Administration of IL-1ra attenuates spinal cord ischemic-reperfusion injury as evidenced by reducing both neuronal necrosis and apoptosis.
Background:Our previous studies showed that transfer of hepatocyte growth factor (HGF) gene or transplantation of marrow stromal cells (MSCs) remarkably attenuated neurologic injuries after spinal cord ischemia. We sought to investigate a novel neuroprotective strategy of transplantation of human HGF gene-modified MSCs on ischemic spinal cords. Methods: Human HGF gene was transferred into MSCs in vitro. The HGF gene-modified MSCs were transplanted by means of intrathecal injection. Two days later, spinal cord ischemia was induced by occlusion of the infrarenal aorta with a balloon catheter for 40 or 50 min. Hind-limb motor function was assessed during a 14-day recovery period with Tarlov criteria, and then histologic examination was performed. Results: Human HGF was detected in the cerebrospinal fluid from 2 to 16 days after transplantation of HGF gene-modified MSCs. Compared with the controls, transplantation of HGF gene-modified MSCs or MSCs alone significantly improved the Tarlov scores 1, 2, 7, and 14 days after spinal cord ischemia of 40 or 50 min (P Ͻ 0.01, respectively) and increased the number of intact motor neurons in the lumbar spinal cord (P Ͻ 0.01, respectively). When the ischemic period was extended to 50 min, the Tarlov scores and the number of intact motor neurons of rabbits transplanted with HGF gene-modified MSCs were markedly higher than those of the rabbits transplanted with MSCs only (P Ