, cerulein-induced acute pancreatitis was more severe in transgenic mice overexpressing JAM-C on endothelial cells under the control of the Tie2 promoter. It is proposed that JAM-C expressed by endothelial cells contributes to the pathophysiology of acute pancreatitis and could be considered a target for clinical applications.

Hepatopulmonary syndrome increases the postoperative mortality rate following liver transplantation: a prospective study in 90 patients.

Hepatopulmonary syndrome (HPS) is a frequent pulmonary complication of patients with end-stage liver diseases. HPS is diagnosed by hypoxemia and pulmonary vascular dilatation and is an independent risk factor of mortality. Orthotopic liver transplantation (OLT) is the only factor that modifies the natural course of HPS. Once patients with HPS have been transplanted, their long-term survival rate is similar to transplanted patients without HPS. Consequently, HPS is an indication of OLT whatever the severity of hypoxemia. However, besides the favorable long-term survival of HPS patients with OLT, a high postoperative mortality (mostly within 6 months) has been suggested. The aim of our study was to analyze the incidence of HPS and postoperative outcome after OLT in 90 consecutive patients. All patients were prospectively included and had blood gas analysis to detect HPS. Patients with hypoxemia had contrast echocardiography to confirm HPS. Nine patients had HPS with a 50 50 mmHg in all HPS patients transplanted.

Acidosis modifies metabolic functions but does not affect vascular resistances in perfused rat livers.

BACKGROUND: Few data exist concerning the consequences of acidosis on intrahepatic vascular resistances and hepatic functions. METHODS: The consequences of pH and PCO2 changes on the intrahepatic vascular reactivity to norepinephrine (NE, 10(-9) to 3 x 10(-5) M) have been investigated in isolated rat livers perfused with solutions bubbled with 5, 10, or 15% CO2 and in solutions in which pH was decreased by replacing HCO3- with NaCl while maintaining a normal PCO2. Hepatic O2 consumption (VO2) and urea release were also measured during these experiments. RESULTS: The NE-induced increase of portal pressure did not change during hypercarbic and normocarbic acidosis. In contrast, the NE-induced increase of urea release was higher when the solution of perfusion was bubbled with 10 and 15% CO2, while during normocarbic acidosis the NE-induced increase of urea release did not change with pH. In the absence of NE, acidosis decreased hepatic VO2 and urea release but portal pressure was not modified by changing % CO2 or pH in the Krebs-Henseleit-bicarbonate solution. CONCLUSIONS: This study clearly shows that, in the liver, the consequences of acidosis are far more important on the metabolism (VO2 and urea release) than on the intrahepatic vascular resistance.

Effect of hyperthermia on NF-kappaB binding activity in cerulein-induced acute pancreatitis.

Although the pancreatic heat shock response has already been reported to confer protective effects during experimental pancreatitis, the mechanism of action remains unknown. We investigated the effects of hyperthermia in cerulein-induced pancreatitis. Heat shock protein 70 (HSP70) expression in rats was induced by a 20-min period of water immersion (42 degrees C). The severity of pancreatitis as well as the pancreatic expression of cytokines, nuclear factor-kappaB (NF-kappaB), and inhibitory factor kappaB-alpha (IkappaB-alpha) were evaluated in the presence and absence of hyperthermia. We found that hyperthermia resulted in time-dependent expression of HSP70 within the pancreas associated with a reduction in the severity of acute pancreatitis. Tumor necrosis factor-alpha and intercellular adhesion molecule-1 expression was significantly reduced in the presence of hyperthermia. Moreover, NF-kappaB activity was delayed in the presence of hyperthermia whereas IkappaB-alpha was stabilized in the cytoplasm. These results suggest that hyperthermia decreases the severity of cerulein-induced pancreatitis by decreasing cytokine expression in the pancreas through the modulation of NF-kappaB activity.

Effects of abdominal Co2 insufflation on renal and hepatic blood flows during acute hemorrhage in anesthetized pigs.

