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Biomedical subjects

T E Ruud

Publications and source records attributed to T E Ruud.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effects of protease inhibitor pretreatment on hemodynamic performances and survival rate in experimental, acute pancreatitis.

Acute pancreatitis was induced in pigs by manual retrograde injection of Na-Taurocholate into the pancreatic duct. Using chromogenic peptide substrate assays, increased plasma kallikrein activity (KK), paralleled by a reduction in functional plasma kallikrein inhibition values (KKI) were found in the peritoneal exudate in untreated animals. Several of the untreated animals experienced an increased trypsin activity (TRY) in the same exudate. Five out of eight animals died during a 6 hour observation period. Pretreatment with either Cl-INH or aprotinin given intravenously, resulted in a significantly increase in KKI capacity paralleled by unchanged KK and TRY activities in the peritoneal exudate. Furthermore, inhibitor pretreatment significantly improved hemodynamic performances (AP and CO) and the survival rate. The study underlines the pathophysiological importance of trypsin and the plasma kallikrein-kinin system during acute, severe pancreatitis.

Acute Disease↗
PubMed1986

Effects on peritoneal proteolysis and hemodynamics of prophylactic and therapeutic infusions of high doses of aprotinin in experimental acute pancreatitis.

Acute pancreatitis was induced in pigs by retrograde injection of Na-taurocholate into the pancreatic duct. Chromogenic peptide substrate assays showed increased trypsin (TRY) and plasma kallikrein activity (KK), parallel with a reduction of plasma prekallikrein (PKK) and functional kallikrein inhibition (KKI) values, in the peritoneal exudate in untreated animals. Intravenous high-dose pretreatment or therapy with aprotinin starting 3 h after the induction of acute pancreatitis resulted in significantly increased KKI capacity and unchanged KK and TRY activities in the peritoneal exudate. In test animals receiving aprotinin intravenously a significantly increased survival rate and improved cardiac output and arterial blood pressure were found during the 6-h observation period. All animals treated with aprotinin survived the observation period, whereas 63% of the untreated animals died. The study emphasizes the pathophysiological importance of the plasma kallikrein-kinin system in acute pancreatitis.

Acute Disease↗
PubMed1986

Effects on peritoneal proteolysis and hemodynamics of prophylactic infusion with C1 inhibitor in experimental acute pancreatitis.

Acute pancreatitis was induced in pigs by manual retrograde injection of Na-taurocholate into the pancreatic duct. Chromogenic peptide substrate assays showed increased trypsin (TRY) and plasma kallikrein activities (KK), parallel with a reduction of prekallikrein (PKK) levels and functional plasma kallikrein inhibition (KKI), in the peritoneal exudate in untreated animals. Pretreatment with C1 inhibitor (C1 INH) concentrate significantly increased the KKI capacity, parallel with unchanged KK and TRY activities in the peritoneal exudate. Furthermore, C1 INH pretreatment significantly improved the hemodynamic performance and the survival rate during a 6-h observation period. The study underlines the pathophysiological importance of trypsin and the plasma kallikrein-kinin system during acute pancreatitis. C1 INH concentrates given intravenously prevent activation of this system locally in the peritoneal exudate during experimental acute pancreatitis.

Acute Disease↗
PubMed1986

Haemodynamic effects of intravenous injection of peritoneal exudate in experimental acute pancreatitis.

The haemodynamic effects of intravenous injection into the test animals themselves of peritoneal exudate obtained during experimental acute pancreatitis in pigs were studied. The exudate had a distinct but moderate vasodilating effect when injected into the test animal. This decrease in afterload and a slight compensatory increase in heart rate led to a small increase in cardiac output. The profound hypotensive effect of intravenous injection of peritoneal pancreatic exudate observed by others when injecting the exudate into healthy animals could not be reproduced. In an organism severely affected by pancreatitis, the added pharmacological insult of peritoneal exudate intravenously seems to be of little haemodynamic consequence. Some of the effects previously reported may be caused by trypsin added to the fluid injected intraductally to produce the ailment.

Acute Disease↗
PubMed1986

Effects on peritoneal proteolysis and hemodynamics by high doses of methyl-prednisolone in experimental acute pancreatitis.

