FURTHER STUDIES ON THE ENDOCRINE CONDITIONING OF THE HEPARIN-INDUCED LIPEMIA CLEARING ACTIVITY (LCA) IN THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 503-510 ◽  
Author(s):  
P. Constantinides ◽  
A. Cairns ◽  
Y. So
Keyword(s):  
Dosage Level ◽  
Rat Plasma ◽  
Mild Stress ◽  
Qualitative Information ◽  
Endocrine Effects ◽  
Oil Emulsion ◽  
Intravenous Heparin ◽  
High Dosage Level ◽  
Males And Females ◽  
Low Dosage

The effects of various endocrines and of stress on the "lipemia clearing activity" (LCA) which is elicited in rat plasma by intravenous heparin injection were studied.High dosage cortisone accelerated LCA, but low dosage cortisone did not affect it. Severe catabolic stress accelerated LCA. Application of a single mild stress was ineffective, but the combination of two mild stressors accelerated LCA. ACTH had no influence on LCA, but adrenalectomy accelerated it. Stilbestrol inhibited LCA at both a low and a high dosage level, but there was no difference in LCA production between males and females or between estrous and diestrous females. Estrous females, however, displayed less LCA than ovariectomized females. Anterior pituitary extract inhibited LCA in females and hypophysectomy accelerated it in both sexes. A synthetic oil emulsion yielded the same qualitative information as lipemic plasma wherever it was used as a substrate for the clearing activity of postheparin plasma.Thus, with the exception of the effects of sex difference and low dosage cortisone, most of the previously reported endocrine effects on the LCA that follows subcutaneous heparin were also obtained when heparin was injected intravenously. The physiological significance of these findings is discussed.

FURTHER STUDIES ON THE ENDOCRINE CONDITIONING OF THE HEPARIN-INDUCED LIPEMIA CLEARING ACTIVITY (LCA) IN THE RAT

1957 ◽  
Vol 35 (7) ◽  
pp. 503-510 ◽  
Author(s):  
P. Constantinides ◽  
A. Cairns ◽  
Y. So
Keyword(s):  
Dosage Level ◽  
Rat Plasma ◽  
Mild Stress ◽  
Qualitative Information ◽  
Endocrine Effects ◽  
Oil Emulsion ◽  
Intravenous Heparin ◽  
High Dosage Level ◽  
Males And Females ◽  
Low Dosage

The effects of various endocrines and of stress on the "lipemia clearing activity" (LCA) which is elicited in rat plasma by intravenous heparin injection were studied.High dosage cortisone accelerated LCA, but low dosage cortisone did not affect it. Severe catabolic stress accelerated LCA. Application of a single mild stress was ineffective, but the combination of two mild stressors accelerated LCA. ACTH had no influence on LCA, but adrenalectomy accelerated it. Stilbestrol inhibited LCA at both a low and a high dosage level, but there was no difference in LCA production between males and females or between estrous and diestrous females. Estrous females, however, displayed less LCA than ovariectomized females. Anterior pituitary extract inhibited LCA in females and hypophysectomy accelerated it in both sexes. A synthetic oil emulsion yielded the same qualitative information as lipemic plasma wherever it was used as a substrate for the clearing activity of postheparin plasma.Thus, with the exception of the effects of sex difference and low dosage cortisone, most of the previously reported endocrine effects on the LCA that follows subcutaneous heparin were also obtained when heparin was injected intravenously. The physiological significance of these findings is discussed.

ENDOCRINE EFFECTS ON THE HEPARIN-INDUCED LIPEMIA CLEARING ACTIVITY (LCA) OF RAT PLASMA

1955 ◽  
Vol 33 (4) ◽  
pp. 530-538 ◽  
Author(s):  
A. Cairns ◽  
P. Constantinides
Keyword(s):  
Sex Difference ◽  
Chronic Stress ◽  
Strong Evidence ◽  
Anterior Pituitary ◽  
Dosage Level ◽  
Rat Plasma ◽  
Female Gonad ◽  
Endocrine Effects ◽  
Long Period ◽  
Adrenal Enlargement

A study was made of the relationships of the gonads, the adrenal, and the thyroid to the "lipemia-clearing activity" (LCA) which appears in rat plasma following heparin injection. Strong evidence was obtained that the induction of LCA by heparin is controlled by the estrogenic secretion of the female gonad: Estradiol inhibited LCA; mature females displayed less LCA than mature males, the sex difference being absent in immature animals; ovariectomy and hypophysectomy accelerated LCA; anterior pituitary extracts inhibited it in the female but not in the male; progesterone, testosterone, and orchidectomy had no effect. The adrenal-LCA relationships were complex: Adrenalectomy accelerated LCA but the effects of injected steroids depended on the dosage level and on the duration of the treatment. Short lasting injections of small amounts of glucocorticoids inhibited LCA, the effect disappearing upon prolongation of treatment. By contrast, massive amounts of glucocorticoids accelerated LCA, whether given for a short or a long period of time. Chronic stress and ACTH had no effect, despite the induction of pronounced adrenal enlargement. Injected thyroxine inhibited LCA but surgical thyroidectomy did not affect it.