OBJECTIVE: To evaluate the consequences of laparoscopy during hemorrhage, we studied the respiratory, renal, and hepatic blood flow changes induced by abdominal Co2 insufflation during severe hemorrhage in anesthetized pigs. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized and ventilated pigs (n = 18). INTERVENTIONS: The right carotid artery was cannulated to measure mean arterial pressure. A pulmonary artery catheter was inserted to measure mean pulmonary arterial pressure and cardiac output. After a midline abdominal incision, three flow probes were positioned around the portal vein, the hepatic artery, and the renal artery to measure portal vein blood flow, hepatic artery blood flow, and renal blood flow. To induce hemorrhage, blood was withdrawn until mean arterial pressure reached 50 mm Hg. Laparoscopy was mimicked by insufflating Co2 until intra-abdominal pressure reached approximately 15 mm Hg. Measurements were collected during hemorrhage, Co2 abdominal insufflation, and the combination of both interventions. MEASUREMENTS AND MAIN RESULTS: Severe pulmonary hypertension and hypercapnic acidosis occurred during abdominal Co2 insufflation. However, the abdominal Co2 insufflation did not aggravate the cardiac output and total hepatic blood flow changes induced by acute hemorrhage, whereas the combination of hemorrhage and abdominal Co2 insufflation markedly altered renal blood flow. CONCLUSIONS: These results suggest that renal function must be monitored carefully when performing laparoscopy in trauma patients. In contrast, hepatic perfusion seems well preserved.

Are genetically modified mice useful for the understanding of acute pancreatitis?

Treatment of patients with acute pancreatitis has greatly improved due to a better understanding of the pathophysiology of the disease. This pathophysiology includes the activation and release of pancreatic enzymes in the interstitium, the autodigestion of the pancreas, and a multiple organ dysfunction after their release into the systemic circulation. Moreover, significant evidence exists that synthesis and release of proinflammatory cytokines and chemokines are also responsible for the local injury and systemic dispersion of the inflammation. The use of knockout mice devoid of active pro- or anti-inflammatory mediators allows examination of the effects of a specific cytokine without any drawbacks induced by pharmacological manipulations. The results obtained from these genetically modified mice show that numerous mediators have a major role in the pathophysiology of acute pancreatitis. They also clearly demonstrate that a single genetic deletion cannot completely prevent the occurrence of pancreatic or distant organ injury. However, the fact that the immune system is characterized by redundancies of ligands and receptors complicates the full understanding of each report. The utility of such experimental models might have limitations, and a full extrapolation of experimental data from genetically modified mice to humans must be done with caution.

Sepsis decreases the spontaneous and agonist-induced contractile activities in the rat portal vein.

BACKGROUND/AIMS: The portal vein has spontaneous and agonist-induced contractile activities and whether sepsis alters these two types of contractile activities is unknown. METHODS: To study the effect of sepsis on the spontaneous contractile activity and the contractile responses to norepinephrine (NE), angiotensin II (AT(II)), and neurokinin B (NKB) in the rat portal vein (RPV), we performed a cecal ligature and puncture (CLP) 24 h before RPV isolation. RESULTS: CLP decreased the spontaneous activity and induced hyporesponsiveness to AT(II) and NKB. The vascular failure was correlated to the severity of sepsis. In contrast, the reactivity to NE was not altered. Although inducible NO synthase was detected in RPV isolated from CLP rats, NO synthase inhibitors did not restore either the responsiveness to AT(II) and NKB or the spontaneous activity. Additionally, hyporesponsiveness to AT(II) and NKB was not modified by indomethacin. CONCLUSIONS: CLP decreases the spontaneous activity of the RPV as well as the contractile responses to AT(II) and NKB. The vascular failure is correlated to the severity of sepsis. The reactivity to NE is not altered in this model. Neither NO nor prostaglandins are responsible for the vascular abnormalities observed during CLP.

Shear stress modulates the vascular tone in perfused livers isolated from normal rats.

Fluid shear stress can be increased either by increasing the flow rate or perfusing increasing doses of norepinephrine (NE) at a constant flow rate. Concomitantly, increased fluid shear stress at the surface of endothelial cells releases nitric oxide (NO). To better understand the role of NO released by shear stress in regulating intrahepatic vascular resistances, we increased fluid shear stress either by changing the flow rate or by perfusing increasing doses of NE at a constant flow rate in perfused livers isolated from normal rats. When concentration-response curves to NE were studied at low, mild, and high flow rates, portal pressure increased during NE perfusion. The higher the flow rate, the lower the response to NE. NO synthase inhibition similarly increased the response to NE at each flow rate. Thus, NO was released by NE-induced increased shear stress, but other vasodilators are likely to be responsible for the flow-induced increased shear stress. In additional experiments, when flow rate was decreased while infusing increasing doses of NE to maintain the portal pressure constant, shear stress remained steady and NO was not released. Hepatic NO production in the different conditions of shear stress could not be detected. Our data are consistent with the fact that in the liver, NO released by shear stress decreases the vasoconstriction to NE and regulates the intrahepatic vascular resistances.

