Search PubMed⌕ Search

Biomedical subjects

T Inoguchi

Publications and source records attributed to T Inoguchi.

34 records · Page 2Linked to original sources
PubMed1988

Reflow of obstructed capillaries in the maculae of humans with diabetic retinopathy, observed by fluorescein angiography.

As diabetic retinopathy progresses, the non-perfused area in the retina gradually enlarges as the capillaries are obstructed. To elucidate the process of capillary obstruction we examined macular capillaries in 104 diabetics, using fluorescein angiography. The follow-up period was three to eight years. We found that some capillaries in the macular were obstructed, then became unobstructed. Reflow of blood into the macula after the obstruction was observed in nine patients (8.7%). The time between obstruction and reflow varied from two months to four years. There were four cases of simple, three of preproliferative, and two of proliferative retinopathy. Reflow in the capillaries was confirmed as occurring at the same position and in vessels with the same diameter as seen before the obstruction. There was no leakage of the fluorescein dye from the capillary where reflow took place. We tentatively conclude that one of the causes of this phenomenon is a functional obstruction.

Adolescent↗
PubMed1986

Plasma fibronectin and platelet aggregation in diabetes mellitus.

Plasma fibronectin (FN) is a high-molecular weight glycoprotein produced by endothelial cells, fibroblasts, and other mesenchymal cells. Plasma FN levels were measured in non-insulin-dependent diabetics (NIDDM) (n = 42) and compared with age-matched control subjects (n = 20). Plasma FN levels were significantly higher in the NIDDM patients (44.2 +/- 2.2 mg/dl, mean +/- SE) than in the control subjects (31.2 +/- 2.2 mg/dl). In addition, the rate of platelet aggregation was studied in 23 of the 42 NIDDM patients. Interestingly, the plasma FN levels were significantly elevated, particularly in diabetic patients with enhanced platelet aggregation. It is suggested that elevated plasma FN may be closely related to the abnormality of platelet function in diabetics, which leads to diabetic vascular lesions.

Adult↗
PubMed1986

Reduced serum-stimulatory activity on prostacyclin production by cultured aortic endothelial cells in diabetes mellitus.

Reduced prostacyclin (PGI2) production by the vascular wall has been proposed as a possible cause of macro- or microangiopathy in diabetes mellitus. In the present study, we confirmed the stimulatory activity on PGI2 (PSA) production in plasma-derived serum (PDS) by cultured aortic endothelial cells. Furthermore, the abnormality of PSA was examined in diabetic PDS. PSA in PDS from non-insulin-dependent diabetics significantly decreased as compared with that in PDS from age-matched control subjects. There was no difference in PSA in PDS between diabetic patients with and without vascular complications such as retinopathy and nephropathy. In addition, after treatment with dialysis, PSA in diabetic PDS was still not restored to that in normal PDS. These findings suggest that relatively heat-stable (56 degrees C, 30 min) and nondialyzable PGI2 stimulatory substance(s) may decrease in diabetic PDS. It is concluded that a reduction in PDS-stimulated PGI2 production by the vascular wall can play an important role in the pathogenesis of vascular lesions in diabetes mellitus.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

[Continuous local application of cytostatics for bronchial carcinoma and mediastinal lymph node metastasisization (author's transl)].

A carcinostatic substance (5-fluorouracil) was instilled into the mediastinal lymph nodes, the pleural cavity or the internal thoracic artery by continuous perfusion before operation on patients with bronchial carcinoma. Degenerative changes could be demonstrated histologically in the cancer cells in the lymph node metastases. This method was also effective for the controlateral lymph node metastases. As a treatment additional to operation, it may improve the chances of survival.

Adenocarcinoma↗
PubMedDate not supplied

Reduction of urinary albumin excretion by thromboxane synthetase inhibitor, OKY-046, through modulating renal prostaglandins in patients with diabetic nephropathy.

We evaluated the effects of thromboxane synthetase inhibitor, OKY-046, on urinary albumin and prostaglandin (PG) excretion in 14 patients with non-insulin-dependent diabetes mellitus (NIDDM). Urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), TXB2 (a stable metabolite of TXA2) and PGE2 in NIDDM patients was comparable with that in control subjects. However, the urinary 6-keto-PGF1 alpha/TXB2 ratio in NIDDM patients with both micro- and macroalbuminuria was significantly (P less than 0.001) lower than that in the controls. By a single administration of OKY-046 (40 mg, i.v.) to the diabetic patients, urinary TXB2 excretion significantly (P less than 0.05) decreased from 169.7 +/- 23.9 to 140.2 +/- 17.9 ng/gCr, but urinary 6-keto-PGF1 alpha and PGE2 excretion did not change significantly. The urinary 6-keto-PGF1 alpha/TXB2 ratio thus significantly (P less than 0.01) increased from 1.02 +/- 0.13 to 1.73 +/- 0.41 as associated with significant increments in urine volume (P less than 0.05), urinary sodium excretion (P less than 0.01) and creatinine clearance (P less than 0.05). Of 14 diabetic patients, 7 with macroalbuminuria (albumin index exceeding 100 mg/gCr) were orally given OKY-046 (600 mg/day) for 8 weeks. After this period, the urinary albumin index significantly (P less than 0.05) decreased from 524.9 +/- 149.6 to 317.6 +/- 90.6 mg/gCr.(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMedDate not supplied

Stimulatory activity on prostacyclin production decreases in sera from streptozotocin-induced diabetic rats.

We recently reported that serum stimulatory activity on prostacyclin (PGI2) production by cultured bovine aortic endothelial cells decreased in noninsulin-dependent diabetic patients. In the present study, this activity was compared in streptozotocin-induced (STZ) diabetic rats and controls. Platelet-poor plasma-derived serum (PDS) from Wistar male rats stimulated 6-keto-PGF1 alpha production (a stable metabolite of PGI2) by cultured bovine aortic endothelial cells, rat lung fibroblasts, and rat aortic rings in a time- and dose-dependent manner. Namely, PDS from rats has a stimulatory activity on PGI2 production (PGI2 stimulatory activity; PSA). Furthermore, PSA in PDS from STZ diabetic rats (n = 12) significantly decreased as compared with that from control rats (n = 10) using three types of in vitro systems. The reduction in PDS-stimulated PGI2 production by the vascular wall may lead to platelet hyperaggregation and thrombus formation in diabetics, which is considered to be involved in the pathogenesis of diabetic macro- or microangiopathy.

6-Ketoprostaglandin F1 alpha↗