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Biomedical subjects

M Siech

Publications and source records attributed to M Siech.

36 records · Page 2Linked to original sources
PubMed1997

Similar morphological and intracellular biochemical changes in alcoholic acute pancreatitis and ischemic acute pancreatitis in rats.

Pancreatic hyperstimulation with simultaneous duct obstruction does not cause the typical features of acute pancreatitis, therefore the role of an additional challenge, such as either ethanol intoxication or short-term ischemia, was studied. Alcoholic pancreatitis was induced in 28 rats by acute ethanol intoxication (0.25 LD50) and an obstruction/hyperstimulation mechanism (clip of the biliopancreatic duct for 20 min and intravenous stimulation with 5 U of cholecystokinin and secretin each). Ischemic pancreatitis was performed by obstruction/hyperstimulation and subsequent pancreatic ischemia by clamping the supplying arteries for 40 min. The macro- and microscopic alterations were evaluated and graded by a scoring system. Additionally, the pancreas was removed in 50% of the animals and the pancreatic acini were prepared. From those acini the intracellular enzymes trypsinogen, kallikreinogen, amylase, lipase, glucuronidase, and acidic phosphatases were determined. While obstruction/hyperstimulation, 40 min of ischemia, or ethanol alone did not induce acute pancreatitis, a combination of obstruction/hyperstimulation with either ethanol or ischemia resulted in acute pancreatitis in 68 and 60% of treated rats, respectively. Similarly, both models were characterized by extrapancreatic fat necrosis and acinar necrosis at the periphery of the lobules. Almost all intracellular enzymes were elevated in both pancreatitis models compared to sham-operated controls. Both alcohol and ischemia were insults that sensitize the pancreas to develop acute pancreatitis after obstruction/hyperstimulation. Since the observed morphologic and enzymatic alterations in both models are very similar, alcohol and ischemia might have some common pathways by which they make the pancreas vulnerable to enzymatic attacks.

Acute Disease↗
PubMed1997

Different changes in high-energy phosphates in alcoholic acute pancreatitis and taurocholate acute pancreatitis in rats using NMR spectroscopy at 2.0 T.

We studied the pancreatic high-energy phosphates in two models of acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo. Alcoholic pancreatitis was induced by acute ethanol intoxication and an obstruction-hyperstimulation mechanism. Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10% taurocholate-Na+. In addition to the obligate control groups, a simple ischemia experiment was performed. The high-energy phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of taurocholate showed an increase in inorganic phosphate with a concomitant decrease in ATP levels, similar to pancreatic ischemia. This irreversible decrease was accompanied histologically by severe pancreatic hemorrhage. After induction of alcoholic acute pancreatitis a reversible decrease in ATP was occasionally seen. Even when alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy phosphates seems to occur as a result of pancreatic cell death rather than being a cause of pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in acute pancreatitis.

Acute Disease↗
PubMed1996

Serous cystadenocarcinoma of the pancreas.

The mucinous type of cystadenoma of the pancreas is known to have malignant potential, whereas the serous type is believed to be benign. Therefore, the therapeutic strategies for serous cystadenomas are less aggressive than in mucinous cystadenoma, where complete operative resection is the procedure of choice. A patient with a biopsy-proven serous cystadenocarcinoma with a lymph node metastasis is reported. Considering the reported case and a review of the literature, the origin of serous cystadenocarcinoma appears to be from cystadenoma lesions. Even if this development of cystadenocarcinoma in pre-existing serous cystadenoma lesions is a rare entity, a less aggressive treatment of this lesion should be avoided in favor of resection procedures because of the good chance of cure.

Aged↗
PubMed1996

[Solid pseudopapillary tumors of the pancreas].

We report on three female patients with solid pseudopapillary tumors of the pancreas. The histogenetic origin of this entity is still unclear. The tumor, usually occurring in young women, forms large masses (up to 10 cm in diameter) before becoming symptomatic. Metastases have very rarely been reported. In contrast to other pancreatic tumors, the main pancreatic duct was displaced, but of normal caliber without stenosis, in all our patients. Despite the large size of the tumors, they were curatively resected in all three cases. Two of the tumors infiltrated the parenchyma or adipose tissue of the pancreas but did not spread into the lymph nodes or other organs. All of the patients are alive and without signs of tumor recurrence up to 8 years after surgical resection.

Adult↗
PubMed1996

[Pancreatic carcinoma in chronic pancreatitis with inflammatory tumor of the head of the pancreas].

