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Biomedical subjects

K Kotzampassi

Publications and source records attributed to K Kotzampassi.

At least 19 recordsLinked to original sources
PubMed2005

Temporary stenting of acquired benign tracheoesophageal fistulas in critically ill ventilated patients.

BACKGROUND: To evaluate the use of esophageal stents for temporary sealing of acquired benign tracheoesophageal fistulas developed in critically ill, ventilated patients. METHODS: This is a retrospective analysis (1992-2003) of the data of 12 mechanically ventilated patients - six of them after major or multiple trauma - being intubated for a median of 30 days before they develop an acquired benign tracheoesophageal fistula. Five of them were in sepsis. Two types of stents were used: the Wilson-Cook esophageal balloon plastic stent in the first four cases and the Ultraflex covered self-expandable stent in the remaining eight. The total procedure was performed at bedside in the intensive care unit, with no special need for supplementary anesthesia or fluoroscopic control. RESULTS: Stent implantation was technically successful in all patients and fistula occlusion was achieved in every case. There was no stent migration and fistulas remained sealed until death or upon decision for removal. Nine patients died between 5 days and 2 months after stent placement, as a result of their diseases. Three patients were referred for fistula surgical repair 33, 36, and 43 days after stent placement. Before surgery the stents were easily removed under direct vision. CONCLUSION: Temporary closure of an acquired tracheoesophageal fistula developed in critically ill ventilated patients is an easy, bedside-applicable, safe, and effective palliative procedure, with no complications or mortality.

Adult↗
PubMed2002

Effect of a novel NSAID derivative with antioxidant moiety on oxidative damage caused by liver and cerebral ischaemia-reperfusion in rats.

Tissue ischaemia-reperfusion evokes toxic and harmful biochemical processes such as oxidative stress and inflammation. The aim of this study is to investigate the indices of tissue damage in rat liver and brain after ischaemia-reperfusion injury of these organs, and to study prospective cytoprotection of molecules such as the novel anti-inflammatory N-(2-thiolethyl)-2-(2-[N'-(2,6-dichlorophenyl)amino] phenyl)acetamide (compound 1) and alpha-tocopherol. Two experimental models were studied: firstly, 30 min liver ischaemia via hepatoduodenal ligament clamping followed by 60 min reperfusion; and secondly, 45 min cerebral ischaemia via bilateral common carotid artery occlusion followed by 90 min reperfusion. Compound 1 and alpha-tocopherol were administered intraperitoneally before induction of ischaemia. We hereby report that compound 1, a molecule that combines potent in-vitro antioxidant and in-vivo anti-inflammatory activity with low gastrointestinal toxicity, offered protection in-vivo against liver or brain ischaemia-reperfusion-induced damage. Both compound 1 and alpha-tocopherol prevented changes in lipid peroxidation in the rat liver and brain tissue and in tumour necrosis factor (TNF-alpha) levels in brain. Also compound 1 attenuated glutathione depletion, evoked by ischaemia-reperfusion, in the rat brain but not in the liver. These results could be explained on the basis of the antioxidant/anti-inflammatory properties of compound 1 and suggest its beneficial effect and potential therapeutic use in post-ischaemic injury.

Acetamides↗
PubMed2001

Percutaneous endoscopic gastrostomy after abdominal surgery.

BACKGROUND: Percutaneous endoscopic gastrostomy (PEG) has been established as a minimally invasive and safe procedure to provide nutritional support in patients unable to swallow food properly. However, a relative contraindication for the procedure is the existence of previous abdominal surgery. METHOD: We described our experience in performing PEG on 37 patients who had undergone surgery for upper abdominal diseases 10 days to 25 years previously. This group of 37 patients, 22 of whom had been subjected to laparotomy in the previous 2 weeks, was compared with 291 patients who had an intact abdomen regarding failure of the procedure to be performed, major and minor complications, and mortality. RESULTS: The two groups were found to be comparable: failure rates of 2.71% (1/37) and 1.72% (5/291), no major complications, no mortality, minor complication rates of 2.77% (1/36) and 2.44% (7/286). CONCLUSIONS: The PEG procedure is associated with minimal risk even in patients previously subjected to upper abdominal surgery, as long as transillumination of the stomach and finger palpation are seen clearly during endoscopy.

