Der Einfluß mesencephaler Strukturen auf die phasische Blutdruckregulation

Summary

Experiments were performed on 45 cats. One group of animals was operated upon utilizing ether anesthesia which was discontinued after brain stem transsection. During the following experimental procedure the animals were immobilized with Flaxedil and artificially respired. Another series of experiments was carried out under Pentobarbital Sodium anesthesia (Nembutal).

The brain stem was successively transsected according to the Horsley-Clarke coordinates A 2 (section I), P 2 (section II), and P 6 (section III). These sections are located rostrally to the rhombencephalic vasomotor center. Blood pressure elevations were produced by intravenous injection of adrenaline.

The height of blood pressure did not change if mesencephalic structures were removed by the three sections. The duration of the adrenaline-induced rise in blood pressure was significantly prolonged after successive removal of the mesencephalic brain stem structures. This effect was abolished under Nembutal anesthesia. In this case the duration of the adrenaline-induced rise in blood pressure was found to be identical with the response to transsection in position III in unanesthetized cats.

The increased duration of the adrenaline-induced blood pressure elevation after successive transsection of mesencephalic structures can still be observed after denervation of the carotid sinus bilaterally. Even though the differences observed were less pronounced, they remained statistically significant.

Comparable results were obtained when both carotid sinus and depressor nerves were interrupted.

If all buffer nerves including both vagi were cut, the duration of the rise in blood pressure continued to increase with each step of the mesencephalic transsection.

In another series of experiments the rhombencephalic vasomotor center was isolated by deafferentiation from all buffer nerves and separated from higher brain stem structures by section III. The duration of an adrenaline-induced rise in blood pressure under these circumstances was not significantly longer than that observed after a subsequently performed spinal section at C₁.

In conclusion it can be said that mesencephalic brain stem structures are involved in the phasic regulation of blood pressure.

The results of the experiments suggest that the baroreceptor reflex arc sends collaterals to the mesencephalon. Since a less pronounced mesencephalic influence on blood pressure regulation can still be observed after deafferentiation from all buffer nerves, the conclusion is reached that additional pressosensitive structures within the mesencephalon participate in the regulation of blood pressure. Application of barbiturates induces complete blockage of the described mesencephalic influence on blood pressure regulation.