Whether chronic pancreatitis is a risk factor for the development of pancreatic cancer is still under discussion. 395 patients operated for chronic pancreatitis with enlargement of the head of the pancreas between 1982 and 1994 were evaluated retrospectively. The frequency of pancreatic cancer in pre-existing chronic pancreatitis was 3.8% (n = 15). This frequency was significantly elevated in comparison to the estimated cancer frequency of the normal population (p < 0.001). The time interval between first diagnosis of chronic pancreatitis and diagnosis of pancreatic carcinoma was 33.3 month in the mean. 474 patients with pancreatic carcinoma without pre-existing chronic pancreatitis were operated in the same period. Histological examination revealed signs of chronic obstructive pancreatitis due to tumor obstruction of the main pancreatic duct in 11.1% (n = 53). The relative risk of patients suffering primarily from chronic pancreatitis to develop pancreatic carcinoma is elevated by a factor of more than 50 in comparison to normal population.

Adult↗
PubMed1996

Papillary cystic and solid tumor of the pancreas.

The papillary cystic and solid tumor of the pancrease (PCSTP) is a primary pancreatic neoplasm of unknown etiology occurring most commonly in young women and regularly containing hemorrhagic areas. Clinical symptoms are non-specific. Although these tumors reach an average diameter of 10 cm, they are often discovered by accident. Because patients with surgically resected PCSTP have very good prognoses, it is important to distinguish these tumors from other growths in the pancreas, for example mucinous cystadenoma. Whereas, due to the variable proportion of fluid components, these tumors offer non-characteristic structure at ultrasonography, computed tomography (CT) possesses high specificity for PCSTP, particularly when calcifications are present. Angiography distinguishes these tumors from hypervascular neoplasms, such as the endocrinologically inactive islet cell tumor. Magnetic resonance tomography (MRT) is especially suited for imaging the hemorrhagic areas in solid tumor formations, as well as hemorrhagic debris in the fluid portions and layer phenomena are frequently observed.

Adult↗
PubMed1996

[Duodenum preserving pancreatic head resection in chronic pancreatitis with inflammatory tumor in the pancreas head].

15 to 30% of the patients with chronic pancreatitis develop an inflammatory mass in the pancreatic head. The leading symptoms of these patients are severe upper abdominal pain and complications of the surrounding organs. From 1969 to 1995, 380 patients were treated with a duodenumpreserving pancreatic head resection. The cause of the disease was alcohol abuse in 81%. 93% of the patients suffered from severe pain with recurrent pain attacks. CT-scan revealed enlargement of the pancreatic head (> 4 cm in diameter) in 79% of the patients. 83% of the patients had an impaired exocrine pancreatic function; 48% of the patients had an impaired glucose tolerance or were diabetic. The hospital mortality was 0.8%; 5% of all patients had to be reoperated. The mean duration of the hospitalization was 13.9 days. 89% of the patients showed an unchanged endocrine function in the early postoperative course. The glucose metabolism was improved in 9%, 2% had a deteriorated function. The duodenum-preserving pancreatic head resection is a procedure with a low postoperative mortality and morbidity without deterioration of the endocrine pancreatic function.

Adolescent↗
PubMed1995

A method for in vivo assessment of reversible rat pancreatic ischemia using 31P NMR spectroscopy at 2.0 tesla.

A surgical method is described which allows in vivo assessment of reversible rat pancreatic ischemia using 31P NMR spectroscopy at 2.0 T. Phosphorous-31 NMR spectra acquired during the ischemic period show the expected increase in inorganic phosphate with a concomitant decrease in ATP levels and pH as compared to controls. Upon reperfusion, inorganic phosphate and ATP returned to control levels while pH recovered to a more alkaline value. This method provides a means of studying in vivo changes in high energy metabolite associated with acute pancreatitis (AP) and maintains the secretory ability of the gland so that different forms of AP, such as those arising from pancreatic juice edema, can be studied.

Adenosine Triphosphate↗
PubMed1992

Influence of ethanol on survival of acinar cells isolated from rat pancreas.