Adolescent↗
PubMed2001

Sustained reduction of portal pressure by administration of octreotide-LAR in portal hypertensive rats.

Objective: Recent studies have demonstrated octreotide as being potentially beneficial for the long-term management of cirrhotic portal hypertension. However, its short-term effects, requiring subcutaneous administration at least twice daily, make it inconvenient, practically, for long-term therapy. Hence, the current study was undertaken to evaluate the effects of the new long-acting-release octreotide formulation (octreotide-LAR) on portal pressure in a prehepatic portal hypertensive rat model. Methods: 14 days after portal vein stenosis or sham operation, rats were treated with either octreotide-LAR (0.25 mg/kg body weight, subcutaneously) or vehicle, after the baseline portal pressure measurements were obtained in each group. On days 10, 15, 18, 21, 24, 27 and 30 post-treatment, eight rats from each sub-group (portal vein stenosis plus octreotide-LAR, or vehicle, sham-operated plus octreotide-LAR or vehicle) were subjected to portal vein pressure measurement. Results: portal vein-stenosed rats exhibited a significantly higher portal vein pressure than sham-operated rats (13.82+/-2.18 vs. 5.82+/-1.08 mmHg, P=0.0001). Octreotide-LAR treatment was found to significantly (P=0.001) reduce portal pressure in portal vein stenosed rats from the tenth post-injection day and thereafter to sustain reduction. Conclusion: the long-acting-release octreotide given in a single dose in a prehepatic portal hypertensive rat model diminishes and sustains diminished portal pressure for 20 days after the tenth post-injection day. These findings seem promising for the portal hypertensive patient and further clinical studies are necessary.

Journal Article↗
PubMed2000

Deterioration of visceral perfusion caused by intra-abdominal hypertension in pigs ventilated with positive end-expiratory pressure.

Experimental studies and clinical experience suggest that the combination of positive end-expiratory pressure (PEEP) ventilation and intra-abdominal hypertension might alter splanchnic hemodynamics to a significantly greater degree than the effect of either of them alone. Therefore, we assessed the intestinal and hepatic hemodynamics in two steps of PEEP ventilation, adding tense pneumoperitoneum in a pig model. The hepatic artery, portal vein, and superior mesenteric artery blood flow, as well as the hepatic and intestinal mucosal microcirculation, and the hepatic pO2 and intestinal mucosal pH, were assessed before, then with 5 cmH2O and 10 cmH2O PEEP alone, and in combination with a 12-mmHg pneumoperitoneum, in ten domestic pigs. Statistical analysis of the hepatic and intestinal measurements revealed a significant decrease (P = 0.001) in all parameters in relation to the baseline, during the 5-cmH2O and 10-mmH2O PEEP ventilation period. The addition of 12 mmHg intra-abdominal pressure led to an extreme deterioration in all parameters (P = 0.001), in relation to both the baseline and the 10-cmH2O PEEP measurement. These findings demonstrate that PEEP and intra-abdominal hypertension act cumulatively on the abdominal viscera, producing conditions of extremely low hypoperfusion and ischemia.

Analysis of Variance↗
PubMed1998

Influence of enteral nutrition-induced splanchnic hyperemia on the septic origin of splanchnic ischemia.

The purpose of this experimental study was to investigate whether enteral nutrition-induced postprandial intestinal hyperemia has a beneficial effect on the splanchnic ischemia due to sepsis. Fourteen dogs, after exposure to Escherichia coli endotoxin via portal vein administration were grouped according to whether they were fed enterally via a jejunostomy or given a placebo. Systemic hemodynamics; portal vein, hepatic, and superior mesenteric artery blood flow; hepatic and intestinal microcirculation; hepatic tissue PO2; intestinal pHi; and hepatic energy charge were assessed before, during, and after endotoxin infusion as well as during and after enteral or placebo feeding. All splanchnic hemodynamic parameters revealed a statistically significant decline (p = 0.001) during the endotoxin shock period relative to the baseline. After enteral feeding all parameters exhibited a statistically significant increase (p = 0.001) relative to the placebo group. The results of this study led us to suggest that enteral nutrition reverses the lipopolysaccharide infusion-induced splanchnic ischemia.

