Search PubMed⌕ Search

Biomedical subjects

M Gardinali

Publications and source records attributed to M Gardinali.

36 records · Page 2Linked to original sources
PubMed1990

Blood--artificial surface interactions during cardiopulmonary bypass. A comparative study of four oxygenators.

Evaluation of the biocompatibility of four different types of oxygenator (bubble, membrane, hollow fibre and 'hybrid') was performed on 26 patients undergoing cardiopulmonary bypass during elective coronary surgery. More platelet derangement and an increased degree of hemolysis, revealed by higher plasmatic concentration of beta-thromboglobulin, platelet factor 4 and plasmatic free hemoglobin (p less than 0.05), was seen when using the bubble oxygenator. Damage to blood cells was minimal with the membrane oxygenator while the 'hybrid' and the hollow fibre oxygenators proved to rank at an intermediate level. Complement activation at the beginning of the cardiopulmonary bypass occurred via the alternative pathway as demonstrated by C3ades arg increase (up to nine times) without a concomitant elevation of C4ades arg. Cardiopulmonary bypass complement activation was quantitatively similar with all the oxygenators. A further activation via the classical pathway occurred in all the patients after protamine injection. Consistent differences as far as clinical and biological effects exist among the various commercially available cardiopulmonary bypass apparatus; our study provides guidelines for the evaluation and selection of devices which might reduce postoperative sequelae.

Anaphylatoxins↗
PubMed1989

Complement activation during hemodialysis.

Hemodialysis, as other extracorporeal circulation treatments, determines activation of the complement system. In this paper molecular mechanism of complement activation by different hemodialysis membranes are reviewed as well as the biological consequences and clinical relevance of the activation.

Anaphylatoxins↗
PubMed1987

Complement activation and membrane lipids in lung vascular injury.

Intravascular complement activation induces a rapid neutropenia and transient hypotension in laboratory animals such as rabbits. Injection of purified C5a causes similar hemodynamic events, and the hematologic changes suggest involvement of components such as polymorphonuclear leukocyte (PMN) and mediators including vasoamines and prostanoids. The anaphylatoxin-induced hypotension coincided with an increase in central venous pressure (CVP), decreased cardiac output (CO), increased plasma prostanoid levels, and neutropenia. These phenomena were repeatable in the animals when C5a was administered as a bolus 45 min after the initial treatment. Animals pretreated with indomethacin failed to exhibit the hypotensive response to C5a but still exhibited the transient neutropenia. Indomethacin effectively eliminated prostanoid release into plasma as expected. Administration of H2, but not H1, histamine-receptor antagonists reduced both C5a-induced hypotension and prostanoid release, suggesting that histamine may contribute to the C5a response in rabbits. Animals rendered neutropenic with nitrogen mustard prior to C5a challenge respond normally to C5a infusion (i.e., elevated prostanoid release and hypotension). The mechanism that we proposed for C5a-induced hypotension requires vascular smooth muscle contraction to be predominant over peripheral vasodilation in affecting cardiac output. Neutropenia occurs as a parallel event to hypotension but seemingly has little influence on the hemodynamic response. Prostacyclin (PGI2) levels were elevated in C5a-treated animals, and this lipid mediator contributes to hypotension by enhancing peripheral vasodilation. Because plasma TGxB2, levels were also elevated and central venous pressure increased as cardiac output decreased in treatment animals, we concluded that thromboxane-dependent pulmonary vasoconstriction contributes significantly to the C5a hypotensive response.

Animals↗
PubMed1986

In vivo study of the complement system during infusion of radiographic contrast media.

It has been claimed that activation of the complement system may play a role in reaction to radiographic contrast media (RCM) infusion. In order to clarify the effects of RCM on the complement system, three different parameters (CH50, C3a, and C1 inhibitor) were measured in 20 patients undergoing intravenous pyelography for diagnostic purposes. We found no significant changes in C3a levels, but CH50 and C1 inhibitor fell significantly at the different sampling times; however, the decreases lost significance when the data were corrected for hemodilution with the total protein content of each sample as a reference. We conclude that RCM infusion does not activate the complement system.

Complement Activation↗
PubMed1985

Acquired C1 inhibitor deficiency with angioedema symptoms in a patient infected with Echinococcus granulosus.

A patient with echinococcosis, acquired deficiency of the inhibitor of the activated first component of complement and angioedema symptoms has been studied. These symptoms started 7 months after the surgical removal of an echinococcus liver cyst. Eight years later, when the complement was investigated, a marked deficiency of the C1 inhibitor, C1, C4 and CH50 was present. The patient was therefore successfully treated with tranexamic acid. After 4 years, the woman needed another operation because of a relapse of echinococcosis; afterwards she was symptom-free without medications, while the complement profile remained unchanged. Circulating immune complexes were detected by the conglutinin method. The patient's serum was demonstrated to possess an anticomplementary activity without affecting the C1 inhibitor when incubated with normal human serum at 37 degrees C. At present, 16 years after the onset of the symptoms, there are no signs of lymphoproliferative disease.

Angioedema↗
PubMed1985

Studies of complement activation in ARDS patients treated by long-term extracorporeal CO2 removal.

To investigate the role of complement activation in the adult respiratory distress syndrome (ARDS) and in the complications of extracorporeal circulation (ECC), several parameters (CH50, C3 split products, C3a, C5a, PMN aggregating activity, carboxypeptidase activity) of the complement profiles of 23 ARDS patients were measured. Twenty patients were treated by long-term extracorporeal support. Before connection to ECC, marked leukocytosis (18,250 +/- 5,950) and significantly high plasma C3a levels (p less than 0.005) were observed. After connection, C3a levels increased further, up to values eight times higher than the basal ones. The WBC count transiently decreased to 41% of prebypass levels after 15 minutes of ECC. At the same time C3 split products appeared and PMN aggregating activity was shown in 52% of the patients. C5a levels remained normal during bypass, even in two samples in which PMN aggregating activity was detected. Later decreases in CH50 titers (p less than 0.001) and carboxypeptidase activity (p less than 0.005) were observed. Complement activation was no longer evident after the 24th hour of bypass. We conclude that there is a low-degree complement activation in ARDS, and ECC is a further strong stimulus for complement activation. This phenomenon appears, however, to be self-limited.

Adolescent↗
PubMed1982

[Pathological effects of recently isolated complement derived peptides].

The C3a and C5a polypeptides release, under conditions of complement activation, causes a change in PMN shape and adhesiveness with formation of leukoemboli in microvascular districts. Those modified granulocytes produce oxygen radicals with toxic activity. This mechanism seems to play a role in different pathological situations like pulmonary distress in hemodialysis, leukapheresis, cardiopulmonary by-pass and extent of necrosis in acute myocardial infarction. The same mechanism has been largely investigated in Adult Respiratory Distress Syndrome (A.R.D.S.). In this condition the leukoembolization toxicity seems to be the most important pathogenetic factor of the alveolo-capillary membrane damage which is the base of the disease.

Animals↗
PubMedDate not supplied

Thrombolytic treatment and complement activation.

Details of possible complement activation in acute myocardial infarction (AMI) and the in vivo effects of fibrinolytic agents on this activation are not yet known. We measured complement activation in 40 patients with AMI: 20 were treated with streptokinase, and 20 did not receive any fibrinolytic agent. Anaphylatoxin C4a, C3a and membrane attack complexes SC5b-9 increased about 10-fold (p < 0.0001) during streptokinase infusion. There were no increases in complement catabolic products in AMI patients not treated with streptokinase. Significant transient leukopenia (-29.5%, 7.0 SEM, p = 0.001) and a drop in systolic pressure (-29%, 3.4 SEM, p < 0.0001) occurred after 15 min of streptokinase infusion simultaneously with the peak of anaphylatoxins in plasma.

Anaphylatoxins↗