Effects of captopril on myocardial protection during cardioplegia.

UNLABELLED: The study aimed at checking effects exerted by captopril (C) on human myocardial ACE system as well as the role played by tissue ACE inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aorto-coronary-by-pass (CABG). Fifty-four patients with coronary artery disease affecting 3 vessels having suffered from acute myocardial infarction anterior (AMI-ant), homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo (P). A total of 4 mg/l Captopril was mixed into the cardioplegic solution with blood according to the method of Buckberg (Buckberg GD. J Thorac Cardiovasc Surg 1987; 93: 127-139). Eight samples (blood/perfusate) were obtained from each patients and norepinephrine (NE), epinephrine (E) were assayed using an HPLC technique. Angiotensin I was assayed by RIA. CK was also assayed (units/ml). Blood/perfusate samples were taken during CABG: (1) pre-pump; (2) pump sample; (3) pump preclamping; (4) coronary sinus; (5) coronary sinus sample during reperfusion; (6) coronary sinus during warm reperfusion; (7) after clamping sample; (8) after decanulation; RESULTS: Captopril group (29 patients): angiotensin I: (1) 8.15; (2) 7.0; (3) 7.31; (4) 8.45; (5) 8.93; (6) 8.73; (7) 9.07; (8) 9.40; versus placebo: (1) 7.09, (2) 7.43; (3) 7.80; (4) 9.31; (5) 9.01; (6) 8.35; (7) 8.85; (8) 8.07 ng/ml, probability, not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of captopril on human myocardial ACE-inhibition: neurohumoral variations during coronary sinus cardioplegia. Cardioprotective effect during aortocoronary bypass]. / Influenza del captopril sul sistema ACE-tissutale miocardico umano: variazioni neuroumorali durante cardioplegia nel seno coronarico. Effetti di cardioprotezione durante bypass aortocoronarico.

UNLABELLED: The present study is aimed at checking effects exerted by captopril on human myocardial ACE system (ACE-T) as well as the role played by tissue ACE-inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aortocoronary bypass graft (CABG): 54 patients with coronary artery disease affecting 3 vessels having suffered from acute anterior myocardial infarction, homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo: 4 mg/l captopril were mixed into the cardioplegic solution with blood according to Buckberg, 8 blood samples were obtained from each patient and norepinephrine, epinephrine were assayed using an HPLC technique. Angiotensin 1 was assayed by RIA. CK was assayed as well (U/L). Blood samples were taken during CABG: pre-pump sample; pump sample; pump preclamping sample; coronary sinus sample; warm reperfusion sample; coronary sinus during warm reperfusion; after clamping sample; after cannulation. RESULTS: captopril group (29 patients): angiotensin 1:8.15; 6.9; 7.45; 8.66; 8.93; 8.70; 9.07; 9.40 versus placebo: 7.09; 7.43; 7.80; 9.31; 9.01; 8.35; 8.85; 8.07 mcg (all NS). Noradrenaline: captopril group: 359; 404; 329; 282; 263; 216; 310; 337 versus placebo: 439; 520; 499; 469; 526; 566; 501; 443 pg (p < 0.001). CK, captopril group: 79.9; 95.1; 100.8; 94.3; 104.2; 94.7; 108.4; 108 versus placebo: 76.2; 120.2; 135.5; 203; 225; 272; 247; 228.7 U/L (p < 0.01). Epinephrine values showed no significant difference between the 2 groups. Norepinephrine and CK decrease as well as angiotensin I increase in treated patients as compared to controls suggest some effect exerted by captopril ACE-T and its capability of reducing reperfusion damage and recommend its use for heart protection during CABG.

[Sea-blue histiocytosis. Clinical and immunological study of a familial case]. / Istiocitosi blu-mare. Studio clinico e immunologico di un caso familiare.

This case (a young man) presented a clinical picture of a hard periorbital edema, hepatosplenomegaly and a mild bilateral pulmonary fibrosis. The histopatological pattern of our case (as well as his sister affected with the same syndrome) was characterized by the presence of macrophages full of blue staining granules and bone marrow macrophagic infiltrations. In the pulmonary function tests the volumes and compliance test and diffusing capacity were normal. The enzymatic deficit of the macrophage leads to the increase storage of phosphoglicerides and phosphosphingolipids responsibles for the blue staining with Wright-Giemsa stain. Our case fit into the specific pathology of the macrophage cell in accordance with the more recent views of the autonomy of the MPS (Mononuclear Phagocytic System). The known relationship between macrophages and T and B lymphocites have prompted us to study the cellular and humoral immunological behaviour of our case. We have observed an increased IgM immunoglobulins and an increase of IgM surface membrane receptors. Our results will be illustrated and compared with the until known 70 publicated cases.