Résumé
When the pathogen infects the fetus,the pathogenic microorganism and the infection product are recognized by the corresponding receptor.The fetus innate immune system is passively activated,which produces proinflammatory cytokines,induces cascade reaction of cytokines,and releases a large number of inflammatory factors secreted by the body.Its toxic effect can cause damage to the brain,lung,small intestine and heart and other important organs of the whole body,which seriously threatens the life of the perinatal infants and their subsequent survival quality.It has been found that fetal cardiovascular system is one of the important target organs of intrauterine infection.Cytokines produced by cardiac inflammation and induced by intrauterine infection can damage myocardial cells,affect the proliferation of myocardial cells,and cause damage to cardiac function.Moreover,the persistent influence of infection on fetus leads to fetal vascular remodeling and changes in fetal cardiopulmonary hemodynamics.This article reviews the effects of pathogens of intrauterine infection and fetal cardiac inflammation,cardiac hemodynamics,cardiomyocyte development,gene program of cardiomyocyte and cardiac structure development on fetal cardiovascular system.
Résumé
The objective of the present study was to evaluate the diagnostic efficiency of the new cardiac-specific marker troponin T (cTnT) compared with the conventional markers creatine kinase (CK) and lactate dehydrogenase (LDH) in detecting myocardial injury in dogs with clinical signs and symptoms of various forms of cardiac diseases including congestive heart failure (CHF). The results showed that in animals with clinical valvular heart disease (n = 20), clinical cardiac arrhythmias (n = 11) and heartworm infection (n = 10) without clinical heart failure, as well as in dogs with clinical CHF (n = 18), there was no significant difference either in the activity of CK or LDH. Levels of cTnT in dogs with CHF, on the other hand, were much higher than those in the other 3 groups. The majority of the 18 dogs with CHF had detectable levels of cTnT, with 6 of them (33%) showing values exceeding the upper reference limit of 0.10 ng/ml. The overall mean cTnT level in this animal group was 0.204 ng/ml. These results may imply that CHF in dogs is associated with a small release of cardiac troponin T indicative of minor myocardial cell damage.