Takehisa Fukuhara

Increased capillary permeability to albumin in diabetic rat myocardium.

To clarify the mechanism for the well-known increase in microvascular permeability that occurs with diabetes mellitus, we investigated capillary permeability to albumin in diabetic rat myocardium by electron microscopy using albumin-gold (Alb-Au) complexes as a tracer. Diabetes was induced by an intravenous injection of streptozotocin. After 24-32 weeks, hearts from diabetic rats and age-matched control rats were perfused with Krebs-Henseleit bicarbonate buffer containing Alb-Au for 5 or 20 minutes and then fixed and processed for electron microscopy. The binding and transport of Alb-Au by capillary endothelium was quantitatively evaluated. In control rats, Alb-Au particles were found preferentially bound to the luminal plasmalemmal vesicles. In diabetic rats, the labeling of luminal vesicles was more extensive and more pronounced after 5 minutes of perfusion when compared with control vesicles. The plasma membrane proper was also heavily labeled in diabetic rats. After 20 minutes, Alb-Au particles were transported across the capillary endothelium via plasmalemmal vesicles, but they did not penetrate the intercellular junctions in either control or diabetic rats. The vesicular transport of Alb-Au across the capillary endothelium was significantly increased in the diabetic myocardium when compared with control myocardium (percentage of abluminal labeled vesicles, 25.9 +/- 5.5% versus 1.3 +/- 0.5%; p < 0.01). The study on food-restricted rats with body weights close to those of diabetic rats suggested that caloric deficiency alone did not have much effect on capillary permeability. The data indicate that capillary permeability to albumin is markedly increased in diabetic myocardium because of enhanced vesicular transport. This may play an important role in the pathogenesis of diabetic cardiomyopathy.

Permeability of small coronary arteries and myocardial injury in hypertensive diabetic rats.

Damage to the coronary artery and myocardium is known to be more marked when hypertension is complicated by diabetes than when either is present alone. The reason is not clear, but one possible factor is vascular permeability. Therefore, we investigated vascular permeability using sodium fluorescein of 70 mg/kg body weight, in 12-week-old streptozotocin-induced diabetic spontaneously hypertensive rats. Non-diabetic spontaneously hypertensive rats, diabetic rats with normal blood pressure, and non-diabetic rats with normal blood pressure of the same age were used as controls and treated similarly. H-E and Azan staining were used to examine vascular abnormality and mycoardial damage. The diabetic spontaneously hypertensive rats showed marked sodium fluorescein in the coronary artery wall and surrounding area, demonstrating greater vascular permeability than non-diabetic spontaneously hypertensive rats, diabetic and non-diabetic normotensive rats. Heart weights and diameters of myocytes were smaller in the diabetic than in the non-diabetic spontaneously hypertensive rats. Diabetic spontaneously hypertensive rats also exhibited marked perivascular fibrosis and focal necrosis. Thus, increased vascular permeability may play a role in vascular and myocardial changes in diabetic spontaneously hypertensive rats.

Congestive heart failure associated with diabetes mellitus

A case of typical congestive heart failure associated with diabetes mellitus is reported. The case was diagnosed on the basis of biopsy findings such as basal laminar thickness and of angiographically normal coronary arteries. The therapy, including insulin, resulted in normalization of electrocardiographic abnormalities and improvement of myocardial contractility.

Capillary permeability to albumin in diabetic rat myocardium

To clarify the mechanism for the well-known increase in microvascular permeability that occurs with diabetes mellitus, we investigated capillary permeability to albumin in diabetic rat myocardium by electron microscopy using albumin-gold (Alb-Au) complexes as a tracer. Diabetes was induced by an intravenous injection of streptozotocin. After 24-32 weeks, hearts from diabetic rats and age-matched control rats were perfused with Krebs-Henseleit bicarbonate buffer containing Alb-Au for 5 or 20 minutes and then fixed and processed for electron microscopy. The binding and transport of Alb-Au by capillary endothelium was quantitatively evaluated. In control rats, Alb-Au particles were found preferentially bound to the luminal plasmalemmal vesicles. In diabetic rats, the labeling of luminal vesicles was more extensive and more pronounced after 5 minutes of perfusion when compared with control vesicles. The plasma membrane proper was also heavily labeled in diabetic rats. After 20 minutes, Alb-Au particles were transported across the capillary endothelium via plasmalemmal vesicles, but they did not penetrate the intercellular junctions in either control or diabetic rats. The vesicular transport of Alb-Au across the capillary endothelium was significantly increased in the diabetic myocardium when compared with control myocardium (percentage of abluminal labeled vesicles, 25.9±5.5% versus 1.3±0.5%; p<0.01). The study on food-restricted rats with body weights close to those of diabetic rats suggested that caloric deficiency alone did not have much effect

A case of cardiac sarcoidosis diagnosed by endomyocardial biopsy

症例は労作時呼吸困難を主訴に,一過性の完全房室ブロック,心房性期外収縮,心室性期外収縮等の種々の心電図異常を呈し入院した63才の女性.何らサルコイドーシスを積極的に疑うべき心臓以外の所見が認められず,心エコー図, 201Tl心筋シンチグラム, 67Gaシンチグラム,心臓カテーテル検査,心内膜心筋生検等により,心サルコイドーシスと生前診断された珍しい症例である.