Animals↗
PubMed1998

Blood digestion-induced splanchnic hyperemia and portal blood flow in portal hypertensive rats and the role of octreotide.

We aimed to investigate whether the presence of blood within the intestinal lumen after variceal bleeding would lead to reactive intestinal hyperemia, which in turn could result in the worsening of portal hemodynamics, and thus bleeding recurrence. Two models of portal hypertensive Wistar rats were used: 32 CCl4-cirrhotics with a low index of portal-systemic shunting and 32 that had been previously subjected to portal vein stenosis, with a high index of portal-systemic shunting; 32 Wistar rats served as controls. The rats were divided into four groups, each comprising 8 cirrhotics, 8 portal vein stenosis rats, and 8 controls. Intestinal microcirculation and portal blood flow were assessed by laser-Doppler and transit-time ultrasonic flow probes, respectively, before and 60 min after the injection of 2 ml of blood (groups 1 and 2) or an equal volume of NaCl 0.9% (placebo; groups 3 and 4) into the intestinal lumen. Octreotide (0.2 microg/100 g body weight [BW]) (groups 1 and 3) or NaCl 0.9% (groups 2 and 4) was then given subcutaneously, and 30 min later the final measurements were performed. The presence of blood within the intestinal lumen resulted in an increase in intestinal microcirculation in rats in all groups, while portal blood flow was increased in portal vein stenosis rats and controls, and decreased in cirrhotics. The presence of NaCl 0.9% had no effect. Octreotide, but not NaCl 0.9%, led to a decrease in both intestinal microcirculation and portal blood flow. The findings of this study suggest that intestinal hyperemia induced by digestion of blood in the enteric lumen increases or decreases portal blood flow, the result being strongly related to the portal hypertension model used. Since the main difference between the models was the extent of portal-systemic shunting, this may suggest a relationship between portal blood flow and portal-systemic shunting. This relationship could explain why variceal bleeding stops in some patients but recurs in others.

Animals↗
PubMed1998

Modulation of intravariceal pressure with pentoxifylline: a possible new approach in the treatment of portal hypertension.

OBJECTIVE: In this study the effect of the hemorheological agent pentoxifylline on the pressure of esophageal varices was investigated in portal hypertensive cirrhotic patients. METHODS: Intravariceal pressure was measured endoscopically using the direct puncture technique in 20 patients. Measurements were obtained under baseline conditions and 30 min after double-blind administration of pentoxifylline (1.4 mg/kg BW, n = 10 patients) or an identical volume of NaCl 0.9% solution (n = 10 patients). RESULTS: Under baseline conditions, intravariceal pressure was similar in pentoxifylline and placebo groups (17.3+/-5.5 mm Hg vs 18.8+/-4.6 mm Hg, respectively; p = N.S.). Placebo administration had no significant effect on intravariceal pressure (18.8+/-4.6 mm Hg vs 18.3+/-4.1 mm Hg; p = N.S.). In contrast, pentoxifylline caused a highly significant reduction of intravariceal pressure, (from 17.3+/-5.5 mm Hg to 11.4+/-5.9 mm Hg; p = 0.0001), the overall mean reduction being 36.1+/-14.1% mm Hg. CONCLUSIONS: We concluded that pentoxifylline, by reducing blood flow viscosity, caused a significant decrease in variceal pressure in patients suffering from portal hypertension.

Double-Blind Method↗
PubMed1998

Long-term measurement of liver microcirculation in dogs and humans.