The role of ethanol in precipitating acute pancreatitis has been studied in model experiments. The influence of ethanol on the survival of isolated pancreatic acinar cells (PAC) and a possible coaction with noxious agents (such as trypsin, chymotrypsin, temporary anoxia, and partial uncoupling of the oxidative phosphorylation by 2,4-dinitrophenol [DNP]) has been investigated. Isolated PACs withstood ethanol levels up to 180 mM without significant decrease of viability within 4 h incubation at 37 degrees C. A 90-min deprivation of oxygen was widely tolerated also. However, with a combination of both ethanol application and oxygen deprivation, a clearly forced cell damage was observed as was true with a combination of ethanol and chymotrypsin. The action of DNP or of extracellular trypsin on cell survival was not amplified by the addition of ethanol (180 mM). This study reveals two possible sites of action at which ethanol may contribute to the pathogenesis of acute pancreatitis.

2,4-Dinitrophenol↗
PubMed1992

Effect of phospholipase A2 and ethanol on the survival of acinar cells isolated from the rat pancreas.

The study was undertaken to investigate the effect of phospholipase A2 (PLA2) on the viability of isolated pancreatic acinar cells (PACs) and its possible synergy with ethanol. The survival of PACs may be reduced by PLA2 in a dose-dependent manner. In the presence of 0.25 microgram PLA2.(10(6) cells)-1, all cells died within less than 4 h of incubation at 37 degrees C. A quantity of 180 mM ethanol, which alone was not lethal for PACs, increased the rate of cell death induced by PLA2 at a certain concentration of this enzyme. The present results imply that (1) PLA2 is able to damage PACs in the absence of additional substrates, and (2) at an appropriate activity of PLA2, ethanol may amplify the toxic effects of this lytic enzyme and force autodigestion of the pancreas.

Acute Disease↗
PubMed1991

Development of acute pancreatitis in rats after single ethanol administration and induction of a pancreatic juice edema.

The effect of an acute gastral ethanol application and an additional induction of a pancreatic juice edema by an obstruction/hyperstimulation mechanism was studied in rats. Neither ethanol administration nor the combination of ductal obstruction and secretory stimulation resulted in an acute pancreatitis when applied independently. A combination of these factors, however, led to the development of AP in two-thirds of the rats treated in this manner. Its severity was evaluated by the degree of extrapancreatic fat necrosis, the increase in serum amylase and lipase activities, and by histologic investigations. It is assumed that a pancreatic juice edema, provoked by pancreatic secretion at temporary ductal obstruction, could be an important cofactor in formation of ethanol-induced acute pancreatitis.

Acute Disease↗
PubMed1991

Transition of rat pancreatic juice edema into acute pancreatitis by single ethanol administration.

The present study was done to determine the influence of single oral, intravenous and intraperitoneal ethanol administration at pre-existing pancreatic juice edema on frequency and severity of acute pancreatitis (AP). The rats were divided into six control (isolated treatment) and five study groups (edema plus varied ethanol application). 24 h postoperatively quality and quantity of macroscopic and histopathologic changes were graded on an arbitrary scale. While in the controls AP was not induced in any rat, in the study groups extrapancreatic fat necrosis and histologic lesions of the pancreas were found in the majority of animals. The individual rats revealed a remarkable variation of the severity of changes. A detailed differentiation of pancreatic necroses revealed a dominance of intrapancreatic fat necrosis and acinar necrosis at the periphery of lobules. The findings observed were widely independent of the way of ethanol administration. The present approach offers a simple and reproducible animal model to study the influence of acute ethanol application on development of AP and hints on the involvement of disturbances of the pancreatic microcirculation and of acinar cell metabolism in the pathogenesis of ethanol-induced acute pancreatitis.

Acute Disease↗
PubMedDate not supplied

Experimental acute pancreatitis in rats after chronic and chronic plus acute ethanol administration in combination with a pancreatic juice edema.

The influence of long-term (26 weeks) and long-term plus acute ethanol administration on the development of acute pancreatitis was studied in rats. While both these treatments alone did not induce pancreatitis in any rat, extrapancreatic fat necrosis and histologic lesions of the pancreas were found in the majority of animal 24 hours after additional establishing of a pancreatic juice edema by an obstruction/hypersecretion mechanism. Severity and frequency of findings were significantly increased by additional short-term ischemia (25 min) of the pancreas. In control rats without ethanol ingestion, the edema receded without any lesions, and after additional ischemia significantly fewer rats exhibited signs of acute pancreatitis when compared to the ethanol-treated groups. An experimental model of acute alcoholic pancreatitis is presented with ethanol ingestion, temporary ductal obstruction and stimulation of secretion being essential constituents, which may be of clinical relevance, too.

Acute Disease↗