Spontaneous high systemic oxygen delivery increases survival rate in awake sheep during sustained endotoxemia.

OBJECTIVE: To study the natural evolution of systemic oxygen delivery (Do2) and oxygen consumption (Vo2) in sheep infused with low or high doses of endotoxin. DESIGN: Prospective, controlled experimental study. SETTING: Animal research laboratory at a medical university. SUBJECTS: Twenty-nine chronically instrumented awake sheep (25-35 kg). INTERVENTIONS: Awake animals were continuously infused with saline (n = 8) or two doses of Escherichia coli endotoxin (20 or 40 ng/kg/min; n = 21) for 72 hrs. No attempt was made to increase Do2, but respiratory failure was treated by mechanical ventilation and metabolic acidosis was corrected. MEASUREMENTS AND MAIN RESULTS: The mortality rate was 25% in the group infused with the low dose and 89% in the group infused with the high dose of endotoxin. During the first 12 hrs of endotoxemia, both surviving (S group; n = 10) and nonsurviving (NS group; n = 11) sheep developed similar pulmonary hypertension, left ventricular failure, and hypotension with low systemic vascular resistance. However, S sheep had less interstitial lung edema (pulmonary lymph protein clearance at 8 hrs was 13+/-3 mL/hr vs. 27+/-6 mL/hr in the NS group and 4+/-1 mL/hr in the control group). During this early phase of endotoxemia, Do2, Vo2, and oxygen extraction ratio did not change significantly in any group. After this phase, animals that ultimately survived had a persistent hyperdynamic syndrome with high cardiac output and hypotension. In this group, the Do2 increase was greater than the Do2 measured in controls and remained steady up to 48 hrs after the start of the endotoxin infusion. Because systemic Vo2 did not change significantly, oxygen extraction ratio decreased progressively to values less than those measured in controls. In contrast, animals that ultimately died had a hypotensive and normokinetic syndrome associated with pulmonary hypertension, persistent depressed left ventricular function, hypothermia, and a progressive deterioration of gas exchange. Systemic Do2 was not significantly different from that in the control group. In contrast, Vo2 decreased progressively to values significantly lower than those measured in controls and remained low until death. CONCLUSIONS: Our results indicate that in the absence of treatment such as fluid challenge or inotropic drugs in sheep infused with endotoxin, the occurrence of spontaneous hyperdynamic syndrome and high Do2 improves the survival rate.

Minor involvement of nitric oxide during chronic endotoxemia in anesthetized pigs.

To study the modifications of hepatic blood flow and hepatic function over time during endotoxemia, 10 pigs received a continuous intravenous infusion of endotoxin (Endo, 160 ng. kg(-1). h(-1)) over 18 h and 7 control (Ctrl) animals received a saline infusion. The involvement of nitric oxide (NO) in this endotoxic model was assessed by measuring plasma concentrations of NO(-)(2), NO(-)(3), and cGMP, by testing vascular reactivity to ACh, and by evaluating inducible NO synthase (NOS 2) expression in hepatic biopsies. Endotoxin induced hypotensive and normokinetic shock in association with few modifications of hepatic blood flow, and hepatic injury was observed in both groups. Endotoxin did not increase plasma concentrations of NO(-)(2), NO(-)(3), and cGMP. The ACh-dependent decrease of mean arterial pressure was reduced in Endo pigs, whereas a minor difference was observed between Ctrl and Endo pigs for ACh-dependent modification of hepatic perfusion. Hepatic NOS 2 mRNA was not detected in Ctrl pigs. In Endo pigs, NOS 2 protein expression was detected only in tissues surrounding the portal vein and the inferior vena cava, whereas NOS 2 mRNA was expressed in all hepatic biopsies. Thus, although endotoxemia induces NOS 2 expression in the liver, our findings show that NO involvement is lower in pigs than in rodents during endotoxemia.

