Katoh Y
Nihon Seikeigeka Gakkai Zasshi. 1979 Jun;53(6):669-71.
The responses of cervical spinal cord blood flow (C-SCBF) to alteration in respiration were examined in gallamine immobilized and respiration controlled cats. Alveolar PCO2 was continuously monitored with an infrared CO2 analyzer. Mean arterial blood pressure (BP) was measured through femoral canula, which also allowed collection of arterial samples for blood gas analysis. C-SCBF was measured using thermoelectrical element which placed on the dorsal surface of the C6 segment. Simultaneously, changes in blood flow of cerebral cortex, L4 segment of spinal cord, heart and skeletal muscles, skin, kidney and spleen were also measured and compared with that of C-SCBF. Cerebrospinal fluid pressure (CSFP) was also measured on C5 segment. Changes in the arterial or alveolar PCO2 increased about 20--30 mmHg following respiration arrest or 10% CO2 inhalation, and decreased about 20 mmHg following hyperventilation during 2 minutes, respectively. Respiratory arrest or 10% CO2 inhalation induced an increase in C-SCBF, and a rise in BP and CSFP. Hyperventilation induced a decrease in C-SCBF, a fall in BP and a rise in CSFP. Effect of the respiration on blood flow of cerebral cortex, L4 segment of spinal cord or heart muscle was similar to the effect on C-SCBF in direction, but that of skin, skeletal muscle, kidney or spleen was conversely. C-SCBF increase by respiratory arrest or 10% CO2 inhalation was incompletely suppressed by pretreatment of propranolol 7 mg/kg i.v., C-SCBF decrease by hyperventilation was also incompletely suppressed by pretreatment of phentolamine 5 mg/kg i.v.. Furthermore, these C-SCBF changes were almost completely suppressed by pretreatment of phentolamine 5 mg/kg, propranolol 7 mg/kg and acetazolamide 250 mg/kg i.v. These results suggest that response of C-SCBF to alteration in respiration is chiefly induced by changes in PCO2, that CO2 acts directly on vascular smooth muscle and also on alpha and beta adrenergic receptors in the cervical spinal cord, and that CO2 has a similar action on the C-SCBF as on the blood flow of cerebral cortex, lumbar spinal cord and heart muscle.
在加拉明固定并控制呼吸的猫身上，研究了颈脊髓血流（C-SCBF）对呼吸变化的反应。用红外二氧化碳分析仪连续监测肺泡PCO₂。通过股动脉插管测量平均动脉血压（BP），该插管还可用于采集动脉血样进行血气分析。使用置于C6节段背侧表面的热电元件测量C-SCBF。同时，还测量了大脑皮层、脊髓L4节段、心脏、骨骼肌、皮肤、肾脏和脾脏的血流变化，并与C-SCBF进行比较。还在C5节段测量了脑脊液压力（CSFP）。呼吸停止或吸入10%二氧化碳后，动脉或肺泡PCO₂分别升高约20-30 mmHg，而在2分钟过度通气期间则降低约20 mmHg。呼吸停止或吸入10%二氧化碳会导致C-SCBF增加，BP和CSFP升高；过度通气会导致C-SCBF减少，BP下降，CSFP升高。呼吸对大脑皮层、脊髓L4节段或心肌血流的影响在方向上与对C-SCBF的影响相似，但对皮肤、骨骼肌、肾脏或脾脏的影响则相反。静脉注射7 mg/kg普萘洛尔预处理不能完全抑制呼吸停止或吸入10%二氧化碳引起的C-SCBF增加，静脉注射5 mg/kg酚妥拉明预处理也不能完全抑制过度通气引起的C-SCBF减少。此外，静脉注射5 mg/kg酚妥拉明、7 mg/kg普萘洛尔和250 mg/kg乙酰唑胺预处理几乎完全抑制了这些C-SCBF变化。这些结果表明，C-SCBF对呼吸变化的反应主要由PCO₂变化引起，二氧化碳直接作用于血管平滑肌以及颈脊髓中的α和β肾上腺素能受体，并且二氧化碳对C-SCBF的作用与对大脑皮层、腰脊髓和心肌血流的作用相似。
