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Biomedical subjects

F Jakab

Publications and source records attributed to F Jakab.

At least 73 records · Page 4Linked to original sources
PubMed1977

The effect of increased inferior vena cava pressure on hepatic circulation in the dog.

Inferior v. cava pressure (IVCP) was raised in the dog by a baloon catheter introduced via the jugular vein. Hepatic artery flow (HAF) and portal venous flow (PVF) were measured with the electromagnetic flow meter. The increase of IVCP reduced uniformly HAF and PVF, the relative contribution of the two vessels to the HBF did not change. The relationship between IVCP increase and HAF reduction and between the decrease of AP-IVCP and the reduction of HAF was linear. There was no sign of autoregulation or vasomotor regulation of HAF. The changes in IVCP are only partially transmitted to the portal venous pressure (PVP). There was no change in intrahepatic portal resistance with increased IVCP. The increase in PVP did not lead to resistance changes in the splanchnic circulation. As a sign of the autoregulation of splanchnic circulation of the AP-PVP versus PVF curve was concave to the pressure axis. It is concluded that as a result of opposing autoregulatory and vasomotor influences in the intact animal the hepatic circulation appears to react passively to the increased outflow pressure.

Animals↗
PubMed1977

The effect of acidifying the duodenal contents on splanchnic blood flow.

Acidifying the duodenal contents with 0.1 N hydrochloric acid in the dog increased both hepatic artery and portal vein flow, and reduced mesenteric vascular resistance as well as hepatic artery and portal venous inflow resistances. The reaction is absent after intraduodenal injection of 30% glucose and physiological saline solutions. More concentrated acid leads to a greater increase in blood flow. The receptors of the circulatory reflex are situated in the duodenal mucosa and can be blocked with lidocaine.

Animals↗
PubMed1976

The effect of the occlusion of liver lymphatics on hepatic blood flow.

In the dog after the ligation of the thoracic duct and of the lymphatics of liver hilum hepatic blood flow decreased in 2hrs by 30.6 per cent. The flow reduction is due to the increase of arterial and venous inflow resistances and of the prehepatic splanchnic arteriolar resistance. The vascular reaction in lymph stasis differs insofar from the reaction seen during biliary duct obstruction that in the latter condition hepatic artery flow is increased. A preexistent lymph stasis does not abolish the increase in the hepatic artery flow produced by raised biliary tract pressure. The differences between the flow reactions observed in bile stasis and in lymph stasis are explained by the accumulation in the latter condition of a protein rich fluid in the liver tissue.

Animals↗
PubMed1976

The escape of bile from the intrhepatic biliary tree in acute bile stasis.

The escape of fluorescent dyes from the bile passages during bile stasis and after a retrograde infusion into the common bile duct was examined in rats and mice. After an intravenous dye injection in bile stasis a strong fluorescence is seen in the periportal spaces. During retrograde dye infusion great amounts of dye accumulate in the periportal spaces but, in consequence of focal disruption of liver cell membranes, escapes also into the spaces of Disse, to be consequently transported by the sinusoidal blood.

Acute Disease↗
PubMed1975

The lymphatic drainage of the liver capsula and hepatic parenchyma.

The lymphatics transport of bilirubin and of 131I-albumin absorbed from the liver capsula was studied in dogs during the early stage of complete biliary obstruction. Bilirubin transport by the right lymph trunc was only 1,5% of the transport by the thoracic duct. Labelled protein absorbed from the Glisson's capsule is transported both by the right lymph duct and the thoracic duct. During an infusion of large amounts of fluid under high pressure into the bile duct labelled protein is transported from the liver parenchyma almost exclusively by the thoracic duct. After the occlusion of about 70% of the lymphatics draining the liver the increase in the transport of the labelled protein by the right duct accounted only for on insignificant fraction of the loss from the thoracic duct lymph. It is concluded, that lymph formed in the hepatic parenchyma is transported by vessels joining the thoracic duct. Capsular lymphatics run both to the thoracic and the right lymph duct. There is practically a complete functional division of the superficial and deep lymphatics of the liver.

Albumins↗
PubMed1975

Bile constituents in blood and lymph during biliary obstruction. I. The dynamics of absorption and transport of ions and colloid molecules.

Na125I and 131I-labeled albumin was infused in dogs into the common bile duct at pressures of 20 to 25 and 40 mmHg. At 40 mmHg, the amounts of the iodide ion and labeled albumin in circulating plasma were, after correction for the secondary loss from the circulation, nearly identical. At 20-25 mmHg more iodid than labeled albumin was found in the circulation. In thoracic duct lymph the same fraction of the infused amount of albumin was recovered at both pressures. Lymphatic concentrations of albumin were in both types of experiments substantially higher than plasma concentrations. It is concluded, that at increased pressure fluid leaks first from the small biliary ducts into the Mall's spaces. In consequence of water absorption and the diffusion of ions and small molecules into the blood capillaries the concentrations of protein or protein bound molecules in this part of the hepatic interstitial fluid increases. This is reflected in their high concentration in the lymph. If bile pressure rises further, fluid leaks also into the Disse's spaces. This leads to a bulk flow of solvent and solutes into the sinusoids and to the near disappearance of the differences in the venous transport of ions and colloids.

Animals↗
PubMed1975

Bile constituents in blood and lymph during biliary obstruction. II. The absorption and transport of bile acids and bilirubin.

