Thalamic injections of kainic acid produce myocardial necrosis.

Bilateral injections of 2–5 nmol of kainic acid into the thalamus produce periarteriorlar myocardial necrosis. In addition, gross hematuria is usually observed. Electrolytic lesions of the same area of brain and intracerebral injections of kainic acid at several other locations fail to produce these peripheral changes. Kainic acid at much higher doses subcutaneously or intraperitoneally is also inactive. Urinary noradrenaline levels are increased up to 10-fold during the post-injection period. Some protection against myocardial damage may be produced by reserpine or 6-hydroxydopamine, but atropine seems to confer no protection. The fact that myocardial damage may result from intracerebral lesions and/or pathological stimulation by kainic acid may have clinical implications. Cardiac damage occasionally results in humans from strokes and intracerebral hemorrhage and no satisfactory explanation has ever been offered for the phenomenon of interstitial myocardial fibrosis. The kainic acid model may be one means of studying this phenomenon.