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L V McIntire

Publications and source records attributed to L V McIntire.

At least 127 records · Page 7Linked to original sources

The structural properties and contractile force of a clot.

When citrated plasma is recalcified, it forms a viscoelastic gel--a clot. The relationship between platelet contractility and clot rigidity was studied by using a rheological technique which simultaneously measured both the dynamic rigidity modulus and the contractile force during gel formation with platelet rich plasma (PRP). Protein network formation in a clot was accompanied by a contractile force throughout the clotting process. PRP demonstrated a maximum elastic modulus of 6,000 dynes/cm2 and a maximum contractile force/area of 1,500 dynes/cm2. The values of these parameters for a platelet-free clot (PFP) were 700 dynes/cm2 and less than 100 dynes/cm2 respectively. Sonicated control PRP and PRP from a Glanzmann thrombasthenia patient both clotted in a manner similar to PFP. Metabolic inhibitors, 2-deoxy-D-glucose and KCN (5 mM each), retarded the clotting curves of PRP. Cytochalasin B and E suppressed both structural rigidity and force generation in a concentration-dependent manner similar to their inhibitory effect on actin polymerization in platelets. Colchicine (2.5 mM) or vinblastine (0.11 mM) did not affect these clotting curves. Thrombin-activated, fixed platelets did not generate any force, nor did they significantly increase clot rigidity. Streptokinase induced a concurrent decrease of both rigidity and force in PRP clots. The elastic modulus of a PFP clot could be increased to 2,500 dynes/cm2 by externally straining the network with an axial force/area of 1,500 dynes/cm2. Our results indicate that clot structure formation in PRP is strongly coupled to the contractile force generated by the platelet microfilament system and that this force modulates clot rigidity.

Blood Coagulation↗

Problems in measurement of erythrocyte calcium.

As calcium has increasingly been the object of study in erythrocyte physiology, we reviewed the current methodologies for determination of calcium by atomic absorption spectrometry. The published normal values for erythrocyte calcium vary from 5 to 500 mumol/liter of packed cells. A method based on Harrison and Long's determination of calcium is presented and shows normal red cell calcium concentration to be 0.0149 +/- 0.0023 mumol/ml of packed red cells. The influence of temperature and type of crucible used in ashing red cells is assessed. The method of additions is employed to corroborate our results.

Calcium↗

Differential effects of cytochalasin B on platelet release, aggregation and contractility: evidence against a contractile mechanism for the release of platelet granular contents.

Cytochalasin B alters the structure and functional properties of filamentous actin. Platelet-mediated clot retraction in dilute platelet-rich plasma (PRP) is inhibited progressively at cytochalasin B concentrations of 0.01 mg/ml, 0.05 mg/ml and 0.1 mg/ml. Dynamic rheological measurements of recalcified PRP in a Weissenberg Rheogoniometer indicate that platelet contractility (as reflected in measurements of elastic moduli) is reduced by 33%, 57% and 63% at cytochalasin B concentrations of 0.01, 0.05 and 0.1 mg/ml, respectively. In contrast, pre-incubation of human platelet-rich plasma (PRP) with 0.01 mg/ml or 0.05 mg/ml cytochalasin B does not inhibit collagen-induced [14C]serotonin release on collagen-induced-platelet aggregation, which is dependent on the release of ADP from platelet dense granules. Even at a cytochalasin B concentration of 0.1 mg/ml, collagen-induced [14C-]serotonin release and aggregation are impaired only moderately. Cytochalasin B does not interfere with the uptake by platelets of [14C-]-serotonin, or with the kinetics and extent of clot formation in platelet-free plasma. Thus, concentrations of cytochalasin B which impair platelet contractility do not inhibit the release of platelet dense granule contents. It is concluded that neither the platelet release reaction nor platelet aggregation is dependent on platelet contractile mechanisms.

Actins↗

Effect of transfusion on hemoglobin flow and oxygen delivery in patients with sickle cell anemia--in vitro evaluation.

A method is given for the in vitro evaluation of transfusion therapy of patients with sickle cell anemia. Changes in volumetric flow rate, hemoglobin flow rate, and oxygen delivery at three values of PO2 (25, 40, and 80 mmHg) induced by transfusion of two units of AA blood in three patients are evaluated. The viscosity-shear rate data are obtained in a precision cone and plate viscometer with controlled environment. This data is then used to calculate flow rates in model tubes of varying diameters (50-500 microns). The increase in oxygenated hemoglobin flow rates at low oxygen tensions after transfusion can be striking-sometimes greater than a factor of two. A preliminary evaluation of the potential effect of auto-transfusion or androgen therapy on these flow rates is also discussed.

Anemia, Sickle Cell↗

Enzyme release and morphological changes in leukocytes induced by mechanical trauma.

Polymorphonuclear (PMN) leukocytes exposed to mechanical trauma in vitro will release enzymes both from azurophilic and specific granules at shear stress levels of between 75 and 150 dyn/cm2 for 10 min. In addition, at these shear stresses the leukocyte count in whole blood decreased only slightly and the number of ruptured leukocytes on Wright-stained blood films increased significantly. At higher shear stresses, enzyme release and leukocyte damage increased monotonically. Transmission electron microscopy evaluation of sheared PMNs revealed that remaining intact cells had minor morphological changes at stresses of 150 dyn/cm2. They were characterized by clublike cytoplasmic potrusions, spherical shape, and a circumferential distribution of cytoplasmic granules. At higher shear stresses (600 dyn/cm2) cell destruction was marked. Intact PMNs contained fewer cytoplasmic granules, a large number of vacuoles, and condensed nuclear chromatin. These studies show that PMN morphology and function are at least as sensitive to mechanical trauma as similar platelet alterations seen in other studies.

Alkaline Phosphatase↗