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Biomedical subjects

M Heideman

Publications and source records attributed to M Heideman.

At least 37 records · Page 2Linked to original sources
PubMed1987

Complement and anaphylatoxin responses to cross-clamping of the aorta. Studies during general anaesthesia with or without extradural blockade.

Complement activation and anaphylatoxin formation were studied in 28 patients undergoing aortic reconstructive surgery under general anaesthesia. In 12 of the patients an extradural catheter was placed in the L1-2 space and 2% mepivacaine was injected until blockade reached the T4 level. The remaining 16 patients were operated upon under general anaesthesia alone. Complement activation was not obvious until aortic cross-clamping. The release of anaphylatoxin was less pronounced during cross-clamping in the extradural group.

Aged↗
PubMed1987

Anaphylatoxin release in association with methylmethacrylate fixation of hip prostheses.

In a prospective study, thirty patients in whom a Charnley hip prosthesis was implanted with cement (methylmethacrylate) and fifteen who received a prosthesis without cement were studied. The activation of complement, as indicated by the release of anaphylatoxins (C3a and C5a), reduced activity of whole complement, and decreased levels of C3, C4, and C5 in plasma, was evaluated. Activation of complement was found when methylmethacrylate was used. In patients in whom components were fixed without cement, no formation of anaphylatoxins occurred, and only slightly reduced whole-complement activity and concentrations of C3, C4, and C5 in plasma were found. A dose-correlated release of the anaphylatoxins was found when monomethylmethacrylate was incubated in fresh serum. One explanation for the hemodynamic instability in these patients might be the biological effects of anaphylatoxins that are released in association with fixation by cement.

Adult↗
PubMed1986

Early activation of humoral proteolytic systems in patients with multiple trauma.

Coagulation, fibrinolytic, kallikrein, and complement systems were studied in 20 patients with multiple trauma. Three of four patients with a trauma score less than 10 on hospital arrival died, compared to one of 16 with a score over 10. Five patients developed disseminated intravascular coagulation. Signs of activated cascade systems were evident in most patients on hospital arrival. Changes were not related to trauma score, but patients with an arterial pressure below 110 mm Hg had significantly lower levels of antithrombin III and alpha 2-antiplasmin than those with higher BP. This study confirms that the cascade systems are activated very soon after multiple trauma.

Adolescent↗
PubMed1986

Altered anaphylatoxin activity during induced hypoperfusion in acute and elective abdominal aortic surgery.

Fifty patients operated on for abdominal aortic aneurysms, ten acutely for ruptured aneurysms and 40 electively, were studied. The anaphylatoxins (C3a and C5a) and the activity of their inhibitor were determined preoperatively, regularly per-, and postoperatively. Increased anaphylatoxin activity was accompanied by altered airway pressure, central hemodynamics, and pulmonary, hepatic, and renal functions. During aortic clamping the anaphylatoxins increased and the activity of their inhibitor decreased. During the clamping period airway pressure, pulmonary artery pressure, and pulmonary vascular resistance increased. These respiratory and hemodynamic changes might partly be explained as biologic effects of anaphylatoxins. The plasma C3a increase correlated with the duration of aortic clamping. Patients with prolonged anaphylatoxin increase were prone to develop multisystem organ failure. Anaphylatoxins released during induced hypoperfusion could be one of the factors influencing respiratory and hemodynamic changes in patients operated on for aortic abdominal aneurysms.

Adult↗
PubMed1985

Immunological interference of high dose corticosteroids.

