scholarly journals OBSERVATIONS ON THE INFLUENCE OF THE HYPOPHYSIS AND THE ADRENAL CORTEX ON BLOOD PLATELET LEVELS

Blood ◽  
1949 ◽  
Vol 4 (8) ◽  
pp. 936-946 ◽  
Author(s):  
ELIJAH ADAMS

Abstract Observations were made to investigate possible endocrine influences on blood platelets. Adrenal cortex extract failed to influence the platelet counts of mice, rats, or rabbits. Adrenalectomy and sham-adrenalectomy were followed by almost identical platelet increases in mice and rats. Administration of adrenal cortex extract, or physiologic saline, to adrenalectomized rats was followed by a consistent fall in platelets not observed in sham-adrenalectomized rats, or after administering distilled water to adrenalectomized rats. Platelet levels in hypophysectomized rats were significantly lower than in unoperated controls. Splenectomy in hypophysectomized rats was followed by a maximum rise in platelets markedly lower than following splenectomy in intact rats. Bone-marrow megakaryocytes in hypophysectomized rats were significantly fewer than in intact rats. No changes in megakaryocyte number or morphology appeared following splenectomy either in intact or hypophysectomized rats.

Blood ◽  
1953 ◽  
Vol 8 (4) ◽  
pp. 342-348 ◽  
Author(s):  
J. D. FELDMAN ◽  
M. RACHMILEWITZ ◽  
O. STEIN ◽  
Y. STEIN

Abstract The intravenous administration of phenylhydrazine caused a significantly greater destruction of red cells in adrenalectomized rats than in controls. Cortisone given to adrenalectomized rats prevented this increased destruction and maintained red cells at a level comparable to controls. ACTH almost completely prevented phenylhydrazine anemia in intact rats and the red cell level was significantly higher than that in intact rats which did not receive ACTH.


Blood ◽  
1952 ◽  
Vol 7 (2) ◽  
pp. 193-206 ◽  
Author(s):  
GERALD F. HUNGERFORD ◽  
WILLIAM O. REINHARDT ◽  
CHOH HAO LI

Abstract The endocrine influences of hypophysectomy, adrenalectomy, and the administration of pituitary and adrenal hormones on the level of thoracic duct lymphocytes have been studied in test animals under standardized conditions. The following effects have been noted: 1. Numbers of thoracic duct lymphocytes are elevated after either hypophysectomy or adrenalectomy in the rat. 2. After the administration of either ACTH protein or pepsin peptide mixtures to normal or hypophysectomized rats, the number of thoracic duct lymphocytes is significantly reduced. This effect was not noted in adrenalectomized rats. These effects were observed two hours after administration of the ACTH preparations. If a shorter time elapsed, no effect was noted with the ACTH protein, nor was any effect noted with an ACTH acid peptide mixture under the conditions employed. 3. Administration of epinephrine to normal or hypophysectomized rats, singly or in combination with ACTH protein (in which case its effect was potentiated), produced a significant reduction in the number of thoracic duct lymphocytes. This effect was not observed in the adrenalectomized rat, suggesting that epinephrine may act directly in producing this effect. 4. Growth hormone (beef anterior pituitary), Pitressin, Pitocin, Adrenal Cortex Extract, cortisone acetate, and desoxycorticosterone glucoside did not alter the levels of thoracic duct lymphocytes under the conditions of these experiments.


1957 ◽  
Vol 191 (2) ◽  
pp. 319-322 ◽  
Author(s):  
Joseph T. Velardo

Previously it was reported that adrenocorticotropin (ACTH) displayed the ability to restrict the action of estradiol-17ß in uterine growth and of progesterone in decidual development. This study concerns the influence of a highly purified and potent preparation of ACTH on pregnancy and litter size in albino rats of known reproductive vigor. Experimental procedures consisted of injecting ACTH prior to, immediately after mating and 11 days after mating. These data indicate that ACTH has the ability to reduce litter size and produce a large number of stillbirths. The most marked effects were observed when ACTH was injected on the day of mating and for 6 subsequent days. Normally, the litter size of nontreated controls is 9.6 ± 0.5. The daily injection of 2.0 and 4.0 mg ACTH daily for 7 days after mating effected reduced litters, 5.0 ± 1.7 and 3.9 ± 1.5, respectively. Furthermore, such treatment produced 27 stillborns on the 2.0-mg dosage and 39 on the 4.0-mg treatment. ACTH administered to adrenalectomized rats neither modified pregnancy nor litter size. ACTH given to intact rats effected a decrease in the fetal body weights. Such was not observed in the adrenalectomized groups nor in the ACTH-treated, adrenalectomized series. These data strongly indicate that the effects observed are mediated by way of the adrenal glands, and additional evidence is offered supporting the contention that there are numerous interactions among hormones of adrenal cortex and the ovaries.


