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Biomedical subjects

A R Quint

Publications and source records attributed to A R Quint.

2 recordsLinked to original sources
PubMed1987

Effect of an insulin-induced decrease in blood glucose on the human diabetic retinal circulation.

The effect of an insulin-induced decrease in blood glucose on the retinal blood flow (Q) was studied in 12 type II diabetics, using bidirectional laser Doppler velocimetry (BLDV) and monochromatic fundus photography. Q was first measured during hyperglycemia and then during normoglycemia which was achieved within approximately 3 hours by intravenous insulin administration. At normoglycemia, Q was 15% lower than at hyperglycemia (P less than 0.001). The decrease in Q was larger in patients with shorter disease duration. The authors also determined the regulatory change in Q during 100% oxygen breathing. Although this response remained subnormal, it was improved significantly in normoglycemia (P less than 0.01), particularly in those patients whose blood glucose level was decreased at a slower rate, suggesting that a gradual decrease in blood glucose may be beneficial.

Adult↗
PubMed1985

Gonadotropin determinations and thyrotropin-releasing hormone and luteinizing hormone-releasing hormone testing in critically ill postmenopausal women with hypothyroxinemia.

Critically ill patients often have altered serum levels of thyroid hormones. The present study was undertaken to further define hormonal changes in such patients. Since postmenopausal women have normally elevated gonadotropin levels, this group was chosen as the study population. Thirteen critically ill patients with serum T4 concentrations below 5 micrograms/dl (group I), 16 critically ill patients with T4 concentrations of 5 micrograms/dl or greater (group II), and 19 normal subjects (group III) were studied. Basal gonadotropin levels (FSH and LH) were significantly lower (P less than 0.01) in both critically ill groups. The LH level in group I was 36.5 +/- 39.3 (+/- SD) mIU/ml, in group II it was 45.3 +/- 30.4, and in group III it was 75.3 +/- 24.4. The FSH level in group I was 43.0 +/- 39.7 (+/- SD) mIU/ml, in group II it was 78.0 +/- 37.9, and in group III it was 133.0 +/- 38.2. Most group I patients had LH and FSH concentrations far below the normal postmenopausal range. The response to dynamic testing with TRH and LRH revealed a significantly lower incremental TSH response to TRH in group I (8.0 +/- 5.6 mIU/ml) compared to that in group III (13.7 +/- 2.8; P less than 0.05). However, the maximal responses of FSH and LH to LRH were not different between groups I and III, despite the fact that 2 of 10 group I patients had no response. These data indicate that a subset of patients with the low T4 syndrome have hypogonadotropism, inappropriate to their menopausal state. This suggests that acute critical illness may cause hypothalamic or pituitary dysfunction, only part of which is recognized as the low T4 syndrome. The mechanism for this dysfunction and its importance in contributing to the overall mortality in this group is unknown.

Adult↗