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Biomedical subjects

H L Goldsmith

Publications and source records attributed to H L Goldsmith.

At least 73 records · Page 4Linked to original sources
PubMed1974

Blood flow and thrombosis.

Platelet thrombi have been observed at bifurcations, constrictions and stenoses in the arterial tree where flow separation with accompanying vortex formation can occur. Hence, studies of the flow behavior of human blood cells in models of a vessel obstruction and a sudden expansion of a vessel lumen were carried out. These showed that the particles were subjected to first high, and then much lower shear stresses as they entered the vortices where the environment appeared favorable for the formation of aggregates. The effects of high and variable shear stress on the release reaction and aggregation of platelets were therefore studied using cells labeled with C14-Serotonin suspended in Tyrodes-albumin undergoing oscillatory tube flow for 20 min at 37degrees C. There was no significant release of serotonin due to flow alone, but the thrombin-induced release of C14-activity was appreciably greater in suspensions subjected to shear rates greater than 2000 sec-1 than in control suspensions which had been incubated at rest. The synergistic effects of the shear flow were also noted in the presence of adrenaline, which increased the release reaction, and when [Ca++] was raised above the physiological level or acetyl salicylic acid added, which inhibited the release of serotonin.

Blood Flow Velocity↗
PubMed1966

Red cells and rouleaux in shear flow.

The rotation and deformation of human red cells and linear aggregates (rouleaux) in dilute plasma suspension were observed in Poiseuille and Couette flow. Single lunideform-led erythrocyte. s and roluleauix rotated in orbits predicted by theory for rigid spheroids. Bending of rouleaux occurred at orientations at which compressive forces act on the particles and the degree of flexibility increased with the number of cells in linear array.

Cell Aggregation↗
PubMedDate not supplied

Effect of hematocrit on adenosine diphosphate-induced aggregation of human platelets in tube flow.

Both chemical and physical effects of red cells are known to play a role in the adenosine diphosphate (ADP)-induced aggregation of human platelets in sheared blood. Using a previously described double infusion technique (Bell et al., 1989a), we studied the effect of increasing hematocrit from 10 to 60% on the rate and extent of platelet aggregation with 0.2 microM ADP in citrated whole blood undergoing tube flow. Blood and agonist were rapidly mixed in a small chamber and the suspensions flowed through lengths of 1.19 mm-diameter polyethylene tubing at mean transit times from 0.2 to 42.8 s at a mean tube shear rate = 335 s-1. Effluent was collected into 0.5% glutaraldehyde, the red cells removed by centrifugation through Percoll, and all single platelets and aggregates in the volume range 1-10(5) microns3 counted and sized using an aperture impedance counter. Both the initial rate (over the first 8.6 s) and the extent of aggregation with time increased with increasing mean hematocrit up to 35.8%, being significantly greater than in citrated plasma (cPRP). However, at 61.5% hematocrit, the extent of aggregation decreased markedly to a level close to that in cPRP. We also studied the effect of washed red cells at 39% hematocrit on the aggregation of washed platelets in Tyrodes-albumin fibrinogen-free suspensions. It had previously been shown that, at > or = 335 s-1, washed platelets in platelet-rich Tyrodes (PRT) aggregated with 0.7 microM ADP. We found that red cells markedly increased the extent of aggregation from that in PRT, and promoted the formation of large aggregates, absent in PRT. Spontaneous aggregation in whole blood or washed cell suspensions in the absence of added ADP at = 42.8 s was < 10% of that in the presence of ADP. The results indicate that a physical effect of red cells, likely manifested as an increase in the efficiency of aggregate formation (Goldsmith et al., 1995), plays an important role at low and normal hematocrits; however, at high hematocrits, particle crowding impedes the formation of aggregates.

Adenosine Diphosphate↗
PubMedDate not supplied

The kinetics of thrombin- and SFLLRN-induced aggregation of human platelets in flow through tubes.

The kinetics of aggregation of human platelets activated by alpha-thrombin (0.17-0.35 nM) and the hexapeptide SFLLRN (2-10 microM) was studied in plasma-free washed cell suspensions undergoing Poiseuille flow at 37 degrees C using a previously described double infusion technique. Platelet-rich Tyrodes, prepared from venous blood by multiple centrifugation, and agonist were rapidly mixed in a small chamber and the suspension flowed through various lengths of 1.19 and 0.76 mm diameter polyethylene tubing at mean transit times t from 0.2 to 43 s and mean tube shear rates = 41.9, 335, and 1335 s-1. Effluent was collected in 0.5% glutaraldehyde and single cells and aggregates in the volume range 1-10(5) micron 3 counted and sized using an aperture impedance counter. The rate and extent of aggregation with thrombin increased with increasing [thrombin] and , and although characterized by a small initial lag time, exhibited a very rapid growth of aggregates to macroscopic size, >> 10(5) micron 3, at low and moderate shear rates. With SFLLRN, the initial lag times were appreciably longer, but subsequently aggregates also rapidly grew to macroscopic size. We hypothesize that the initial lag time is due to the time required for sufficient secretion and surface organization of ligands such as vWF (known to be released by the platelet) to occur, in order for cross-bridging of the GPIIb-IIIa receptors on adjacent platelets to take place. It appears that thrombin, which, at the low concentrations used, primarily activates the platelet via binding to the GPIb alpha receptor, can more rapidly facilitate secretion of the ligand than SFLLRN, which activates the cell via binding to the seven transmembrane domain receptor.

Adult↗