Clot retraction facilitates clot lysis.

Platelet facilitation of clot lysis was studied using the dilute clot lysis assay, a standardized assay for fibrinolysis shown to correlate with the development of postoperative deep vein thrombosis. Clots prepared from dilute platelet poor plasma showed prolonged clot lysis when compared with clots prepared in a similar fashion from dilute platelet rich plasma. Since in the presence of platelets clot retraction or contraction occurred, we evaluated a possible direct contribution of retraction to clot lysis. Dilute platelet poor plasma clots were compacted by centrifugation, to a similar extent as that achieved during clot retraction in dilute platelet rich plasma. These clots now lysed at a rate that approached that seen with dilute platelet rich plasma clots. Using an alternate alternate approach, dilute platelet rich plasma clots were treated with cytochalasin B to prevent clot retraction. Such clots now showed prolonged lysis similar to that seen with dilute platelet poor plasma. The prolonged lysis of cytochalasin B treated dilute platelet rich plasma clots was corrected by artificial compaction of the clots. The results suggest that clot retraction markedly facilitates clot lysis, and shows that a major role of platelets to facilitate clot lysis is the effect of these cells to cause clot retraction.

A phenomenologic description of clot lysis in dilute human plasma correlating structure and function of platelets.

Platelets in a dilute platelet-rich plasma clot formed by the addition of thrombin at 4 C do not lose their alpha-granules or develop platelet-fibrin interconnections. These clots do not retract or lyse. If after clot formation for 30 minutes the clots are transferred to 37 C, the alpha-granules then disappear from the platelet, extensive platelet-fibrin interconnections develop, and the clots retract and lyse. When the dilute plasma clots, however, are formed at 37 C, alpha-granules are quickly lost, few platelet-fibrin interconnections develop, and the clots do not retract or lyse. Deoxyglucose and antimycin, when added before thrombin at 4 C, prevent the loss of alpha-granules and development of platelet-fibrin interconnections after transfer of the clot to 37 C. These inhibited platelets did not retract or lyse. From the results reported here we conclude that the development of platelet-fibrin interconnections as well as the retraction and lysis of the clot occur in conjunction with the release of alpha-granules from the platelet. It may be necessary for this release to occur after the fibrin network is completed, since release of the alpha-granules in the 37 C clot before clot formation did not result in formation of many platelet-fibrin interconnections or in clot retraction or lysis.

Lanthanide ion-induced isotropic shifts and broadening for nuclear magnetic resonance structural analysis of model membranes.

The effects of a series of aquated lanthanide ions on the nuclear magnetic resonance spectrum of phospholipid bilayer suspensions are reported. The ability of these ions to provide a spectral distinction between morphologically exterior resonances and their interior counterparts was confirmed. Measurements of the relative shifting and broadening capabilities of these ions are reported, and their correlation with solid-state magnetic susceptibility anisotropies is shown to implicate a dipolar (pseudocontact) mechanism as the source of this effect. The potential for the use of dipolar shifts as structural probes is discussed and an alternative method using dipolar shifting and broadening reagents simultaneously is presented.