延髄血管運動中枢の血圧維持機構に関する研究 ―延髄機能脱落に伴う血圧下降現象およびその機序に関する実験的研究―
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Since the repiratory center and vasomotor center are located in the medulla oblongata, the medulla oblongata has been called the vital center. However, regarding the function of both centers reports on investigations seem to be insufficient. On the other hand, in the field of neurosurgery, in brain tumor cases and brain edema due to various causes when high increased intracranial pressure results in cerebral herniation, cessation of spontaneous respiration is seen. Following this, an abrupt fall of blood pressure, it has been postulated that loss of the function of the vasomotor center in the medulla oblongata is the main cause. Among the various factors involved in the mechanism of maintenance of arterial blood pressure in additiont to neural control such as the vasomotor function in the medulla oblongata and the spinal maintenance mechanism, inasmuch as heart function, humoral factors, total blood volume and the vascular bed of each organs are involved, it would seem presumptuous to judge the function of the vasomotor center in the medulla oblongata sends vasoconstrictory impulses to arteries throughout the entire body and thus maintains the blood pressure. Since vasoconstrictory impulses are recorded as sympathetic efferent activity, in order to know the function of the vasomotor center in the medulla oblongata, it is important to observe the changes of vasoconstrictory impulses in parallel with changes in blood pressure. The author in the present paper studied the neural mechanism of control of arterial blood pressure from the stand point of sympathetic efferent activity by bilateral selective destruction of vasomotor center in the medulla oblongata and transection of medulla oblongata. 1. When the vasomotor center in the medulla oblongata is selectively destructed in the level of obex bilateraly, irreversible cessation of spontaneous respiration is seen. The blood pressure shows a two phase change. The blood pressure first shows a rapid rise and for 30～60 seconds a rise of systolic blood pressure of 73.6% in average is seen. This followed by a progressive fall and at 12～48 minutes after destruction of the medulla oblongata the blood pressure shows lowered values of 54.3～32.4 mmHg and in a 2 hours follow up the same blood pressure values were seen. Further at a later time, when total transection at the same high level of the medulla oblongata is additionally conducted, a further fall in the blood pressure was not recognized. 2. The impulse of the renal branch of the abdominal sympathetic nerve which consists of vasoconstrictory sympathetic nerve fiber alone, has a tonic discharge of 10～20 μV, 10～20/sec and a superimposing phasic discharge of 100 μV, 3～15/sec. It was noted that when bilateral selective destruction of vasomotor center in the medulla oblongata is conducted the phasic discharge disappeared immediately and this was irreversible. The tonic discharge showed an enhancement to 30 μV or thereabout 20～30/sec during the initial rise in the blood pressure. When the blood pressure reached to the maximal lowered value, the tonic discharge is inhibited to 10 μV or thereabout 10/sec or thereabout. In other words a decrease in sympathetic efferent activity was seen from the vasomotor center self by bilateral selective destruction of the vasomotor center in the medulla oblongata. 3. When bilateral selective destruction of the vasomotor center in the medulla oblongata is conducted it was noted that changes appeared in the E.C.G.. Namely, there were two groups which showed temporary cardiac. arrest immediately after destruction of the medulla oblongata followed by irregular cardiac rhythm and strong bradycardia followed by irregular cardiac rhythm. It was noted in both groups 3～6 minutes after destruction of the medulla oblongata, the irregular cardiac rhythm disappeared and at a low electric potential bradycardia made its appearance. 4. Following bilateral selective destruction of the vasomotor center in the medulla oblongata, it was noted that pressure response arising from peripheral stimulation of the somatosensory nerve and hypoxia disappeared and in addition the phasic discharge was not enhanced. It was concluded that the fall of blood pressure following destruction of the medulla oblongata can be attributed to the blocking of sympathetic efferent activity. 5. The initial temporary rise in blood pressure and abnormalities of the cardiac rhythm seen immediately after bilateral selective destruction of the vasomotor center in the medulla oblongata, cannot be seen when denevation of the vagal nerves has previously been conducted and in this experiment a lowering of blood pressure and bradycardia were seen immediately after the destruction of the medulla oblongata. Therefore it may be summarized that the initial temporary rise in blood pressure and abnormalities of cardiac rhythm are temporary phenomena arising from stimulation of the vagal nucleus. 6. The maximal lowered blood pressure value of 54.3～32.4 mmHg. following bilateral selective destruction of the vasomotor center in the medulla oblongata, when blocking of conduction of spinal sympathetic ganglia by infusion of lidocain into the spinal epidural space, lowered to 20 mmHg which is maintained by heart as pace maker and tonic discharge of the renal branch of the abdominal sympathetic nerve completely disappears. These phenomena suggest the presence of a spinal mechanism of maintenance of blood pressure.
- 札幌医科大学の論文
- 1976-08-30
札幌医科大学 | 論文
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