Platelet Activation In Coronary System Of Patients With Coronary Artery Stenosis (CAS)

Platelets and platelet mediator substances are thought to play a role in the genesis of atheroma and spasm of coronary arteries. In the present study, indices of platelet activation (PA) were studied in the basal state and under conditions of exercise [Pacing (P) ; Handgrip (HG)] in patients with CAS and controls (CO). Pat, and methods; 22 pat. (14 with CAS > 75% in angiography; 8 with normal coronary arteries). No premedication, heparin or contrast media; Judkins technique; simultaneous sampling in the sinus coronarius (CS) and in the aorta (A) (basal, 5 min. P, 3 min. HG). Measurements: Platelet counts (PC), Beta-thromboglobulin (B-TG), platelet factor 4 (PF 4) with RIA, thromboxane B2 (RIA), ADP/collagen induced platelet aggregation (MA). Results : In the basal state no difference between A and CS was demonstrable for CO and CAS with respect to any of the above parameters. Both after P and during HG, a significant (p < 0.05) increase of B-TG was found in CAS; however, a significant increase was found in CO. In contrast to literature, no change of PC was observed. However, under P and HG a significant decrease of collagen and ADP-induced platelet aggregation (p< 0.05) was observed in CAS but not in CO. In some, but not all, CAS-patients, elevated TXB2 was demonstrable in A and CS blood. Conclusion: The present study demonstrates PA in the coronary system of pat. with CAS. Reduced aggregability but no change of PC may be due to subthreshold activation in proximity to the stenosis. This study (which avoided the use of heparin and contrast agents) also shows that PA, as measured by local sampling, is neither a sensitive nor a specific indicator of CAS.

Active state prolongation associated with depolarization in frog's skeletal muscle

If the K+ content of normal Ringer solution is increased, the duration of the plateau of the active state begins to rise at 8–10 mM [K]out. If the Cl− of the Ringer solution is replaced by NO3−, the active state duration begins to rise at 4–5 mM [K]out, and increases markedly with further depolarization. The observed dependence of active state duration on [K]out is similar to the known relation between resting metabolism and [K]out and is taken as evidence in support of the concept of subthreshold activation of the excitation–contraction coupling system by depolarization.