Comparison of the protective effects of direct ischemic preconditioning and remote ischemic preconditioning in a rabbit model of transient spinal cord ischemia.

INTRODUCTION: This study aimed to determine the relative potency of direct ischemic preconditioning (DIPC) and remote ischemic preconditioning (RIPC) for protection against ischemic spinal cord injury in rabbits and to explore the mechanisms involved. METHODS: In experiment 1, we compared the neurological and histopathological outcomes of DIPC, kidney RIPC, and limb RIPC. The DIPC and kidney RIPC groups received two cycles of 5-min occlusion/15-min reperfusion of the abdominal aorta and left renal artery, respectively. The limb RIPC group received two cycles of 10-min occlusion/10-min reperfusion of the femoral arteries bilaterally. Thirty minutes after the conditioning ischemia, spinal cord ischemia was produced by occluding the abdominal aorta for 15 min. In experiments 2 and 3, we investigated whether pretreatment using a free-radical scavenger, dimethylthiourea (DMTU), an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), or a mitochondrial ATP-sensitive potassium channel antagonist, 5-hydroxydecanoate (5HD), could attenuate the protective effects of DIPC. In experiment 4, comprehensive analysis of phosphorylated proteins in the spinal cord was performed using a Proteome Profiler Array followed by immunoblotting to elucidate the signal pathway activated by DIPC. RESULTS: In experiment 1, DIPC improved the neurological and histopathological outcomes, whereas kidney and limb RIPC had no protective effects. In experiments 2 and 3, strong protective effects of DIPC were reconfirmed but were not attenuated by DMTU, DPCPX, or 5HD. In experiment 4, DIPC induced phosphorylation of Akt2. CONCLUSIONS: DIPC, but not kidney or limb RIPC, protected against ischemic spinal cord injury in rabbits. Akt2 might contribute to this protective effect.

Monitoring of central venous pressure and stroke volume variation in a case with a ruptured brain arteriovenous malformation and Fontan circulation.

BACKGROUND: Patients with complex congenital heart disease increasingly undergo noncardiac surgeries because of advancements in surgical techniques and medical management. In Fontan circulation, maintaining an adequate transpulmonary gradient is essential for preserving both pulmonary blood flow and cardiac output. However, intraoperative circulatory monitoring of Fontan patients has not been established. CASE PRESENTATION: A 17-year-old girl required an emergency craniotomy for ruptured arteriovenous malformation. She had a surgical history of bidirectional Glenn operation and Fontan palliation for her congenital hypoplastic left heart syndrome and double outlet right ventricle. We performed general anesthesia with continuous monitoring of central venous pressure (CVP) and stroke volume variation (SVV). Transesophageal echocardiography was not conducted because of difficulty in manipulating the probe due to the patient's position and surgical setting. After incision of the dura, approximately 1700 ml of rapid blood loss from the arteriovenous malformation was observed in 30 min. In this period, CVP decreased from 15 to 5 mmHg or less. In contrast, there was only a slight rise in SVV from 5 to 8%. We rapidly administered fluid and then transfused blood, and CVP gradually recovered to 10-15 mmHg. During the surgery, circulatory collapse was not observed. The patient was transferred to the intensive care unit under sedation and controlled ventilation. CONCLUSIONS: CVP decreased sharply, whereas SVV rose only slightly during acute bleeding in the present case. CVP monitoring may have been useful for the management of an acute bleeding case with a Fontan circulation but SVV may not have been reliable. As more patients with a Fontan circulation undergo noncardiac surgeries, appropriate circulatory monitoring in these patients should be further investigated.