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Biomedical subjects

M Kusagawa

Publications and source records attributed to M Kusagawa.

At least 145 records · Page 8Linked to original sources
PubMed1978

Surgical treatment of infantile lobar emphysema in cardiovascular disease with left-to-right shunts.

Serious symptoms associated with the lobar emphysema in congenital heart diseases with left-to-right shunt disappeared after radical operation for cardiac lesion. The study of seven autopsied cases revealed that the lobar emphysema resulted from check valve mechanism created by compression of the bronchi by distended pulmonary artery. Eight cases of our experience of lobar emphysema disappeared shortly after the operation for congenital heart disease with left-to-right shunt seems to indicate infantile lobar emphysema in congenital heart diseases with left-to-right shunt should not be treated by resection but rather by radical operation for cardiac lesion as soon as possible even in infancy.

Bronchi↗
PubMedDate not supplied

The role of the protein C-thrombomodulin system in physiologic anticoagulation during cardiopulmonary bypass.

Changes in the protein C-thrombomodulin (PC-TM) system in relation to other coagulofibrinolytic parameters were examined in 25 patients undergoing open heart surgery. Although all patients were given heparin, a decrease in antithrombin III (ATIII) and progressive increase in thrombin-ATIII complex (TAT) and fibrinopeptide A (FPA) levels were noted during cardiopulmonary bypass, which indicated that heparinization did not completely inhibit the formation of thrombin and its function. C1-inactivator (INA) resistant fibrinolytic activity increased markedly during CPB, in parallel with the change of tissue plasminogen activator antigen (t-PA;Ag), which indicates that fibrinolytic activity during CPB is mainly of extrinsic origin caused by t-PA. Protein C antigen (PC;Ag), protein S antigen (PS;Ag), and thrombomodulin antigen (TM;Ag) were all decreased significantly during CPB. This is considered to reflect the activation and consumption of the PC-TM system in response to generated thrombin. Furthermore, enhancement of the extrinsic fibrinolytic system is easily explained by the action of activated PC, which counteracts plasminogen activator inhibitor (PAI-1), to cause enhancement of t-PA activity.

Adult↗