ENDOCRINE EFFECTS ON THE HEPARIN-INDUCED LIPEMIA CLEARING ACTIVITY (LCA) OF RAT PLASMA

1955 ◽  
Vol 33 (1) ◽  
pp. 530-538
Author(s):  
A. Cairns ◽  
P. Constantinides
Keyword(s):  
Sex Difference ◽  
Chronic Stress ◽  
Strong Evidence ◽  
Anterior Pituitary ◽  
Dosage Level ◽  
Rat Plasma ◽  
Female Gonad ◽  
Endocrine Effects ◽  
Long Period ◽  
Adrenal Enlargement

A study was made of the relationships of the gonads, the adrenal, and the thyroid to the "lipemia-clearing activity" (LCA) which appears in rat plasma following heparin injection. Strong evidence was obtained that the induction of LCA by heparin is controlled by the estrogenic secretion of the female gonad: Estradiol inhibited LCA; mature females displayed less LCA than mature males, the sex difference being absent in immature animals; ovariectomy and hypophysectomy accelerated LCA; anterior pituitary extracts inhibited it in the female but not in the male; progesterone, testosterone, and orchidectomy had no effect. The adrenal-LCA relationships were complex: Adrenalectomy accelerated LCA but the effects of injected steroids depended on the dosage level and on the duration of the treatment. Short lasting injections of small amounts of glucocorticoids inhibited LCA, the effect disappearing upon prolongation of treatment. By contrast, massive amounts of glucocorticoids accelerated LCA, whether given for a short or a long period of time. Chronic stress and ACTH had no effect, despite the induction of pronounced adrenal enlargement. Injected thyroxine inhibited LCA but surgical thyroidectomy did not affect it.

Anticoagulation Kinetics Following Bolus Heparin Injections

1979 ◽  
Author(s):  
L F. Mockros ◽  
S.D. Hirson ◽  
L. Zuckerman ◽  
J.A. Caprini ◽  
W.P. Robinson ◽  
...  
Keyword(s):  
Least Squares Method ◽  
Test Methods ◽  
Assay Method ◽  
Heparin Dose ◽  
Intravenous Heparin ◽  
Using Data ◽  
Kinetics Of ◽  
Dose Dependent ◽  
Low Dosage ◽  
Clot Time

Anticoagulation (AC) levels were monitored simultaneously in dogs by 3 whole blood (WB) and 2 plasma CP) clotting assays. Three levels of heparin (50,100 and 200 U/kg were tested in 26 experiments by Intravenous injection. Blood was sampled at 10 and 30 min then repeated every 30 min for 4 hours. The WB clotting tests provided more sensitivity with respect to the kinetics of neutralization of the heparin than did the P assays. The levels of AC determined by each assay method was fit to exponential curves using a computerized iterative least squares method. The points were weighted inversely with the variance and the censored data was used by fitting the known values to a gamma distribution and deriving the average and SEN of the series. The coagulation curves were dependent upon the heparin dose and test methods. Extrapolated levels of initial AC demonstrate from 3 to 67 fold increases in relative clotting times for 50 and 200 U/kg dosages respectively, depending on the assay method. The AC half lives (T½) with the three WB assays varied from 15 to 41 min for the low dosage and 24 to 34 min and 27 to 30 min for 100 and 200 U/kg dosages respectively. The shortness of these T½ is a consequence-of using data acquired at 10 to 30 tnin post injection. Reanalysis of our data using sampling periods >60 min significantly prolonged the derived T½. Finally there was a marked post heparin shortening (less than pre-heparin values) of the WB assays at 2-4 hours. The values appeared to be dose dependent, as the shortest values occurred In those animals receiving the highest heparin dose. Therefore, intravenous heparin can be associated with high Initial AC followed within 2-4 hours by a quicker than normal clot time.

Endocrine Effects of Chronic Administration of Psychoactive Drugs to Prepubertal Male Rats. II. LSD

1975 ◽  
Vol 53 (6) ◽  
pp. 1023-1026 ◽  
Author(s):  
Robert Collu ◽  
Jacques Letarte ◽  
Gilles Lebœuf ◽  
Jacques R. Ducharme
Keyword(s):  
Plasma Levels ◽  
Tail Length ◽  
Chronic Administration ◽  
Male Rats ◽  
Dosage Group ◽  
Sprague Dawley ◽  
Endocrine Effects ◽  
High Dosage Group ◽  
Hydroxyindoleacetic Acid ◽  
Low Dosage

The endocrine effects of chronic D-lysergic acid diethylamide (LSD) administration to prepubertal animals were studied by injecting intraperitoneally three times a week for a month either 100 μg or 500 μg of the psychoactive drug per kilogram or the vehicle to groups of Sprague–Dawley male rats starting at 21 days of age. Animals injected with either dosage of LSD had smaller body weights than controls and tail length was significantly reduced in the high dosage group, plasma levels of growth hormone (GH) were decreased in the high dosage group, and pituitary levels in the low dosage group. Plasma levels and pituitary concentrations of luteinizing hormone and follicle stimulating hormone were not significantly modified by the drug. The low dosage of LSD decreased the brain levels of noradrenaline and increased those of dopamine, while the high dosage decreased those of 5-hydroxyindoleacetic acid. These data suggest that LSD, when administered chronically to developing animals, can inhibit body growth probably by altering the secretion of GH through modifications of its neuroendocrine control.

