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Biomedical subjects

M Heideman

Publications and source records attributed to M Heideman.

At least 19 recordsLinked to original sources
PubMed1991

Activation of the complement cascade by trypsin.

In twenty-three patients with acute pancreatitis, the plasma levels of immunoreactive trypsin were determined with a RIA method. The patients were divided into groups according to the severity of the disease. Ranson's criteria and the development of multisystem organ failure were used for the classification. Elevated plasma levels of immunoreactive trypsin were found in all groups after admittance. Incubation of fresh human serum and plasma with bovine trypsin in concentrations between 10(-6) and 10(-4) M at 20 degrees C activated the complement cascade. The anaphylatoxins C3a and C5a were determined with a RIA and the terminal complement complex (TCC) with an ELISA method. C3a and C5a were released and TCC was formed. The effect of trypsin on leukocyte activation was determined with a chemiluminescence technique. Trypsin dissolved in saline did not activate the leukocytes. However, serum digested by trypsin-activated leukocytes in a dose-dependent manner. The present study supports the theory that trypsin can activate complement components and results in formation of split products which have potent vascular, and leukocyte activating effects.

Acute Disease↗
PubMed1990

Trypsin-induced vascular permeability and leukocyte accumulation in hamster cheek pouch: the role of complement activation.

Trypsin-induced acute inflammation was studied in hamster cheek pouch using intravital microscopy, correlative histology, and electron microscopy. Vascular permeability changes were monitored with intravital fluoroscopy, after intravenous injection of FITC-dextran (Mw 150,000), by counting the number of FITC-dextran leakages around the vessels. The number of extravasated polymorphonuclear leukocytes (PMNLs) was calculated by a histological technique. A dose-dependent increase in the number of FITC-dextran leakages, as well as the number of accumulated PMNLs, was found when trypsin was locally deposited in concentrations of 0.25-2.5 microM (15 microliters during 5 min). Local deposition of autologous serum treated with trypsin at final concentrations of 0.25-2.5 microM caused an increase in vascular permeability as equally pronounced as that of pure trypsin, but only a moderate PMNL accumulation which was not dose dependent. Trypsin at a 25 microM concentration resulted in numerous microbleedings and cessation of flow. The electron microscopy demonstrated inflammatory events (PMNL adhesion, diapedesis, and interstitial infiltration) in all treatment groups but they were more pronounced after trypsin exposure. Trypsin did not cause disintegration, cellular lysis, or increased mast cell degranulation. The permeability changes induced by trypsin (2.5 microM) and trypsinated serum (2.5 microM) were significantly suppressed by the addition of the chelating agent potassium-EDTA to the reaction mixture, indicating a calcium- or magnesium-dependent mechanism. Pretreatment of the animals with cobra venom factor (CVF), by which the plasma C3 concentration was reduced to less than 10%, inhibited the vascular leakages almost completely. The trypsin-induced accumulation of PMNLs was significantly reduced by potassium-EDTA as well as by pretreatment with CVF (P less than 0.01). These findings indicate a central role of complement activation in trypsin-induced acute inflammation in the hamster cheek pouch.

Animals↗
PubMed1990

Complement activation and reinfusion of wound drainage blood.

Eighteen patients undergoing total hip replacement (n = 13) or knee arthroplasty (n = 5) due to osteoarthritis or osteoarthrosis were prospectively studied in an investigation of complement activation and anaphylatoxin release in association with reinfusion of aspirated wound blood. Twelve of the patients needed blood transfusions and received an average of 390 +/- 75 ml (+/- SD) of autologous blood within 45 min. Plasma complement components, anaphylatoxins, and inhibitors were studied 1 min before and 15 min after the start of and 15 min after the completion of autologous transfusion. Samples also were taken from the collected blood, before and after passing it through a microporous filter. Blood gases and systemic complement samples were drawn simultaneously. There were no significant changes in systemic complement variables before, during, or after transfusion of autologous blood. However, in the aspirated blood, increased concentration of anaphylatoxins (C3a and C5a) and terminal complement complexes (TCC) were present (P less than 0.001). There were no differences observed between samples drawn before and after filtration of the blood. The concentration of C5 was less in the collected blood than in the systemic blood (P less than 0.05). No changes in blood gases were observed. This study demonstrated that postoperatively salvaged whole blood underwent anaphylatoxin formation and complement activation. However, after reinfusion of this blood, neither systemic complement activation nor clinical complications were observed.