Blood ◽  
1946 ◽  
Vol 1 (1) ◽  
pp. 27-51 ◽  
Author(s):  
WILLIAM DAMESHEK ◽  
EDWARD B. MILLER

Abstract 1. The megakaryocytes of the sternal bone marrow at biopsy were studied in 11 cases of idiopathic thrombocytopenic purpura and compared with those of 10 normal cases, 5 of thrombocytopenic purpura associated with various types of splenomegaly, and of a large group of miscellaneous hematologic conditions, including leukemia, associated with a reduction in platelets. 2. Megakaryocyte counts expressed in terms of a million nucleated red cells and differential counts of megakaryocytes were performed. The megakaryocytes were classified as megakaryoblasts, promegakaryocytes, and mature forms, and were further subdivided into those showing granularity, platelet production, degenerated forms, and mitoses. 3. In the normal cases, not more than 300 megakaryocytes per million nucleated red cells were present, and an average of 68.6 per cent showed platelet production. 4. In acute idiopathic thrombocytopenic purpura, although the platelets in the circulating blood were rare, megakaryocytes were increased, being present in a proportion of 366 to 743 per million nucleated red cells. Platelet production was, however, greatly diminished and found in only 8 to 19 per cent of all megakaryocytes. Following splenectomy, there was a striking increase in platelet production, which was now present in 69 to 85 per cent of all cells; the large masses of new platelets in the marrow were often very striking. 5. In chronic idiopathic thrombocytopenic purpura, the megakaryocytes were considerably increased over normal values, but showed great diminution in platelet production; following splenectomy, extreme degrees of platelet production from megakaryocytes took place. 6. In splenomegaly of nonleukemic origin (cirrhosis, splenic vein thrombosis, Gaucher's disease, Felty's syndrome), the megakaryocytes were somewhat increased, but platelet production was normal. 7. In aplastic anemia, lymphosarcoma, acute leukemia, and other diseases invading or destroying the bone marrow, the megakaryocytes were conspicuously reduced, the few remaining cells present being of normal morphology. 8. The origin of the blood platelets from megakaryocytes, certain regulatory mechanisms for platelet production and delivery, and the possible relationship of the spleen to these mechanisms are discussed. 9. The findings of increased megakaryocytes and greatly diminished platelet production in the marrow before splenectomy and the striking increase in platelet production after splenectomy indicate a definite pathogenetic relationship of the spleen to the disease. Idiopathic thrombocytopenic purpura is probably a form of hypersplenism (splenic thrombopenia) in which, through a possible hormonal mechanism, the megakaryocytes of the bone marrow are inhibited from normal platelet production and delivery. 10. The marrow findings in idiopathic thrombocytopenic purpura are sufficiently characteristic to be of diagnostic value in differentiating the disease from leukemia and other conditions associated with a low blood platelet count.


2020 ◽  
Vol 133 (20) ◽  
pp. jcs244731
Author(s):  
Julie Boscher ◽  
Ines Guinard ◽  
Anita Eckly ◽  
François Lanza ◽  
Catherine Léon

ABSTRACTThe main function of blood platelets is to ensure hemostasis and prevent hemorrhages. The 1011 platelets needed daily are produced in a well-orchestrated process. However, this process is not yet fully understood and in vitro platelet production is still inefficient. Platelets are produced in the bone marrow by megakaryocytes, highly specialized precursor cells that extend cytoplasmic projections called proplatelets (PPTs) through the endothelial barrier of sinusoid vessels. In this Cell Science at a Glance article and the accompanying poster we discuss the mechanisms and pathways involved in megakaryopoiesis and platelet formation processes. We especially address the – still underestimated – role of the microenvironment of the bone marrow, and present recent findings on how PPT extension in vivo differs from that in vitro and entails different mechanisms. Finally, we recapitulate old but recently revisited evidence that – although bone marrow does produce megakaryocytes and PPTs – remodeling and the release of bona fide platelets, mainly occur in the downstream microcirculation.


Author(s):  
O. Behnke ◽  
J. Tranum-Jensen

Within the last decade the mammalian blood platelet has enjoyed a rapidly increasing popularity as a research object. It is widely appreciated that platelets are multifunctional, and that they play a role in a variety of physiological and pathological processes besides their main function: the formation and consolidation of a haemostatic plug (for a recent monograph, and for references, see Gordon, 1976). The platelet is an anucleate piece of cytoplasm, pinched off from megakaryocytes (MK) in the bone marrow or in the circulation (Tinggaard Petersen, 1974). Vital microscopy has shown that in the circulation the platelet is disc-shaped, that it normally does not stick to endothelium or to other blood cells, and that it is the least deformable cell in blood - the latter observation does suggest the presence of a rigid skeleton in the platelet cytoplasm.


1980 ◽  
Vol 87 (1) ◽  
pp. 131-NP ◽  
Author(s):  
F. C. LEUNG ◽  
H. T. CHEN ◽  
S. J. VERKAIK ◽  
R. W. STEGER ◽  
J. J. PELUSO ◽  
...  