BACKGROUND: We verified the possibility of using laser Doppler fluxmetry for prolonged monitoring of hepatic perfusion; we confirm the ability of an implantable laser Doppler microprobe to be in constant 'optical contact' with the liver and thus to transmit a stable microcirculatory signal for a prolonged period of time, and we correlate the response of liver microcirculation to the hepatic artery blood flow reduction in order to estimate this flow by continuous monitoring of microcirculation. METHOD: Hepatic microcirculation was recorded by a single-fiber microprobe implanted in the livers of 8 dogs and of 5 surgical ICU patients. In another 7 dogs, liver microcirculation as well as hepatic artery blood flow were recorded digitally, while an occluder was used to decrease hepatic artery flow. RESULTS: Analysis of the initial data of microcirculation revealed a nonsignificant variation between consecutive time segments, a finding confirming the hypothesis that laser Doppler gives a very stable signal over a long period of time. Polynomial regression analysis, performed on data pairs obtained from microcirculation and hepatic artery blood flow revealed a regression coefficient y = -54.22 + 1.07x + 0.0046x2 (y = hepatic artery blood flow, x = liver microcirculation). CONCLUSION: This finding means that it is possible to watch the hepatic artery flow values continuously by the use of this equation and simple monitoring of liver microcirculation. Thus, the use of laser Doppler fluxmetry with implantable microprobes seems promising as a novel method for continuous assessment of hepatic artery blood flow.

Animals↗
PubMed1996

Splanchnic ischemia during laparoscopic cholecystectomy.

BACKGROUND: Experimental studies have shown that elevation of intraabdominal pressure by means of gas insufflation produces hemodynamic disturbances in the peritoneal viscera, leading to splanchnic ischemia. The purpose of this clinical investigation is to reproduce the experimental data in humans undergoing laparoscopic cholecystectomy. METHODS: Sixteen females participated in this study. Eight of them (the control group) were subjected to open laparotomy for biliary surgery, while on the remaining eight laparoscopic cholecystectomy was performed. In all patients hepatic microcirculation was registered during the time of operation using the laser-Doppler technique. A single-fiber laser-Doppler microprobe was introduced transcutaneously within the hepatic parenchyma, through a Chiba needle, under direct or laparoscopic vision. Additionally, gastric intramucosal/intramural pH, a low level of which indicates tissue ischemia, was assessed by means of a tonometric nasogastric catheter. Hepatic microcirculation and gastric intramucosal/intramural pH were assessed between controls and pneumoperitoneum-subjected patients, and within the laparoscopic surgery group, i.e., during pneumoperitoneum and after abdominal deflation. RESULTS: Hepatic microcirculation was found to be significantly decreased in laparoscopic surgery patients in relation to controls (22.21 +/- 5.48 vs 57.52 +/- 18.06 perfusion units of flow, P = 0.0001) as was gastric intramural pH (7.15 +/- 0.16 vs 7.37 +/- 0.02, P = 0.003). Similarly, immediately after abdominal deflation, hepatic microcirculation exhibited a sudden elevation (22.21 +/- 5.48 vs 67.49 +/- 7.93 perfusion units of flow, P = 0.0001), while gastric intramural pH return to its normal values (7.15 +/- 0.16 vs 7.43 +/- 0.07, P = 0.0001). CONCLUSIONS: It is concluded that during laparoscopic cholecystectomy abdominal organs are hypoperfused, leading to a splanchnic ischemia environment. The clinical significance of these events remains to be clarified.

Adult↗
PubMed1996

Gut ischemia, oxidative stress, and bacterial translocation in elevated abdominal pressure in rats.

The purpose of this experimental study was to investigate whether the increased intraabdominal pressure due to gas insufflation creates intestinal ischemia leading to oxygen free radical production and bacterial translocation. A group of 88 rats were studied, 40 of which were subjected to a 15 mmHg pressure pneumoperitoneum for 60 minutes, with the following parameters being studied: mean arterial pressure after carotid catheterization; intestinal microcirculation by means of the laser-Doppler technique; gut metabolic activity (O2 extraction) by blood sampling from portal vein and carotid artery; intestinal, hepatic, splenic, and lung free radical production (malondialdehyde); and bacterial translocation toward the mesenteric lymph nodes, liver, and spleen at 3 and 18 hours after pneumoperitoneum deflation. The mean arterial pressure exhibited no alterations, whereas the jejunal mucosa microcirculation was significantly decreased (p = 0.0001), as was the gut metabolic activity (p = 0.025). Malondialdehyde was increased in gut mucosa (p = 0.0002), liver (p = 0.02), spleen (p = 0.03), and lung (p = 0.017). Bacterial translocation toward the mesenteric lymph nodes (p = 0.002), spleen (p = 0.002), and liver (p = 0.05) was increased in the 3-hour group; in the 18-hour group bacteria were not found in mesenteric lymph nodes but were in liver (p = 0.008) and spleen (p = 0.035). It is concluded that elevated intraabdominal pressure in the rat leads to intestinal ischemia, oxygen free radical production, and bacterial translocation. These results must be reproduced in humans and their clinical significance clarified.

