[An experimental study on the regional blood flow in the cervical spinal cord --the influence of respiration (author's transl)]
- PMID: 490014
[An experimental study on the regional blood flow in the cervical spinal cord --the influence of respiration (author's transl)]
Abstract
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.
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