Adult↗
PubMed1990

Accumulation of anaphylatoxins and terminal complement complexes in inflammatory fluids.

The presence of anaphylatoxins (C3a and C5a) and terminal complement complexes (TCC) in different inflammatory fluids and plasma was studied in 33 patients. Anaphylatoxins were assayed using a radioimmunoassay technique, and the terminal complement complexes were determined by an ELISA method. Patients with peritoneal (n = 14), pleural (n = 7), pericardial (n = 6) or burn bullae fluid (n = 6) were studied. High C3a and TCC concentrations were found in all these fluids. Elevated C3a and TCC concentrations in inflammatory fluids were found not only in patients with elevated plasma C3a and TCC concentrations, but also in patients with normal plasma levels. No increases in C5a concentration were observed in pleural or burn bullae fluid. In one patient with pericarditis, and in subjects with acute pancreatitis with ascites, high C5a levels were found in the fluid. However, the high TCC concentration in the fluids suggests that C5a had been formed but was probably removed by leucocytes present in the fluid.

Acute Disease↗
PubMed1989

Anaphylatoxin generation in acute pancreatitis.

Fifty-one patients with elevated serum amylase and clinical signs of acute pancreatitis were studied prospectively. The concentrations of anaphylatoxins (C3a and C5a) were measured with a radioimmunoassay and the activity of their inactivator was determined. The pancreatitis was classified as mild, moderate, or severe according to Ranson's 11 signs, appearance of peritoneal fluid, and development of multisystem organ failure (MSOF). Plasma C3a and C5a concentrations were elevated during attacks of acute pancreatitis. Anaphylatoxin levels correlated with the severity of the disease (C3a, P less than 0.001; C5a, P less than 0.05). The highest and most persistent levels were found in the group with MSOF. C3a levels decreased rapidly during recovery. In patients with complications like abscess or pseudocyst, the C3a elevation persisted until adequate treatment was instituted. In this study, no significant changes of the inactivator levels were found, except at discharge when the inactivator level of the severe group was elevated compared to that of the moderate and mild groups (P less than 0.05).

Acute Disease↗
PubMed1989

Altered concentrations of terminal complement complexes, anaphylatoxins, and leukotrienes in the coronary sinus during cardiopulmonary bypass.

The aim of this study was to determine if the hypoperfused heart activates complement with formation of anaphylatoxins, terminal complement complexes (TCC), or leukotrienes during cardiopulmonary bypass. Fifteen patients undergoing elective cardiopulmonary bypass surgery were studied regarding complement and leukotriene activation. Blood samples were drawn serially from the radial artery and coronary sinus. The plasma concentrations of the complement components C1INH, C3, C4, and C5 decreased during the procedure, whereas C3a and TCC increased. Protamine reversal of heparin further increased the plasma levels of C3a and TCC. No significant changes in plasma levels of C5a and leukotriene C4 were observed during cardiopulmonary bypass. The activity of the anaphylatoxin inactivator (AI) decreased in both the radial artery and the coronary sinus. There were no significant differences between the concentrations of complement components and leukotriene C4 in blood from the radial artery and coronary sinus. The levels of C3a and TCC increased and C1INH, C3, C4, C5, and the anaphylatoxin inactivator activity decreased to the same extent in the coronary sinus and the radial artery. Thus, the heart does not appear to be the primary site for the altered concentrations of these endogenous vasoactive substances.

Aged↗
PubMed1989

Complement activation and anaphylatoxin (C3a and C5a) formation in preeclampsia and by amniotic fluid.