The lymphatic and venous transport of bilirubin and total bile acid was examined in dogs after the occlusion of the common bile duct. Lymphatic concentrations of both substances attained maximum levels between the 4 th and 6 th hours, but remained during the entire time of observation (24 hours) above plasma concentrations. The concentrations in blood plasma rose more slowly, but continuously. The amounts of both substances transported by the lymphatics rose steadly for 6 or 8 hours respectively and exceeded after 2 hours of occlusion the amounts transported by the veins. The results are explained by the changes in bilirubin and bile acid formation and secretion during biliary obstruction and on the basis of observations made in experiments with electrolyte and colloid infusions into the biliary passages.

Animals↗
PubMedDate not supplied

The retention of bile constituents in biliary stasis.

The biliaro-lymphatic reflux of bilirubin and bile salts is present in the dog only in the first 24 hrs of complete biliary obstruction. The reflux has been demonstrated also in rats, but it is absent in dogs with functioning gall bladder, when bile pressure does not attain the "secretory pressure". Alkaline phosphatase and GOT do not regurgitate in bile stasis into the lymph. The biliaro-lymphatic reflux of bile pigments and bile salts stops in consequence of the cessation of their secretion into the bile. This is corroborated by the observation that in the rat the excretion of BSP into the bile ceases after a prolonged bile stasis. The uptake by the hepatocytes of BSP and other substances does not stop, however, after several days of complete biliary obstruction. The bile constuents are released in prolonged bile stasis from the liver cells directly into the sinusoidal blood. This is probably the consequence of some damage of the cell function.

Alkaline Phosphatase↗
PubMedDate not supplied

First clinical data of a natural immunomodulator in colorectal cancer.

BACKGROUND/AIMS: MSC (trade-name AVEMAR) is a per os applicable complex of multiple, biologically active molecules obtained from fermented wheat-germ extract. Preclinical studies suggest potent anti-metastatic activity and it has a favorable toxicity profile. It has been aimed in a pilot-scale, phase II clinical study to document whether or not MSC as a support to surgery or plus chemotherapy adds any therapeutic benefit compared to the same combination without MSC in colorectal cancer. METHODOLOGY: From 1998 to June 1999, 18 control patients and 12 consecutive colorectal cancer patients respectively, were enrolled into this study. All patients underwent curative surgery. The control group (18 patients) received no other therapy or adjuvant chemotherapy alone. The MSC group (12 patients) received MSC alone or plus adjuvant chemotherapy. Until now, the median follow-up has been 9 months. RESULTS: Interim data of the study document that in the MSC group no new metastases, neither hepatic nor other, have occurred, so far. On the contrary, several new metastases have developed in the control group. CONCLUSIONS: Orally administered MSC is a potent candidate to be regarded as a supportive therapy to surgery or plus chemotherapy for colorectal cancer patients.

Adjuvants, Immunologic↗
PubMedDate not supplied

The first histological demonstration of pancreatic oxidative stress in human acute pancreatitis.

Necrotizing acute pancreatitis is associated with an inflammatory explosion involving numerous pro-inflammatory mediator cascades and oxidative stress. Acinar oxygen free radical production aggravates pancreatic tissue damage, and promotes cellular adhesion molecule upregulation resulting in leukocyte adherence and activation. The cerium capture oxygen free radical histochemistry combined with reflectance confocal laser scanning microscopy allows the "in situ" histological demonstration of oxygen free radical formation in live tissues. Here we present a case report, where oxidative stress is demonstrated on a histological level for the first time in human acute pancreatitis. A 44-year-old male patient suffering from acute exacerbation of his chronic pancreatitis developed a pancreato-pleural fistula with amylase-rich left pleural exudate causing respiratory compromise. Subsequent to an urgent thoracic decompression a distal pancreatectomy and splenectomy was performed with the closure of abdomino-thoracic fistula. The postoperative course was uneventful, except for a transient pancreatico-cutaneous fistula, which healed after conservative treatment. To carry out cerium capture oxygen free radical histochemistry the resected pancreas specimen was readily perfused with cerium-chloride solution through the arteries on the resection surface. Frozen sections were cut, E-, P-selectin, ICAM and VCAM were labeled by immunofluorescence. The tumor-free margin of an identically treated pancreas carcinoma specimen served as a control. Intrapancreatic oxidative stress and cellular adhesion molecule expression were detected by confocal laser scanning microscopy. Numerous pancreatic acini and neighboring capillaries showed oxygen free radical-derived cerium-perhy-droxide depositions corresponding to strong local oxidative stress. Acinar cytoplasmic reflectance signals suggested xanthine-oxidase as a source of oxygen free radicals. These areas presented considerably increased endothelial P-selectin expression with adherent, oxygen free radical-producing polymorphonuclear leukocytes displaying pericellular cerium-reflectance. Modest ICAM upregulation was noted, E-selectin and VCAM expression was negligible. The control pancreas specimen showed minimal oxidative stress with weak, focal P-selectin expression. The development of deleterious pancreatic oxidative stress was based on indirect evidence in human acute pancreatitis. To the best of our knowledge this is the first report demonstrating persistent intrapancreatic oxidative stress histologically in human acute pancreatitis. We have noted P-selectin overexpression with a preponderance in the areas of acinar oxidative stress.

Adult↗