Related Experiment Videos
[Calcium metabolism of the thrombocytes in ischemic heart disease]
Insights
Platelets in patients with acute myocardial infarction show elevated calcium levels, which normalize over time. These calcium changes suggest disturbances in calcium metabolism are key in ischemic heart disease.
Area of Science:
- Cardiology
- Biochemistry
- Platelet Physiology
Background:
- Platelet activation and calcium signaling are crucial in ischemic heart disease (IHD).
- Understanding intracellular calcium changes in platelets can offer insights into IHD pathogenesis.
Purpose of the Study:
- To investigate intracellular calcium (Ca++) concentration changes in platelets of patients with acute myocardial infarction, unstable angina, and stable angina compared to healthy donors.
- To assess the influence of aggregation inducers on platelet Ca++ levels in these patient groups.
Main Methods:
- Utilized the fluorescent probe Quin-2 AM to measure intracellular Ca++ concentration in platelets.
- Administered aggregation inducers like Platelet-Activating Factor (PAF) and Adenosine Diphosphate (ADP) to stimulate platelets.
- Conducted dynamic follow-up of acute myocardial infarction patients and monitored platelet sensitivity during therapy for angina patients.
Main Results:
- Patients with acute myocardial infarction exhibited significantly increased intracellular Ca++ concentrations upon stimulation with PAF and ADP.
- Patients with unstable and stable angina also showed elevated calcium responses to stimulators.
- A significant decrease in intracellular Ca++ concentration was observed in acute myocardial infarction patients from day 14 onwards.
- Platelet sensitivity to inducers showed no significant change in stable angina but tended to decrease in unstable angina patients during therapy.
Conclusions:
- Elevated platelet aggregability and calcium responses in IHD patients indicate disturbances in calcium metabolism.
- These calcium metabolism disturbances play a significant role in the pathogenesis of ischemic heart disease.
Abstract:
Changes in Ca++ concentration were studied in platelets of patients with acute myocardial infarction, unstable or stable angina pectoris and those of healthy donors by means of fluorescent probe Quin-2 AM. Influence of aggregation inductors on the process of Ca++ level increase in these cells was also investigated. Intracellular Ca++ concentration increased in patients with acute myocardial infarction in the presence of PAF 2.10(-7) M (1337 +/- 255 nM) and in the presence of ADP 10(-5) M (1767 +/- 296 nM). A certain increase in calcium responses to stimulators was observed also in patients with unstable or stable angina pectoris. Dynamic follow up of patients with acute myocardial infarction starting from the 14th day demonstrated significant fall in intracellular Ca++ concentration (from 1767 +/- 296 nM to 834 +/- 186 nM, p less than 0.01). Platelet sensitivity to inductors during the course of therapy did not change significantly in patients with stable angina pectoris and tended to decrease in those with unstable angina pectoris (from 707 +/- 274 nM to 410 +/- 95 nM, p greater than 0.05). Increase in platelet aggregability and in calcium responses to stimulators in patients with IHD is an evidence of calcium metabolism disturbances which play an important role in the pathogenesis of the disease.