[Subepithelial hemorrhage of renal pelvis (Antopol-Goldman lesion). Report of 4 cases and review of the literature]. / Hemorragia subepitelial de pelvis renal (lesión de Antopol-Goldman). Presentación de cuatro casos y revisión de la literatura.

OBJECTIVES: The subepithelial hematoma of renal pelvis (Lesion of Antopol-Goldman) is a rare entity that preferably is diagnosed clinically as a neoplasic lesion. METHODS: We present four new cases of subepithelial hematoma of renal pelvis diagnosed in our hospital from 1989. RESULTS: Our cases presented clinically with hematuria and flanc pain, preferably in the left side (3 out of 4). After nephrectomy, all the cases showed a subepithelial hematoma of variable extension that can occupy the renal pelvis and calices, associated to hidronefrosis, cortical infartion, renomegaly or renal angioma. Additionally, two of our patients presented with dilation of the pielocalicial system, and a third one presented with urotelial carcinoma of the ureter, being therefore the lesion of Antopol-Goldman an incidental discovery. In the remaining case, the presence of multiple renal hemangiomas was identified as cause of the renal pelvic hematoma. CONCLUSIONS: The preoperatore diagnosis of the lesion of Antopol-Goldman is difficult although it should be included as differential diagnosis in those cases with hematuria and alterations of renal pelvis in the image techniques, because an early diagnosis could imply a conservative treatment with pieloplastia or partial nephrectomy.

Hepatic and splanchnic oxygen consumption during acute hypoxemic hypoxia in anesthetized pigs.

OBJECTIVE: To compare the hepatosplanchnic oxygen consumption (VO2) with the hepatic and splanchnic VO2 and to calculate the critical oxygen delivery (DO2crit) below which VO2 decreases in the hepatic, splanchnic, and hepatosplanchnic regions in a model of hypoxemic hypoxia. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized and ventilated pigs (n = 7). INTERVENTIONS: The right carotid artery was cannulated to measure mean arterial pressure. A pulmonary artery catheter was inserted to measure mean pulmonary arterial pressure and cardiac output. After a midline abdominal incision, two flow probes were positioned around the portal vein and the hepatic artery to measure portal vein blood flow and hepatic artery blood flow. Oxygen and lactate contents in the carotid artery, the portal vein, and the hepatic vein were measured in blood samples obtained from the appropriate catheters. MEASUREMENTS AND MAIN RESULTS: After a 2-hr stabilization period, hemodynamic and biological variables were recorded during acute hypoxemic hypoxia (FIO2 = 0.5, 0.4, 0.3, 0.21, 0.15, 0.10, and 0.07). VO2, DO2, and DO2crit were determined in the hepatic, splanchnic, and hepatosplanchnic regions. The hepatosplanchnic VO2 was 48 +/- 5 mL/min at high FIO2 (40% for the liver and 60% for the splanchnic organs) and decreased below FIO2 of 0.15. Lactate uptake in the whole hepatosplanchnic region remained steady at FIO2 values of 0.5 to 0.15 and then switched to a lactate release at low FIO2. However, the splanchnic region released lactate, whereas lactate was taken up by the liver. DO2crit in the hepatic, splanchnic, and hepatosplanchnic regions was 24 +/- 3, 38 +/- 2, and 49 +/- 4 mL/min, but the systemic DO2crit, below which regional VO2 became oxygen supply dependent, did not differ in the liver, splanchnic, and hepatosplanchnic regions. CONCLUSIONS: The variables of oxygenation and lactate flux measured in the hepatosplanchnic region summarize the metabolic changes of various organs that may vary in different ways during hypoxemic hypoxia.

Hepatic vascular response to norepinephrine during endotoxemia in anesthetized pigs.

To investigate the systemic and hepatic reactivity to norepinephrine (NE) during chronic endotoxemia, we measured the reactivity of the drug in pigs infused with endotoxin (End, 160 ng/kg/min) during an 18-h period. At the end of the experiments, the hepatic vessels were removed to test the hepatic vascular reactivity in vitro. The pressive response to NE did not change over time in control (Ctrl) pigs, but endotoxin infusion decreased the response at t = 11 and 17 h. The reactivity of the portal vein blood flow did not change in Ctrl pigs but was significantly increased in End pigs at t = 5 h. Finally, endotoxin decreased the contractile response to NE only in transversal strips of portal veins isolated from End pigs. Thus, in this model, the decreased pressive response to NE develops over time, but the modifications of the hepatic vascular reactivity remain minor.

