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Biomedical subjects

T W Gardner

Publications and source records attributed to T W Gardner.

47 records · Page 3Linked to original sources
PubMed1988

Retinal histamine synthesis is increased in experimental diabetes.

We examined retinal de novo histamine synthesis mediated by retinal histidine decarboxylase in normal and streptozotocin-diabetic male, Sprague Dawley rats that were diabetic for 21 days. We also examined effects of insulin and alpha-hydrazinohistidine (alpha HH) treatments on retinal histamine synthesis in this diabetic model. alpha HH is a specific inhibitor of histidine decarboxylase. Results indicate that the retina contains an active histidine decarboxylase enzyme system, and that in streptozotocin diabetes retinal histamine synthesis is increased 197%. Both insulin and alpha HH independently reverse and normalize retinal histamine synthesis. These data thus indicate that the retinal inducible histamine pool is increased in experimental diabetes, and that insulin is an important modulator of retinal histamine metabolism. This newly described retinal metabolic alteration may be one factor responsible for increased retinal vascular permeability in diabetic retinopathy.

Animals↗
PubMed1984

Mucinous adenocarcinoma of the eyelid. A case report.

A 52-year-old man had a rapidly growing cystic-appearing lesion on his lower eyelid. Excisional biopsy disclosed a mucinous sweat gland adenocarcinoma and the mucinous material (presumably sialomucin) accounted for the transillumination property of the tumor. These carcinomas should be considered in the differential diagnosis of cystic eyelid lesions.

Adenocarcinoma, Mucinous↗
PubMed1984

Congenital optic nerve colobomas: CT demonstration.

Patients with ocular coloboma and its variants may exhibit notching of the iris, peripapillary staphylomas, crater-like excavation of the optic disc, funnel-shaped widening of the retrobulbar optic nerve, cup-shaped filling defects in the perioptic subarchnoid space, and concurrent anomalies of the face, skull, and brain. Combined ophthalmological and radiological evaluation identifies these lesions successfully and differentiates them from other ocular pathology.

Abnormalities, Multiple↗
PubMed1983

Congenital pulmonary lymphangiectasis. A case complicated by chylothorax.

A case is reported of an infant with features of Noonan Syndrome and congenital pulmonary lymphangiectasis. Soon after birth, persistent respiratory distress developed, and, at 4 months of ge, a chylothorax was noted. Medium chain triglyceride therapy by the enteral route was tried, but parenteral alimentation and chest-tube drainage were required. Diagnosis of pulmonary lymphangiectasis was confirmed by biopsy.

Chylothorax↗
PubMed1982

Photic maculopathy secondary to short-circuiting of a high-tension electric current.

A 21-year-old man was exposed accidentally to the flash of a high-tension short circuit. He subsequently developed a yellow-gray foveolar lesion with mild central visual loss. Fluorescein angiography demonstrated the area of retinal pigment epithelial disruption and was used to follow its evolution over eight months. The energy level at the retina was estimated at 0.87 Joules/cm2, insufficient to create a thermal burn. Therefore, although the patient suffered thermal facial burns, the foveolar lesion represents a photochemical injury to the retinal pigment epithelium and, hence, is similar to solar retinopathy, eclipse blindness, and arc-welder's retinopathy.

Adult↗
PubMedDate not supplied

Antihistamines reverse blood-ocular barrier breakdown in experimental diabetes.

Retinal and other tissue histamine synthesis is increased in experimental diabetes; histamine infusion causes blood-ocular barrier breakdown in nondiabetic rats. We have examined the hypothesis that antihistamines prevent blood-ocular barrier breakdown in streptozotocin diabetes using male Sprague-Dawley rats held 28 days. During the last 7 days they were divided into these treatment groups: control (C), untreated diabetic (D), diabetic rats receiving diphenhydramine-HCl (B), diabetic rats receiving ranitidine (R) and diabetic rats receiving diphenhydramine and ranitidine (BR). Vitreous albumin content was measured 6 hr following fluorescein isothiocyanate bovine serum albumin (FITCBSA) injection. Data show that D had a 98.3% increase in vitreous body FITCBSA over C (p less than 0.05) while B and R showed respective decreases of 34.9% and 51.4% compared to D, R being significantly lower than D (p less than 0.05). BR showed a decrease of 71% (p less than 0.05) compared to D, and R and BR groups were not significantly different from C (p less than 0.05). Leakage into the vitreous was from the retina, not the ciliary body. These data indicate that 1) experimental diabetes results in elevated blood-ocular barrier permeability, which can be reversed by diphenhydramine-HCl and ranitidine; and 2) histamine H1- and H2-receptor activation and interaction by altered endogenous histamine metabolism may mediate blood-ocular barrier breakdown, implicating a pathogenic role of histamine in diabetic retinopathy.

Animals↗
PubMedDate not supplied

Astemizole reduces blood-retinal barrier leakage in experimental diabetes.

We examined the potential of astemizole, a histamine H1-receptor antagonist that does not cross the blood-brain barrier, to reverse blood-retinal barrier leakage to albumin in streptozotocin diabetic rats. Four groups of nondiabetic and four groups of diabetic rats received vehicle or astemizole at dosages of 5, 10, or 20 mg/kg body weight for days 22-28 of a 28-day holding period. There were no significant differences in nondiabetic plasma-vitreous albumin ratios between animals receiving vehicle or any of the three astemizole dosages. Only diabetic rats receiving vehicle showed a significant (p < 0.05) 100% increase in the plasma-vitreous albumin ratio over their nondiabetic counterparts. Diabetic rats receiving either 5, 10, or 20 mg/kg astemizole exhibited total normalization of vitreous albumin accumulation, despite persistence of diabetes. These data indicate that astemizole, an H1-receptor antagonist that does not cross the blood-retinal barrier, is effective in reversing blood-retinal barrier leakage of albumin in experimental diabetes.

Animals↗