The aim of this study was to determine whether the biologically active complement peptides C3a and C5a are formed in pregnancy and whether amniotic fluid can activate complement. C3a and C5a are formed when complement is activated. They increase smooth-muscle contraction, vascular permeability, and histamine release from mast cells and basophils. Thirty pregnant women were studied, 16 with uncomplicated and 14 with preeclamptic pregnancies. The plasma C3a and C5a concentrations before delivery were significantly higher in the preeclamptic than in the normal group. The concentrations returned to normal within 1 week. Plasma, serum, and amniotic fluid from 12 pregnant women (eight uncomplicated and four preeclamptic pregnancies) were drawn in connection with delivery. Amniotic fluid was incubated in fresh autologous serum at 37C for 15 minutes. A dose-dependent formation of C3a and C5a was registered with increasing amounts of amniotic fluid.

Adult↗
PubMed1979

The effect of thermal injury on hemodynamic, respiratory, and hematologic variables in relation to complement activation.

The effects of thermal injury on circulation, respiration, and complement activity was studied in dogs. An aggregation of platelets in the blood and trapping in the lung were observed following burn injury. Leukopenia appeared first, then leukocytosis. Hemolysis of red cells corresponding to a destruction of about 30% of the erythrocytes was observed. A blood pressure decrease and a tracheal insufflation pressure increase followed thermal injury. Blood gas and lactate changes like those seen during a low perfusion state were recorded, but signs of impaired oxygenation of arterial blood were also observed. A possible mechanism by which denatured proteins might initiate some of the symptoms seen after thermal injury is suggested and its relation to complement activation is evaluated.

Animals↗
PubMed1979

The general and local response to injury related to complement activation.

Injury can activate the complement system as well in vivo as in vitro. This activation might contribute to some of the phenomena seen after large injuries. Such general effects as fall in blood pressure, impaired ability to oxygenate blood and local effects such as accumulation of granulocytes and oedema formation might be influenced by complement activity. The in vitro experiments indicated an alternative pathway activation of whole complement by injured tissue or endotoxin.

Animals↗
PubMed1978

Complement activation and hematologic, hemodynamic, and respiratory reactions early after soft-tissue injury.

The effect of soft-tissue trauma was studied in dogs. Following injuries to the hind leg an aggregation of thrombocytes in blood and trapping in the lung was noted. Injury was initially followed by leukopenia and later by leukocytosis. Early hemolysis of red cells was observed. The injury was accompanied by complement activation. Its possible relation to hemolysis, leukopenia, thrombocytopenia, and increased insufflation pressure is discussed.

Animals↗
PubMed1977

Surgical management of gastroduodenal haemorrhage.

We have presented a retrospective study of the surgical management of 299 patients bleeding from duodenal ulcer, gastric ulcer or gastritis. The overall mortality rate was 15%-5% for elective and 25% for emergency operations. The mortality increased with age and reached 50% for emergency operations in patients over the age of 70. Patients with low admission haemoglobin values, who had episodes of hypovolemic shock or who required immediate transfusions were also at risk. A Billroth I gastric resection proved to be the safest operative procedure. Based on our results, we are supporting a program calculated to reduce the mortality attending gastroduodenal bleeding, especially in those patients requiring an emergency operation. The basic principles of this program are constant observation, prompt diagnosis and early surgical intervention.

Blood Transfusion↗
PubMed1976

The risk of renal allograft rejection following angiography.

In a retrospective study of 173 immediately functioning primary kidney transplants, correlation between agiography and renal allograft rejection was studied during the first 14 days. It was found that rejection was more frequent in kidneys undergoing angiography than in those not undergoing angiography. It was also found that in kidneys undergoing angiography an overwhelming number of the rejections started the day after angiography. These differences in rejection frequency could not be explained by differences in HLA matching or the origin of the kidneys. These findings suggest a possible connection indicating that the angiography might elicit an acute rejection episode. A possible mechanism for starting this reaction might be activation of the complement system which was found in 50% of the patients undergoing angiography in peripheral blood and in 100% when studied in vitro.

Angiography↗