Effect of Triton on Lipoprotein Lipase of Rat Plasma

1957 ◽  
Vol 188 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Michael C. Schotz ◽  
A. Scanu ◽  
Irvine H. Page
Keyword(s):  
Fatty Acids ◽  
Lipoprotein Lipase ◽  
Intravenous Injection ◽  
Optical Density ◽  
Lipase Activity ◽  
Coconut Oil ◽  
Rat Plasma ◽  
Plasma Lipoproteins ◽  
Lipoprotein Lipase Activity ◽  
Oil Emulsion

When postheparin plasma was incubated with a coconut oil substrate, a decrease in optical density and an increase in unesterified fatty acids occurred. The increase in unesterified acids was prevented by previous intravenous injection of Triton to rats. Addition of post-Triton plasma to a system containing postheparin plasma and coconut oil emulsion inhibited the lipoprotein lipase activity. Incubation of Triton with coconut oil substrate before addition of postheparin plasma caused inhibition of lipoprotein lipase activity. It is concluded that inhibition of lipoprotein lipase activity by Triton is due to modification of the substrate such that the enzyme can no longer act. Further, it is suggested that the chief cause of Triton hyperlipemia is coating of the plasma lipoproteins by Triton resulting in their faulty catabolism.

scholarly journals Histopathological changes in kidney, Adrenal gland and Skin due to the Effect of Captopril in Mice

2010 ◽  
Vol 9 (3) ◽  
pp. 118
Author(s):  
H.A. N.AL-Zaiydi And S. K.Majeed
Keyword(s):  
Adrenal Gland ◽  
Therapeutic Dose ◽  
Dosage Level ◽  
Epidermal Layer ◽  
Histopathological Changes ◽  
High Toxicity ◽  
Visceral Organs ◽  
Target Organs ◽  
Males And Females ◽  
Intermediate Dose

The present study project was on toxic pathology of captopril (antihypertension drug). Thestudy was done on 44 white mice of 1-1.5 months old (males and females), the mice weredivided into four equal groups of 10 mice (5 of each sex), for 6 months. The groups included:untreated control, low therapeutic dose( 2.1 mg / kg), intermediate dose( 6.3 mg / kg) and highdose (toxic) 18.9 mg / kg, daily for 6 months . In addition a peracute high toxicity group treatedat 56.7 mg/kg day, dosage level for two weeks (2 males and 2 females). Histopathologicalexamination showed that captopril affected certain visceral organs as target organs, such askidney which showed dilated cortical tubules, adrenal gland with evidence of reduced size ofmedulla and angioedema of the lip region and areas of thickened epidermal layer.

scholarly journals Subchronic Feeding Study of N,N-Dimethylformamide in Rats and Mice

1983 ◽  
Vol 2 (6) ◽  
pp. 371-378 ◽  
Author(s):  
Peter J. Becci ◽  
Kenneth A. Voss ◽  
William D. Johnson ◽  
Michael A. Gallo ◽  
John G. Babish
Keyword(s):  
Body Weight ◽  
Food Consumption ◽  
Body Weight Gain ◽  
Dosage Level ◽  
Female Rats ◽  
Male Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
High Dosage Level ◽  
Related Increase

Wistar rats (25/ sex • group) and CD-1 mice (30/sex • group) were fed either a control diet or diet supplemented with N,N-dimethylformamide at the levels of 215, 750, and 2500 ppm for rats and 160,540, and 1850 ppm for mice. The duration of feeding was 104 days for rats and 119 days for mice. Body weight gain, food consumption, hematological and clinical chemical data, ophthalmic, gross, and microscopic examinations were used to study possible toxic or pathologic effects. A significant reduction in body weight gain was noted for male and female rats at the high dosage level. Food consumption in male rats at the high-dosage level and female rats at both the middle- and high-dosage levels was decreased. A significant dose-related increase in relative liver weights was noted in male and female rats. Absolute liver weights of male rats were comparable among groups, however, a dose-related increase was noted in female rats. No significant differences among groups were noted in body weight and food consumption data for mice. A significant dose-related increase in relative and absolute liver weights was noted in male and female mice. Histopathological evaluation revealed no evidence of a toxic effect related to feeding of N.N-dimethylformamide to Wistar rats and CD-1 mice. The increase in liver weight is considered to be a normal phenomenon (physiological adaptation) required for the biotransformation of N,N-dimethylformamide. The lack of hepatotoxicity in the present study may be the result of feeding N,N-dimethylf ormamide over waking hours versus bolus dosing (in other studies) in which hepatotoxicity was noted.

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