Interleukin-1α is interesting lymphokine to cardiologists because it has been implicated as a regulatory protein in the development and clinical sequale of atherosclerosis, including the modulation of low density lipoprotein metabolism, the regulation of vascular smooth muscle cell mitogenesis, the stimulation of leukocyte adherence to endothelium, and procoagulant activity.

But most interleukin-1α remains in the cytosol of cells in its precursor form, and is transported to cell surface. and associated with cell membrane. Therefore considerable amount of interleukin-1α, contrast to interleukin-1β, is not released by cells into the extracellular space and the circulation. Despite of increased production of interleukin-1α, circulating level may not be elevated because of autocrine and paracrine action of that. In order to elucidate whether interleukin-1α is systematically elevated or not in patients with coronary artery disease who are complaining of chest pain, we undertook this study.

We isolated lymphocytes from peripheral blood in patients and control group. After the peripheral lymphocytes were cultured in the presence or absence of phytohemmagglutinin in RPMI-1640 media for 24 hours, we measured the content of interleukin-1α in supernatant by radioimmunoassay.

1) In the absence of phytohemagglutinin, the mean value of Interleukin-1α in the supernatant was 29.13±17.42 pmol/ml in control group and 27.28±18.80 pmol/ml in patients group(p=NS).

2) In the presence of phytohemagglutinin, the mean value of Interleukin-1α in the supernantant was 36.53±20.72 pmol/ml in control group and 152.13±91.85 pmol/ml in patient group(p<0.0001).

Significant increase of interleukin-1α in the presence of phytohemagglutinin in the patient group means that the peripheral lymphocytes in patients with coronary artery disease are activated to produce interleukin-1α.