LEUKOCYTE MOTILITY: I. METHOD OF STUDY, NORMAL VARIATION, EFFECT OF PHYSICAL ALTERATIONS IN ENVIRONMENT, AND EFFECT OF IODOACETATE

1966 ◽  
Vol 44 (3) ◽  
pp. 475-485 ◽  
Author(s):  
Bruce M. Carruthers
Keyword(s):  
Physical Environment ◽  
Venous Blood ◽  
Small Population ◽  
Normal Variation ◽  
Peripheral Venous Blood ◽  
Human Leukocytes ◽  
Directed Motility

A method for the study of random and directed motility of human leukocytes obtained from small amounts of peripheral venous blood is presented in which the cells are studied in vitro under standardized conditions and the results are expressed quantitatively. A small population of subjects in varying states of health was studied. Considerable variation in the amount of leukocyte motility was found. Small variations in the physical environment (direction of motility in relation to gravity, and the presence of currents) had little if any influence on motility. No motility was observed in the presence of iodoacetate at a concentration of 10−4 M. These results suggest that the motility observed is active and metabolism dependent.

Activation of the Kinin-Forming System during Therapy with Cyclophosphamide

1974 ◽  
Vol 20 (1) ◽  
pp. 19-21 ◽  
Author(s):  
A Cuschieri
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Venous Blood ◽  
In Vitro Studies ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Peripheral Venous Blood ◽  
Human Whole Blood ◽  
Maximum Decrease

Abstract Venous blood kininogen is significantly decreased during therapy with cyclophosphamide in cases of advanced breast cancer. The maximum decrease in plasma kininogen coincided with onset of maximal leukopenia in the peripheral venous blood. In vitro studies showed that both human whole blood and mononuclear cell suspensions liberate free kinin when incubated with cyclophosphamide, but plateletfree human plasma does not. Evidently, the kinin-forming system is activated during therapy with cyclophosphamide, and this may account for some of its reported side effects. The in vitro studies suggest that this activation results from damage to peripheral blood leukocytes by the cyclophosphamide, with the release of intracellular proteases.

FORMATION OF EPITESTOSTERONE BY HUMAN BLOOD AND ADRENAL TISSUE

1967 ◽  
Vol 54 (2) ◽  
pp. 208-214 ◽  
Author(s):  
Jorge Blaquier ◽  
Ralph I. Dorfman ◽  
Enrico Forchielli
Keyword(s):  
Venous Blood ◽  
Endocrine Gland ◽  
Men And Women ◽  
Peripheral Venous Blood ◽  
Adrenal Tissue ◽  
Idiopathic Hirsutism ◽  
Normal Human ◽  
Normal Men ◽  
Peripheral Production

ABSTRACT Whole peripheral venous blood from normal men and women, and from females with idiopathic hirsutism was incubated in vitro with labelled testosterone, androstenedione and dehydroepiandrosterone. Epitestosterone was formed consistently from added testosterone, in some cases from androstenedione but not from dehydroepiandrosterone. The rate of formation of epitestosterone from testosterone by blood of normal men and women is similar, whereas the rate of formation in blood from female idiopathic hirsutes was several fold greater. In a similar manner, normal human adrenal tissue also formed epitestosterone from added testosterone but not from androstenedione nor dehydroepiandrosterone. These results suggest that the origin of urinary epitestosterone can be the resultant of both peripheral production and endocrine gland secretion.

INTERCONVERSION OF PROGESTERONE AND 20α-DIHYDROPROGESTERONE AND OF ANDROSTENEDIONE AND TESTOSTERONE IN VITRO BY BLOOD AND ERYTHROCYTES

1968 ◽  
Vol 58 (3) ◽  
pp. 419-444 ◽  
Author(s):  
H. J. van der Molen ◽  
D. Groen
Keyword(s):  
Dehydrogenase Activity ◽  
Venous Blood ◽  
Hydroxysteroid Dehydrogenase ◽  
Linear Increase ◽  
Equivalent Amount ◽  
Men And Women ◽  
Peripheral Venous Blood ◽  
Normal Men

ABSTRACT Peripheral venous blood and erythrocytes from normal men and women, as well as from dogs, rabbits and sheep were incubated with 14C-labeled progesterone*, 20α-dihydroprogesterone, androstenedione and testosterone. The presence in blood and erythrocytes of a 20α-hydroxysteroid dehydrogenase activity, catalyzing the interconversion progesterone ⇄ 20α-dihydroprogesterone, and of a 17β-hydroxysteroid dehydrogenase activity, catalyzing the interconversion androstenedione ⇆ testosterone was observed. Incubation with washed erythrocytes in the presence of glucose and several co-factors favoured the formation of the reduced compounds: 20α-dihydroprogesterone or testosterone. Incubations with washed erythrocytes, without addition of glucose and co-factors, favoured the formation of the oxidized compounds: progesterone and androstenedione. Incubation of steroids with whole blood, resulted in metabolism of progesterone to 20α-dihydroprogesterone and of androstenedione to testosterone. The formation of the product during incubation in vitro increased linearly with time of incubation (15—180 min). Incubations of 20 ml blood or the equivalent amount of erythrocytes with substrate amounts of steroids varying from 0.5 to 3000 μg, gave a linear increase in the amount of product formed. The possible significance of these observations in vitro for steroid metabolism in vivo is discussed.