Acute pancreatitis was induced in 15 anesthetized pigs by injection of Na-taurocholate into the pancreatic duct. Seven animals were pretreated with methyl-prednisolone sodium succinate 30 mg/kg intravenously. Using chromogenic peptide substrate assays, values of trypsin (TRY), plasma prekallikrein (PKK), plasma kallikrein (KK) and functional plasma kallikrein inhibition capacity (KKI) were studied in the peritoneal exudate. Cardiac output (CO) and arterial pressure (AP) were regularly monitored before and during a six hour observation period. In acute untreated pancreatitis a 40% reduction of PKK levels was found paralleled by an increased KK activity and a reduction of KKI capacity. High TRY levels were found in several animals. The mortality rate was 63%. The pretreated animals all survived. CO and AP were significantly less reduced than in the untreated animals. Components of the plasma kallikrein-kinin system and TRY in the exudate remained mainly unchanged. Methyl-prednisolone given as pretreatment significantly improves hemodynamic parameters and increases the survival rate. Methyl-prednisolone suppresses generation of trypsin activity and activation of the plasma kallikrein-kinin system in the peritoneal exudate which may be of significant importance to the outcome.

Acute Disease↗
PubMed1986

Evaluation of patients with acute pancreatitis by means of chromogenic peptide substrate assays and the proenzyme functional inhibition index.

Using chromogenic peptide substrate assays the severity and clinical course were evaluated in 37 patients with acute pancreatitis. Retrospective clinical evaluation revealed that 20 patients had a severe disease, whereas 17 patients had mild acute pancreatitis. Seven of the patients with severe acute pancreatitis died. The proenzyme functional inhibition index (PFI index) is defined as the sum of deviations from the normal plasma pool values of plasma prekallikrein, functional kallikrein inhibition, plasminogen, antiplasmin, prothrombin and antithrombin III. Increased values are counted as positive, whereas reductions compared with the normal plasma pool values are recognized as negative. During the second day after admission the PFI index revealed significantly more negative values in severe cases than in patients with mild acute pancreatitis, -159 in severe case, -74 in mild cases (median values, P less than 0.05). The PFI index values were maintained strongly negative for the following 3 days in severe cases whereas the index was brought to positive values during the same period in patients with mild acute pancreatitis. The fatal cases revealed strongly negative PFI index values for the whole observation period. The patients with severe acute pancreatitis were earlier identified by means of the PFI index than by individual parameters also used for calculating the index. The results show that by means of the PFI index severity of acute pancreatitis can be recognized during early stages of the disease.

Acute Disease↗
PubMed1985

Studies on the plasma kallikrein-kinin system in peritoneal exudate and plasma during experimental acute pancreatitis in pigs.

Acute pancreatitis was induced in pigs by retrograde injection of Na-taurocholate into the pancreatic duct. By means of chromogenic peptide substrate assays, increased plasma kallikrein activity, parallel with a reduction of plasma prekallikrein and functional kallikrein inhibition values, was found in peritoneal exudate. In plasma, however, no changes in the kallikrein-kinin system were found during the 6-h observation time. The study demonstrates the presence of components of the plasma kallikrein-kinin system in peritoneal fluid and suggests that the peritoneal cavity to a great extent is a functionally separate compartment from plasma. Activation of the plasma kallikrein-kinin system in peritoneal exudate during acute experimental pancreatitis appears to be of importance for the initial symptoms and the development of shock seen during this condition.

Acute Disease↗
PubMed1985

Modulation of the proteolytic cascade systems by high dose corticosteroids.

The effects of high-dose corticosteroids (HDC) on activities within the proteolytic cascade systems were studied in vitro and in vivo using chromogenic peptide substrate assays. In in vitro experiments 20 mg methylprednisolone sodium succinate (Solu-Medrol) per ml plasma significantly inhibited activation of plasma prekallikrein, prothrombin and plasminogen and reduced functional plasma kallikrein inhibition, antithrombin and antiplasmin activities. The effects of HDC on activities within these proteolytic cascade systems were further evaluated in experimental acute pancreatitis in pigs. Acute pancreatitis was induced by injection of Na-taurocholate into the pancreatic duct. Seven test animals received methylprednisolone sodium succinate 30 mg per kg intravenously for 30 minutes before the induction of pancreatitis as pretreatment. Eight animals remained untreated. Trypsin (TRY), plasma prekallikrein (PKK), plasma kallikrein (KK) and functional plasma kallikrein inhibition capacity (KKI) were studied in the peritoneal exudate. Cardiac output (CO) and mean arterial pressure (MAP) were monitored regularly before and during a 6 hour observation period. During untreated pancreatitis a reduction of PKK levels of about 40% were found, paralleled by an increased KK activity and a reduction of KKI capacity. Several of the animals experienced high TRY activities. The mortality rate was 63% (5 out of 8 animals). In the pretreated groups, all animals survived the observation period. CO and MAP were significantly less reduced than the untreated group at 6 hours. HDC was also found to reduce significantly plasma kallikrein activities in the peritoneal exudate compared with untreated animals. No changes in TRY activities were found in pretreated animals. Furthermore, plasma prekallikrein and functional plasma kallikrein inhibition values in the exudate were elevated significantly in HDC treated animals compared with untreated animals.

