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Biomedical subjects

C L Chang

Publications and source records attributed to C L Chang.

At least 199 records · Page 11Linked to original sources
PubMed1985

Effects of sodium nitroprusside-induced hypotension on the cerebral and hindlimb blood flow in dogs.

Sodium nitroprusside (SNP) has been commonly used as a vasodilator agent for deliberate hypotension with general anesthesia. The purpose of this study was to observe whether cerebral blood flow (CBF) was significantly reduced when SNP infusion was accomplished to decrease peripheral blood flows with systemic hypotension. We conducted the experiments in 15 pentobarbital-anesthetized dogs. CBF was measured in 7 dogs using a venous outflow method. Hindlimb blood flow (HBF) serving as a representative of the peripheral circulations was obtained by flow measurement in the femoral artery in 8 dogs. The systemic arteral pressure (SAP) was decreased stepwise (approximately 5 mmHg for each step) by adjusting the SNP infusion rate. During the systemic hypotension, the CBF remained fairly constant despite a marked decline in the mean SAP to 40 mmHg. The calculated cerebral vascular resistance was progressively decreased with the systemic hypotension. On the contrary, a reduction in the HBF was observed accompanying the fall in SAP. When the mean SAP was decreased to 50 mmHg, the HBF was only 46.3 +/- 7.6% of the control value. The calculated hindlimb vascular resistance was slightly elevated during the whole course of SNP-induced hypotension. The results reveal the disparity between the brain and hindlimb in the resistance and flow responses to SNP-induced hypotension. The constancy of CBF subserves adequate brain perfusion when deliberate hypotension is conducted for surgery in the peripheral organs.

Animals↗
PubMed1984

The effect of pituitary homografts on the accessory sex organs and serum hormonal levels with or without androgen in mature male rats.

The effect of pituitary homografts on the accessory sex organs and hormonal levels were studied in Wistar mature male rats. Grafted rats were further divided into four experiments: rats were bled once daily via a jugular vein cannula for seven days to investigate when serum prolactin began to rise after transplantation. rats were decapitated on the seventh day after transplantation to test whether 7 days were long enough to show the effect of pituitary grafts on the weight of prostate and seminal vesicles. rats were orchiectomized or orchiectomized and adrenalectomized on the seventh day after transplantation and then decapitated 4 weeks later to test a long term action of pituitary grafts and hormonal levels on the accessory sex organs without androgen. Rats grafted with several pieces of muscle were used as controls in each experiment. The initial rise in serum prolactin level was observed on the fourth day after pituitary transplantation, and then a higher serum prolactin level was maintained thereafter. Despite the higher prolactin level in the pituitary-grafted rat than in the control, no significant differences from the control in the weight of prostates and seminal vesicles and adrenal gland and the concentrations of serum luteinizing hormone (LH) and follicular stimulating hormone (FSH) were measured. This result showed that the weight of accessory sex organs was not affected by a higher serum prolactin within seven days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1983

Insulin resistance in the liver in fasting and diabetes mellitus: the failure of insulin to stimulate the release of a chemical modulator of pyruvate dehydrogenase.

To further define the mechanism(s) of insulin resistance in the liver associated with diabetes and fasting, we evaluated the ability of insulin to release an activator of pyruvate dehydrogenase activity from a liver particulate fraction. Insulin reproduceably and significantly enhanced the release of mediator from the liver particulate fraction of control animals. The particulate fractions from fasted and diabetic animals were resistant to this effect of insulin. Refeeding and insulin treatment, respectively, restored responsiveness to insulin. These data support the concept that alterations at or near the plasma membrane can be responsible for or accompany the insulin resistance observed in the liver in fasting and diabetes mellitus.

Animals↗
PubMed1983

The effects of glucocorticoids on insulin-stimulated lipogenesis in primary cultures of rat hepatocytes.

