Treatment of proximal aortic hypertension after thoracic aortic cross- clamping in dogs: Phlebotomy versus sodium nitroprusside/isoflurane

Abstract

Thoracic aortic cross-clamping causes proximal aortic hypertension. Theoretically, the method used to treat hypertension can influence spinal cord perfusion pressure and neurologic outcome. Phlebotomy was compared to sodium nitroprusside/isoflurane in terms of ability to treat increased proximal mean aortic pressure (MAP(p)) after thoracic aortic cross-clamping in dogs. Dogs were assigned randomly to one of three groups depending on the method used to treat hypertension after cross clamping: 1) phlebotomy (n = 10); 2) sodium nitroprusside/isoflurane (n = 11); and 3) control (no treatment) (n = 8). In each dog, anesthesia was maintained with isoflurane in oxygen, 1.4% end-tidal. The thoracic aorta was occluded 2.5 cm distal to the left subclavian artery for 50 min and then was released. Hemodynamics, cerebrospinal fluid pressure (CSFP), and regional blood flows by the radioactive microsphere technique, were measured at 1) baseline; 2) 2 min after aortic cross-clamping; 3) after treatment of proximal aortic hypertension; 4) 5 min after aortic unclamping; and 5) 30 min after resuscitation. At 24 h, a neurologic assessment was performed. Thoracic aortic cross-clamping increased MAP(p), decreased distal MAP (MAP(d)), and reduced lumbar spinal cord perfusion pressure (SCPP1), [SCPP1 = MAP(d) - CSFP], in all three groups. Control of increased MAP(p) necessitated removal of 36 ± 9 ml/kg of blood in the phlebotomy group. In the sodium nitroprusside/isoflurane group, sodium nitroprusside (16 μg · kg-1 · min-1) was infused and end-tidal isoflurane concentration increased to 2.5 ± 0.7 %, restoring MAP(p) to baseline level. After treatment of increased MAP(p) in the phlebotomy and sodium nitroprusside/isoflurane groups and nontreatment in controls, SCPP1 was similar in the control and phlebotomy groups (7 ± 3 vs. 5 ± 6 mmHg) but significantly lower in the sodium nitroprusside/isoflurane group (-12 ± 5 mmHg, P = 0.04; group x time interaction). The uniformly negative SCPP1 after sodium nitroprusside/isoflurane was associated with significant increases in total cerebral blood flow, cervical spinal cord blood flow, and CSFP. In contrast, phlebotomy decreased central venous pressure and, secondarily, CSFP, without changing cerebral blood flow or cervical spinal cord blood flow. The intergroup differences in SCPP1 were not associated with measurable differences in lumbar spinal cord blood flow. After aortic unclamping, lumbar spinal cord blood flow exhibited a hyperemic response in all three groups. Higher MAP(d) in the control group during the period of aortic cross-clamping was associated with significantly more favorable acid-base status immediately after unclamping. Twenty-five dogs survived for 24 h. Eight of eight dogs in the sodium nitroprusside/isoflurane group and seven of eight in the control group had spastic paraplegia. In the phlebotomy group, three of nine dogs could walk. Neurologic outcome did not differ significantly between groups. In this experimental model (50 min of thoracic aortic cross-clamping in isoflurane-anesthetized dogs), the method of treating proximal aortic hypertension did not significantly influence either lumbar spinal cord blood flow or neurologic outcome.