The enzymatic studies of the liver in acute experimental pancreatitis in dogs treated with prostacyclin (PGI2).

The liver affection in acute experimental pancreatitis (AEP) could be reflected by changes of enzymatic activity in the liver and in serum. The histoenzymatic studies of the liver of dogs with AEP of different severity and time of duration induced according to Elliott's method were performed and the constellation of serum enzymatic activities considering treatment with prostacyclin was estimated. The histoenzymatic reactions on succinic dehydrogenase, lactic dehydrogenase and alkaline phosphatase were depressed with progression of time and severity of AEP. In contrast, the reaction on acid phosphatase was augmented at the same time. Serum AspAT, AlAT and alkaline phosphatase were augmented in the later phase of AEP, but acid phosphatase and beta-glucuronidase were not significantly changed. The treatment with PGI2 limited both histoenzymatic reactions and alterations of serum enzymatic activities. These results support the significance of changes in enzymatic activities in the course of liver reaction on pancreatogenic noxa during acute pancreatitis, and suggest the protective effect of PGI2 against liver injury in this disease.

The lung lysosomal hydrolases and phospholipase A in acute experimental pancreatitis with reference to heparin treatment.

The pulmonary complications are severe sequeles of acute pancreatitis. The pathogenesis of these complications is unsolved. The purpose of this work was to evaluate the status of lung lysosomes and phospholipase A activity in acute experimental pancreatitis (AEP) and the effect of heparin as a potentially protective agent. Taurocholate-induced AEP in rats lasting 24 and 48 hours was treated with heparin intraperitoneally (2 mg/kg every 8 hours). The total activity of cathepsins and B-glucuronidase in lysosomal enriched subfraction increased markedly during 48 hours of AEP in untreated animals, but the relative free activity was maximal after 24 hours. Free activity of cathepsins and acid phosphatase in supernatant was maximal after 24 hours. The phospholipase A activity was maximally elevated (more than twofold) after 48 hours. Heparin prevented the increase of activity of B-glucuronidase, depressed the relative free activity of all investigated lysosomal hydrolases and inhibited the phospholipase A activity in the lung homogenate. Our results indicate the significance of labilization of lung lysosomes and increment of phospholipase A activity in the lungs in the damage of this organ during AEP in the rats, and suggest the beneficial effect of heparin on these factors.

Fibrin stabilization, factor XIII transamidase activity and subunits "A" and "B" concentration in plasma of patients with liver cirrhosis.

The parameters found in the last phase of blood clotting were measured in patients with liver cirrhosis against a background of some coagulation and fibrinolysis tests. The significant decrease of the fibrin stabilizing activity of plasma and the fall of plasma free -SH groups concentration were documented in the patients. It was accompanied by impaired whole blood clot elasticity in the thrombelastogram. Cirrhotic patients also revealed diminished factor XIII transamidase activity as well as decreased concentrations of its subunits "A" and "B". The data emphasize the necessity of factor XIII substitution and -SH groups supplement in patients with liver cirrhosis.

The renal lysosomes in acute experimental pancreatitis in dogs treated with prostacyclin (PGI2).

The inflammatory process in pancreas affects the function and structure of kidneys both by enzymatic toxemia and impairment of the renal circulation. In this study the stability of renal lysosomes in AEP in dogs treated with cytoprotective agent PGI2 was investigated. AEP was induced by injection of the bile and trypsin into the pancreatic duct; experiments were terminated after 12 hours. In lysosomal enriched subfraction of the kidney cortex (sedimenting in 15 000 x g) in untreated group (N = 5) relative free activity (r.f.a.) of cathepsins (Cs), acid phosphatase (APh) and beta-glucuronidase (BG) increased to 51,67 and 62% respectively, whereas in healthy dogs (N = 6) these activities were 20,38 and 25%. In dogs (N = 6) treated with PGI2 at the dose of 20 ng/kg/min. during 12 hrs, the r.f.a. of Cs, APh and BG was 18,40 and 49%, whereas in dogs (N = 5) additionally pretreated during 1 hr before induction of AEP with the same dose of PGI2, its values achieved 19,40 and 47% respectively. Our results suggest the stabilizing effect of PGI2 on kidney lysosomes damaged in acute experimental pancreatitis in dog. As possible mechanisms of prostacyclin action are discussed: limitation of necrotic process in the pancreas; improvement of renal haemodynamics; direct cytoprotective effect on the kidney.

Prostacyclin (PGI2) stabilises hepatic lysosomes during acute experimental pancreatitis in dogs.

In 15 mongrel dogs acute experimental pancreatitis (AEP) was induced by injection of bile and trypsin into the pancreatic duct. After 12 hrs in lysosomal enriched subfraction of the liver in untreated group (N = 5) relative free activity of cathepsins (Cs), acid phosphatase (AP) and beta-glucuronidase (beta G) increased to 50,62, and 53% respectively in comparison to the healthy dogs (N = 6) : 19,43 and 20%. In dogs with AEP treated with prostacyclin (PGI2) in the dose of 20 ng/kg X min for 12 hrs these activities of Cs, AP and beta G were lowered to 30,55 and 41% in comparison with the untreated group. In dogs with AEP (N = 5) additionally pretreated during 1 hr before the induction of AEP with the same rate of PGI2 i.v. infusion, the relative free activity of enzymes was similar to the treated group. After two hrs incubation of lysosomal enriched subfraction in acidic medium (pH = 5,0), the highest values of relative free activity were observed in untreated group, the difference being more pronounced in comparison with control group than before incubation. In those animals treated and pretreated with PGI2, postincubation activities were much lower than in untreated dogs. These results suggest the stabilising effect of PGI2 on hepatic lysosomes, damaged during the course of AEP in dogs.

Effect of acute cold exposure on the mobilization of intramuscular glycogen and triglycerides in the rat.

Male Wistar rats, 300-360 g of body weight, were exposed to cold (1 degree) for 3 and 24 h. The levels of glycogen and triglycerides (TG) were estimated in "white" and "red" portions of the quadriceps muscle (FG and POG muscles respectively) in the soleus muscle (SO muscle), and in the heart muscle. It was found that 3 h cold exposure decreased significantly the glycogen level only in the heart muscle and had no effect in the other muscles examined. Exposure to cold for 24 h reduced the glycogen level in FG and FOG muscles, and lowered further the heart glycogen level. No change of glycogen level during cold exposure was observed in SO muscle. The level of TG in each examined muscle was significantly reduced already after 3 h of cold exposure. After 24 h it remained further unchanged in FG and FOG muscles whereas in SO and heart muscles a partial recovery of TG occurred. It is concluded that in warm-acclimatized rats the intramuscular TG play an important role as a local source of free fatty acids during the first period of acute exposure to cold.