Reflexogenic areas of the cardiovascular system.

Abstract

After the discovery ofthe pulmonary circulation by Ibn-an-Nafis in the thirteenth century and by Servetus in the sixteenth century and the discovery of the systemic circulation of the blood by Harvey in 1628, arterial pressure was first measured by Stephen Hales in 1733 and then by Poiseuille in 1828 and Ludwig in 1847, wno recorded arterial blood pressure by means ofa glass tube or a mercury manometer connected with an artery. As a result of numerous observations, the physiologists concluded that the arterial pressure was subject to regulation and tried to clarify the mechanisms. In 1836 Astley Cooper observed that compression of both common carotid arteries, which induced a fall of arterial pressure in the head and brain, provoked acceleration of the heart rate and a rise in the systemic arterial pressure (1). This observation was confirmed by Magendie in 1838 (2). Experiments done between 1877 and 1926 by several workers (3-10) showed that a rise of blood pressure in the carotid-cephalic circulation induces bradycardia and a fall of the systemic arterial pressure, while a drop in the carotid-cephalic pressure provokes acceleration ofthe heart rate and a rise ofsystemic arterial pressure. All these experimental observations were considered to be a demonstration ofa direct sensitivity of the cardiovascular centers to blood pressure variations. The direct central regulation and homeostasis of arterial pressure by means of the action of blood pressure variations on the cardiovascular centers was thus generally accepted. But as early as 1900 Pagano (11) and Siciliano (12), of the laboratory of Spallitta in Palermo, published an interesting series of experiments. Siciliano showed that while clamping of both common carotid arteries induced tachycardia and a rise in the systemic arterial pressure, clamping of