Animals↗
PubMed1984

Studies on the kallikrein-kinin system in plasma and peritoneal fluid during experimental pancreatitis.

Using chromogenic peptide substrate assay technique, components of the plasma kallikrein-kinin system and trypsin activity were studied in plasma and peritoneal exudate during acute pancreatitis in pigs. In the plasma no significant changes occurred, but increased kallikrein activity was found in the peritoneal exudate. This finding was paralleled by a reduction in prekallikrein levels and functional kallikrein inhibition values. The trypsin activity in peritoneal exudate, however, increased inconstantly. These results emphasize the significance of peritoneal protease-antiprotease imbalance during acute pancreatitis.

Acute Disease↗
PubMed1984

Heparin treatment of deep venous thrombosis in 280 patients: symptoms related to dosage.

280 patients with phlebographically proven deep venous thrombosis received intravenous heparin infusion, mean duration 6.8 days, mean dose 370 U/kg/day. In 58 patients (21%) there was no apparent predisposing factor. Leg pain diminished more rapidly than edema. At discharge, 46% had edema. Symptoms suggesting pulmonary embolism (PE) occurred in 13 patients (4.6%) whose mean daily heparin dose was similar to that of the others. The only fatal PE occurred three days after cessation of heparin administration. Eight patients (3%) experienced major bleeding, the only fatal occurring after thoracocentesis. The frequency of major bleeding in patients above 70 years was 8% in females and 4% in males, in those below 70 years it was 0.5%; 22 patients (8%) had minor bleeding. Control phlebography after one week revealed completely cleared thrombus in 3%, partial clearance in 36%, unchanged in 39% and increased thrombosis in 22%. Dosage was significantly correlated to thrombus resolution.

Adult↗
PubMed1984

Bacterial shock due to transfusion with Yersinia enterocolitica infected blood.

A fatal case (a 55-yr-old man) of bacterial shock and sepsis following a transfusion with erythrocytes infected with Yersinia enterocolitica serotype 03, is reported. The blood donor had slight diarrhea 6 days before the blood donation. A serum sample from the donor showed high titre of both IgG and IgM antibodies against Y. enterocolitica 03, indicating a recent infection. Y. enterocolitica 03 was isolated from blood cultures from the patient. The remaining portion of the transfused erythrocyte concentrate also yielded abundant growth of the same organism on direct plating of the material on blood agar indicating that profuse multiplication of the organism had occurred within the transfusion bag during storage at 4 degrees C.

Blood Donors↗
PubMed1982

Studies on pathological plasma proteolysis in patients with acute pancreatitis. A preliminary report.

Changes in the plasma proteolytic enzyme systems were studied in 14 patients with acute pancreatitis. Ten patients survived whereas four died. In both survivors and fatal cases a high frequency of reduced values of plasma prekallikrein (PKK) functional antithrombin III (AT III) and platelets were found during the first week after admission. These changes were seen together with increased serum FDP values and the presence of soluble fibrin. In the fatal cases PKK, AT III, platelets and functional kallikrein inhibition values observed during the first week after admission, were found significantly more reduced than in the survivors. These observations underline that activation of proteases in plasma is an important pathophysiological mechanism in this state, and that evaluation of this process in patients with acute pancreatitis might give information of prognostic value.

Acute Disease↗
PubMed1982

Chromogenic peptide substrate assays in patients with multiple trauma.

Daily monitoring of the plasma proteolytic enzyme systems i.e. the coagulation, the fibrinolytic and the kallikrein-kinin system in multitraumatized patients with chromogenic substrate assays disclosed significant differences in the levels of Prekallikrein, Hageman Factor, Antithrombin-III, Prothrombin in survivors (N = 9) and fatal cases (N = 6) during the first week after admission. Since chromogenic peptide substrate assays are simple, cheap and easily automated, close monitoring of critical care patients may be rewarding.

Adult↗
PubMed1982

Studies on components of the plasma kallikrein-kinin system in peritoneal fluid and plasma before and during experimental acute pancreatitis in pigs. A preliminary report.

Acute pancreatitis was induced in pigs by retrograde injection of Na-Taurocholate into the pancreatic duct. Using a chromogenic peptide substrate assay, increased plasma kallikrein activity was found in the peritoneal exudate. This finding was paralleled by reduced prekallikrein and functional kallikrein inhibition values. In plasma, however, no changes in the kallikrein-kinin system were found during the 6 hours observation time. These findings emphasize the significance of peritoneal protease-antiprotease imbalance during acute pancreatitis.

Acute Disease↗