Platelet Hyperaggregability in Ischemic Cerebrovascular Disease and Effects of Aspirin

1982 ◽  
Vol 48 (02) ◽  
pp. 117-119 ◽  
Author(s):  
M Kusunoki ◽  
K Kimura ◽  
K Nagatsuka ◽  
Y Isaka ◽  
O Uyama ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Venous Blood ◽  
Second Phase ◽  
Cerebral Angiogram ◽  
Peripheral Venous Blood ◽  
Chronic Stage ◽  
Ischemic Cerebrovascular Disease ◽  
Carotid Arterial ◽  
Platelet Hyperaggregability ◽  
The Brain

SummaryPlatelet aggregation was studied in 24 patients in the chronic stage of ischemic cerebrovascular disease (CVD), with cerebral affluent and effluent blood, i.e., carotid arterial and internal jugular venous blood, and also with peripheral venous blood. Aggregation tests were performed at various final concentrations of sodium arachidonate (A.A.) and ADP. In 17 patients, not taking aspirin, platelet aggregability in jugular venous blood was significantly accentuated compared with that in arterial and peripheral venous blood. This tendency was more marked in the patients with cerebral artery stenosis and/or occlusion than in those with normal cerebral angiogram. In 7 patients taking 500 mg or more oral aspirin, aggregation differences across the brain were not observed and A.A. aggregation and the second phase of ADP aggregation were completely suppressed. These results suggest that a prophylactic administration of aspirin may be beneficial for patients in chronic stage of CVD.

Maternal and Fetal Platelet Responses and Adrenoceptor Binding Characteristics

1985 ◽  
Vol 53 (01) ◽  
pp. 095-098 ◽  
Author(s):  
C R Jones ◽  
R McCabe ◽  
C A Hamilton ◽  
J L Reid
Keyword(s):  
Adenylate Cyclase ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Binding Characteristics ◽  
Receptor Coupling ◽  
Threshold Response ◽  
Alpha Receptors ◽  
Maternal Responses ◽  
Epidural Anaesthetic

SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to the inhibition of adenylate cyclase by adrenaline.Alpha2 adrenoceptors were investigated using [3H] yohimbine binding receptor number and were reduced modestly but significantly on fetal compared to maternal platelets. The failure of fetal platelet aggregation in response to adrenaline appears to be related to a failure of receptor coupling and may represent a delayed maturation of fetal platelet alpha receptors or a response- to increased circulating catecholamines during birth.

Increased erythrocyte adhesiveness/aggregation in the peripheral venous blood of patients with ischaemic heart disease and an eventful course

2001 ◽  
Vol 56 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Schlomo BERLINER ◽  
Rivka ROTSTEIN ◽  
Renato FUSMAN ◽  
Itzhak SHAPIRA ◽  
Ori ROGOWSKI ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Venous Blood ◽  
Peripheral Venous Blood

The procoagulant effects of factor V Leiden may be balanced against decreased levels of factor V and do not reflect in vivo thrombin formation in newborns

2006 ◽  
Vol 95 (03) ◽  
pp. 434-440 ◽  
Author(s):  
Satu Hyytiäinen ◽  
Ulla Wartiovaara-Kautto ◽  
Veli-Matti Ulander ◽  
Risto Kaaja ◽  
Markku Heikinheimo ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Factor V Leiden ◽  
Factor V ◽  
Cord Plasma ◽  
Adult Plasma ◽  
Thrombin Formation

SummaryThrombin regulation in newborns remains incompletely understood.We studied tissue factor-initiated thrombin formation in cord plasma in vitro, and the effects of Factor VLeiden (FVL) heterozygosity on thrombin regulation both in vitro and in vivo in newborns. Pregnant women with known thrombophilia (n=27) were enrolled in the study. Cord blood and venous blood at the age of 14 days were collected from 11 FVL heterozygous newborns (FVL-positive) and from 16 FVL-negative newborns. Prothrombin fragment F1+2 and coagulation factors were measured. Tissue factor-initiated thrombin formation was studied in cord platelet-poor plasma (PPP) of FVL-negative and -positive newborns, and in both PPP and platelet-rich plasma (PRP) of healthy controls. The endogenous thrombin potential (ETP) in cord PPP or PRP was ∼60% of that in adult plasma, while thrombin formation started ∼55% and ∼40% earlier in cord PPP and PRP, respectively. Further, in FVL-positive newborns thrombin formation started significantly earlier than in FVL-negative newborns. Exogenous activated protein C (APC) decreased ETP significantly more in cord than in adult PRP. In FVL-negative cord plasma 5nM APC decreased ETP by 17.4±3.5% (mean±SEM) compared with only 3.5±3.8% in FVL-positive cord plasma (p=0.01). FVL-positive newborns showed similar levels of F1+2 but significantly decreased levels of factor V compared with FVL negative newborns both in cord plasma (FV 0.82±0.07 U/ml vs. 0.98±0.05 U/ml, p=0.03) and at the age of two weeks (FV 1.15±0.04 U/ml vs. 1.32±0.05 U/ml, p=0.03). In conclusion, newborn plasma showed more rapid thrombin formation and enhanced sensitivity to APC compared with adult plasma. FVL conveyed APC resistance and a procoagulant effect in newborn plasma. Lack of elevated F1+2 levels in FVL-positive infants, however, suggested the existence of balancing mechanisms; one could be the observed lower level of factor V in FVL heterozygous newborns.

Sign in / Sign up

Export Citation Format

Share Document