No immediate clinical implications from feline model; leaves open translation of LV receptor mechanisms to human ischemia.
The activity in unmyelinated afferents from left ventricular receptors was examined in cats during shortlasting general asphyxia and during transient occlusion of one coronary artery. After 40–70 s of asphyxia the receptors increased their activity. The firing initially displayed a cardiac rhythm but became continuous when the asphyxia was prolonged and intensified. This increased activity was closely related to a mechanical distension of the left ventricle when the nutritional supply was compromised suggesting a mechanoreceptor rather than a chemo‐receptor function of the recepton. Coronary occlusion also caused an activation of the ventricular receptors after a latency of about 35 s with an initial cardiac rhythmicity which became continuous with prolonged occlusions. The receptor activation appeared also in this situation to be caused by the mechanical bulging of the ischemic area of the left ventricular wall, rather than by chemical factors.
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Peter Thorén (1971) studied this question.
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