The possible direct effect of corticosterone on release of pituitary prolactin was examined in a system using incubation for 8 h. Corticosterone at either 0·1 or 1 μg/ml medium had no significant effect on in-vitro prolactin release but 10 or 100 μg/ml medium produced a significant inhibition of release of prolactin. Release of LH, FSH and thyroid-stimulating hormone were not altered by 0·1, 1 or 10 μg corticosterone/ml, indicating that its action at the concentration of 10 μg/ml was specific on release of prolactin. Corticosterone injected at doses of 1 or 5 mg/kg into hypophysectomized rats with two pituitary grafts underneath the kidney capsule produced a significant fall in serum levels of prolactin when compared with control hypophysectomized rats with two pituitary grafts. Examination with the electron microscope showed that about one third of the lactotrophes from adrenalectomized rats after corticosterone injection exhibited patterns which suggested a decrease in protein synthesis when compared with lactotrophes from adrenalectomized rats given only the vehicle injection. These observations indicated that inhibition of release of prolactin by corticosterone could be exerted directly on the pituitary gland, and that the rise of serum levels of prolactin after adrenalectomy might have been due to the removal of direct inhibition by corticosterone. Male rats were adrenalectomized and 2–3 weeks later, concentrations of dopamine and noradrenaline in the medial basal hypothalamus were measured and found not to be different from values in intact rats. Dopamine metabolism also was not altered in the median eminence. The dopaminergic agonist, l-DOPA, inhibited, and the antagonists, pimozide and haloperidol, stimulated release of prolactin in both adrenalectomized and intact rats. Serotonin (5-HT) metabolism in the medial basal hypothalamus and anterior hypothalamus of adrenalectomized rats was not significantly different from values in intact rats, but a higher concentration of 5-HT was observed in the medial basal hypothalamus of adrenalectomized rats when compared with the values in intact rats. A serotonergic agonist, fluoxetine, and an antagonist, cyproheptadine, had no apparent effect on release of prolactin in intact rats, but fluoxetine produced a significant rise, and cyproheptadine, a significant lowering of serum levels of prolactin in adrenalectomized rats. These results suggest that 5-HT, but not dopamine, may be involved in the rise of prolactin after adrenalectomy.


1967 ◽  
Vol 54 (3) ◽  
pp. 428-438 ◽  
Author(s):  
B.-A. Lamberg ◽  
T. Pettersson ◽  
A. Gordin ◽  
R. Karlsson

ABSTRACT The effect of angiotensin-II-amide (Val-5-Hypertensin-II-amide, Hypertensin®, Ciba) and methopyrapone (Metopiron®, Ciba) on the lipid accumulation and activities of glucose-6-phosphate and succinic acid dehydrogenase (G-6-PD and SAD) in the zona glomerulosa (ZG) of intact and hypophysectomized rats was studied. Angiotensin induced lipid accumulation and activitation of the enzyme activity in intact rats. Hypophysectomy produced widening of the ZG and lipid accumulation. In hypophysectomized animals, the enzyme activity decreased markedly in zona fasciculata but appeared fairly intense in the enlarged ZG. The effect of angiotensin on the ZG of hypophysectomized rats was not as clearly defined as in intact animals. Angiotensin, however, seemed further to stimulate the activity of G-6-PD. Methopyrapone alone did not induce any marked changes in ZG of intact rats but when given in conjunction with angiotensin, the effect clearly exceeded that of angiotensin alone with regard to lipid accumulation and the activities of both G-6-PD and SAD. No synergistic effect was found in hypophysectomized animals.


1964 ◽  
Vol 12 (01) ◽  
pp. 179-200 ◽  
Author(s):  
Torstein Hovig

SummaryThe effect of calcium and magnesium on the aggregation of rabbit blood platelets in vitro was studied, with the following results:1. Platelet aggregation induced by ADP or collagen could be prevented by EGTA or EDTA. The aggregating effect was restored by recalcification. The effect was also restored by addition of magnesium in EDTA-PRP, but not in EGTA-PRP unless a surplus of calcium was present.2. Calcium remained in concentrations of the order of 0.15–0.25 mM after dialysis or cation exchange of plasma. Aggregation of washed platelets resuspended in such plasma could not be produced with ADP or collagen, unless the calcium concentration was increased or that magnesium was added.3. The adhesiveness of blood platelets to collagen was reduced in EGTA-PRP and EDTA-PRP. Release of ADP from platelets influenced by collagen could not be demonstrated either in EGTA-PRP (presence of magnesium) or in EDTA-PRP.4. It is concluded that calcium is a necessary factor both for the reaction leading to release of ADP and for the the aggregation produced by ADP.5. Thrombin induced aggregation of washed platelets suspended in tris-buffered saline in the presence of calcium. No effect of magnesium could be observed unless small quantities of calcium were present.


2012 ◽  
Vol 37 (5) ◽  
pp. 888-892 ◽  
Author(s):  
Jean-Michel Pontier ◽  
Emmanuel Gempp ◽  
Mihaela Ignatescu

Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.


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