Beneficial effects of leukocyte-depleted blood and low-potassium dextran solutions on microvascular permeability in preserved porcine lung.

Modified Euro-Collins (EC) solution, a crystalloid intracellular-type solution, has been commonly used for pulmonary preservation. Several experimental studies have shown the advantages of using extracellular colloid-based solutions. The aim of this study was to compare the quality of preservation of two extracellular colloid solutions, leukocyte-depleted blood (BL) and low-potassium dextran (LPD) solutions, with that of EC solution. Lungs of 22 domestic pigs were flushed and preserved with EC (n = 8), BL (n = 7), or LPD (n = 7) solution. After harvesting, one of the lungs was reperfused immediately in an ex vivo circuit (control lungs), whereas the contralateral lung was reperfused after 8 h of cold (4 degrees C) storage (preserved lungs). Besides the lung function parameters (gas exchange, pulmonary hemodynamics and mechanics), the permeability of the endothelial-epithelial barrier was assessed by determining the transferrin leak index (TLI) using a double radioisotopic method, by measuring the alveolar/arterial protein concentration ratio, and by analyzing histopathologic changes. The functional quality (oxygenation, airway resistance, dynamic compliance [CL, dyn]) of both BL and LPD lungs was slightly but significantly superior to that of EC lungs. However, pulmonary vascular resistance was lower in BL-preserved than in EC- or LPD-preserved lungs. The TLI was increased in EC control and preserved lungs, whereas it was low in BL and LPD control lungs and did not increase after preservation. The alveolar/arterial protein concentration ratio was not different between control groups, but was increased fourfold in EC-preserved compared with BL- or LPD-preserved lungs. Finally, EC-preserved lungs presented a weight gain about twice that of BL- and LPD-preserved lungs. Morphologic analysis confirmed these results, because in the EC-preserved lungs, rupture of alveolar septa and severe alveolar edema and hemorrhage were observed, whereas BL- and LPD-preserved lungs showed a relatively well-preserved structure. The results demonstrate that both BL and LPD flush solutions preserve the endothelial-epithelial barrier better than does EC solution. Although the quality of preservation is similar, pulmonary vascular resistance is higher in LPD-preserved than in BL-preserved lungs.

Vascular hyporesponsiveness of the renal circulation during endotoxemia in anesthetized pigs.

OBJECTIVE: To compare the vascular reactivity of the renal circulation in control and septic conditions. DESIGN: Prospective, randomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized pigs (n = 17). INTERVENTIONS: Ten pigs received a continuous intravenous infusion of endotoxin from Escherichia coli (160 ng x kg(-1) x hr(-1)) during 18 hrs, whereas seven control animals received a saline infusion. To test the vascular reactivity, norepinephrine (NE) (1 microg x kg(-1)), acetylcholine (10 microg x kg(-1)), and sodium nitroprusside (10 microg x kg(-1)) were intravenously injected for 20 secs and changes of mean arterial pressure and renal blood flow were observed during the 200 secs after the drug administration. To compare the evolution of the vascular reactivity over time, three tests were performed 5 hrs, 11 hrs, and 17 hrs after initial endotoxin or saline administration. MEASUREMENTS AND MAIN RESULTS: Endotoxin infusion induced a hypotensive and hypokinetic syndrome with renal hypoperfusion. The mean arterial pressure increase after NE injection and the mean arterial pressure decrease after acetylcholine and nitroprusside were lower in endotoxin than in control pigs. In the renal circulation, the increase of resistance after NE injection and the decrease of renal resistance after acetylcholine and nitroprusside injections were lower in endotoxin than in control pigs. CONCLUSIONS: This study shows a hyporesponsiveness of the renal circulation to vasoactive agents during endotoxemia. Vasoconstriction to NE, endothelium-dependent as well as endothelium-independent relaxations are altered during endotoxemia but not abolished, and despite the continuous infusion of endotoxin for 18 hrs, no recovery was observed over time.