We used primary cultures of rat hepatocytes to evaluate the effects of glucocorticoids on insulin-responsive hepatic lipogenesis. The data indicate that hepatocytes incubated for 20 h with dexamethasone (0.1 microM) alone are profoundly resistant to the ability of insulin to stimulate lipogenesis acutely. In contrast, primary cultures of hepatocytes incubated with dexamethasone plus insulin are hyper-responsive to the ability of insulin to stimulate lipogenesis chronically. This potentiation of insulin action by a glucocorticoid occurs at physiological concentrations of the two hormones. Exposure to dexamethasone plus insulin for more than 4 h is required for the two hormones to enhance insulin action either by overcoming the insulin resistance induced by dexamethasone alone or by stimulating insulin action induced by insulin alone. Despite the marked potentiation of insulin action, hepatocytes exposed to dexamethasone plus insulin are less sensitive to insulin, as demonstrated by a shift to the right in the dose-response curve for insulin-stimulated lipogenesis. The resistance of hepatocytes to the acute effects of insulin after exposure to dexamethasone alone and the potentiation of insulin action and decreased sensitivity to insulin after exposure to insulin plus dexamethasone are all mediated by post-insulin-binding events. These studies demonstrate potentiation of insulin action in the liver by physiological concentrations of glucocorticoids and may have physiological significance for the regulation of normal hepatic lipogenesis, for the hyperlipidaemia observed with the pharmacological use of glucocorticoids, and for disease states in man associated with hyperinsulinaemia and hypercortisolism.

Animals↗
PubMed1982

Insulin-induced alterations in insulin binding and insulin action in primary cultures of rat hepatocytes.

The exposure of primary cultures of hepatocytes to insulin. 10(-8) M, for 16 h results in a decrease in high affinity insulin binding with no alterations in lower affinity binding. This is reflected in a decrease in the sensitivity, but normal responsiveness, of cultured hepatocytes to the acute effect of insulin on the uptake of aminoisobutyric acid. The shift in sensitivity, however, can only be partially explained by the decrease in insulin binding. With regard to lipid synthesis, hepatocytes cultured in the presence of insulin, 10(-8) M, are normally sensitive and hyperresponsive to the acute effects of insulin. These data indicate that the insensitivity or resistance of a given tissue to insulin may be specific for the biologic response being evaluated, that postbinding events may be more important than alterations in insulin binding in determining both the sensitivity and responsiveness of a tissue to insulin, and that generalizations concerning the sensitivity or responsiveness of a tissue to insulin based on binding data alone may be unwarranted.

Acetates↗
PubMedDate not supplied

Relationship between radioprotective and neuromotor effects of S-2(3-aminopropyl-amino)ethylphosphorothioate (WR-2721) in mice.

The radioprotective and neuromotor effects of WR-2721 were studied in male albino ICR strain mice. The protective activity was evaluated by graded doses of WR-2721 (50-400 mg/kg, IP) against whole body 60Co gamma irradiation at a single maximal lethal threshold dose rad (i.e., 1250 rad). The neuromotor effects of the drug were assayed by its action, at the same dose range as used in the protection assay, on spontaneous motor activity (SMA) and wire hanging performance (WHP). Drug doses were administered 30 min before radiation exposure and neurobehavioral testings. The results showed a dose-dependent increase in radioprotection and an inhibition in the neuromotor tasks. The radioprotective efficacy was seen at doses at which intrinsic neuromotor deficits were detected (100-400 mg/kg). A dose-related parallelism of protective efficacy and neurobehavioral toxicity (i.e., SMA inhibition and WHP disruption) was also observed. The present findings suggest that WR-2721 induces neuromotor dysfunctions along with its radioprotectivity.

Amifostine↗
PubMedDate not supplied

Computer-aided diagnosis: detection and characterization of hyperparathyroidism in digital hand radiographs.

An automated method is developed for the detection and staging of skeletal changes due to hyperparathyroidism on digitized hand radiographs. Subperiosteal bony resorption, particularly along the radial margins of the middle and proximal phalanges, is among the earliest manifestations of secondary hyperparathyroidism. In order to quantify the severity of bone resorption in these regions, the computer method analyzes the roughness of the phalangeal margins, as projected on the radiograph. The regions of interest, which contain the phalanges, are obtained from the digitized hand radiographs by an image preprocessor. The radial margin of each phalanx is detected by a model-guided boundary-tracking scheme. The roughness of these boundaries is then quantified by the mean-square variation and the first moment of the power spectrum. A receiver operating characteristic (ROC) study comparing the computer detection of hyperparathyroidism with the diagnosis by three experienced skeletal radiologists was performed by evaluating 84 hand images from 22 patients. Our present computer method can achieve a true-positive rate of 94% and a true-negative rate of 92%. Such a computer-aided diagnosis system may assist radiologists in their assessment of primary and secondary hyperparathyroidism, since it is both accurate and not subject to either intra- or interobserver variations.

Algorithms↗