High-dose corticosteroids (HDC) will influence cellular as well as humoral participants of the immune response. The lymphoid tissue will decrease in size and weight after prolonged treatment with HDC. Lymphocyte functions will be impaired. Reduced synthesis of B- as well as T-lymphocytes will be seen. The inhibitory effect on B-cell function can be observed both as decreased serum levels of immunoglobulins and as impaired binding of antibodies and complement to the cellular surface. Reduced T-cell function indicated by impaired stimulation by PHA and porkweed as well as by impaired lymphokinin effects on leukocyte migration inhibition has been reported. Reduced lymphocyte adherence to antigen and suppressed lymphocyte reaction have also been observed. Humoral factors involved in chemotaxis, opsonisation, phagocytosis, vascular permeability leading to leakage of fluid and cells and factors involved in lysis of antigens are impaired. This can be explained partly by the observed reduced complement activation via the alternative as well as the classical pathway in association with HDC therapy. Acute processes with increased vascular permeability and accumulation of leukocytes as impairing factors could be influenced beneficially by HDC therapy. This positive effect can be seen in treatment of septic shock or rejection of a transplant. However, if sepsis or rejection is not rapidly reversed, complications such as multisystem organ failure and bacteremia are prone to appear.

Adrenal Cortex Hormones↗
PubMed1984

Anaphylatoxin generation in multisystem organ failure.

Complement components were studied in 44 patients with extensive injuries or infections. The concentrations of anaphylatoxins (C4a, C3a, and C5a) and other complement components (C1INH, C4, C3, and C5) were determined in plasma using radioimmunoassay and rocket immunoelectrophoresis techniques. The results were correlated with the development of multisystem organ failure (MSOF). In particular, plasma concentrations of C3a and C4a were found elevated in trauma patients. These elevated anaphylatoxin levels were correlated with severity of the injury. As reported in other types of patients, the apparent C5a plasma levels were not elevated. Therapy reduced the plasma levels of C3a with great predictability. It appears that plasma C3a and C4a levels may relate not only to severity of the injury but may signal onset of secondary events such as bacteremia. Consequently, longitudinal monitoring of anaphylatoxin levels may prove helpful in diagnosing the status of trauma patients.

Adolescent↗
PubMed1982

Effect of nonviable tissue and abscesses on complement depletion and the development of bacteremia.

Complement concentrations and blood cultures were compared in 58 patients within 24 hours of injury and weekly thereafter. Extensive amounts of nonviable tissue (n = 40) were associated with a mean depletion of C4, C3, and C5 by 56%, and minor injuries (n = 18) by 22% of normal concentration within 14 hours after injury. The C4, C3, and C5 concentrations returned to normal or above within a week after minor injuries, but not following major injuries. However, C4, c3, and C5 levels remained depressed after major injuries unless necrotic tissue was removed or abscesses were drained. If complement concentration was below 50% of normal for more than a week all patients developed bacteremia. Following debridement or drainage complement returned to normal in 11 patients and blood cultures became negative in seven. Possible consequences by activation and altered availability of complement for chemotaxis, opsonization, and lysis of bacteria have been analyzed and related to the development of bacteremia.

Abscess↗
PubMed1982

A shared effect of abscesses and nonviable tissue influencing the development of sepsis and acute respiratory distress syndrome.

The influence of extensive accumulation of pus (n=20) or nonviable tissue (n=50) on complement has been studied. Plasma concentrations of C1 esterase inhibitor, C4, C3 and C5 were determined by electroimmunodiffusion technique. A good correlation between the extent of complement depletion and the amount of nonviable tissue or pus present was found. A prolonged state with reduced plasma concentrations of complement was in high frequency followed by the development of bacteremia. Patients with ongoing extensive complement activation were prone to develop ARDS. The relation between a depleted complement system and the development of bacteremia has been analysed and so has a relation between impaired oxygenation of arterial blood and products formed when complement is activated.

Abscess↗
PubMed1980

Septic shock.

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Animals↗
PubMed1980

The cascade systems in posttraumatic pulmonary insufficiency.

The cascade systems - the coagulation, fibrinolytic, kallikrein-kinin and complement systems - are all activated after trauma. These systems are involved in the post-traumatic pulmonary reaction. The complexity with which all the systems are intimately related is stressed. The specific role of the different systems in the development of post-traumatic pulmonary insufficiency remains to be evaluated.

Blood Coagulation↗
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↗