Animals↗
PubMed1995

Increased capillary endothelial leakage in portal hypertensive gastric mucosa: fluorescence microscopy in CCl4-induced cirrhotic rats.

Since portal hypertension affects the gastric mucosa, leading to congestive gastropathy and thus to increased incidence of bleeding, it is one of the possible causes of increased permeability of gastric mucosal capillaries. The aim of this study was the quantitative assessment of the permeability of the gastric mucosal endothelial cells. Eight CCl4-induced cirrhotic rats and eight matched controls were subjected to i.v. injection of FITC-albumin, and a morphometric evaluation of fluorescence in serial histological sections of the gastric mucosa was performed by a video image analysis system. Fluorescence was found to be 0.351 +/- 0.01% of the area scanned in experimental animals versus 0.073 +/- 0.005% in controls, i.e. it was significantly increased by the treatment, which implies a significant endothelial leakage into the extravascular space.

Albumins↗
PubMed1993

The influence of hemorrhage on liver microcirculation of the cirrhotic rat.

Bleeding from esophageal varices is highly lethal in cirrhotics, the main cause of death being liver failure. Because adequate hepatic perfusion is a prerequest for the maintenance of liver function, the present study was designed to evaluate the influence of hemorrhagic shock on liver microcirculation in rats with portal hypertension due to cirrhosis of the liver induced by CCl4. In 16 cirrhotic rats and an equal number of controls, hepatic microcirculation was continuously assessed--by means of laser-Doppler flowmetry, through a self-adhesive probe attached to the liver surface, before and during a 15 min period of arterial hypotension (40 mmHg) induced by blood withdrawal. Our findings revealed that immediately following hemorrhage there is a statistically significant reduction of microcirculation in cirrhotics versus controls. The results of this study assist in the better understanding of the hemodynamic conditions which prevail in the cirrhotic liver during the first minutes of hemorrhage.

Acute Disease↗
PubMed1992

Gastric mucosal blood flow distribution in the CCl4-induced cirrhotic rat--a model of portal hypertensive gastropathy?

Because the carbon tetrachloride-induced cirrhotic rat model is considered to be the closest to the clinical situation of the cirrhotic patient, the discovery of congestive gastropathy in such rats would enable the development of a useful research model. By the use of laser-Doppler technology, gastric mucosal blood flow was assessed on 14 defined points of the stomach in 16 cirrhotic and 16 matched healthy rats, in an effort at in vivo mapping of the gastric mucosal microcirculation. Our findings of mucosal congestion in the cirrhotic stomach (reduced mucosal blood flow in the gastric corpus) are well matched with the distribution of gastric mucosal blood flow in the cirrhotic patient. These findings suggest that a rat's gastric mucosa could be used for studies of portal hypertensive gastropathy.

Animals↗
PubMed1992

Experimental and clinical evaluation of capsular and parenchymal total liver perfusion. Liver microcirculation.

Liver blood flow measurements obtained from both the liver surface and deep within the parenchyma, were correlated in an effort to assess the usefulness of laser-Doppler flowmetry for non-invasive monitoring of total liver blood flow, the probe being positioned on either the surface or within the liver parenchyma. In 23 Wistar rats and 10 biliary surgery patients, anaesthetized prior to gallbladder removal, liver microcirculation was measured at 4 points on the capsular surface, and consequently at 4 points deep within the parenchyma, using probes connected to a laser-Doppler flowmeter. The findings revealed that laser-Doppler measurements on the liver surface and within the parenchyma were well correlated, as no statistically significant differences were found either in rats or humans. It is concluded that laser-Doppler flowmetry for monitoring of total liver perfusion can be applied either on the capsular surface or within the hepatic parenchyma.

Animals↗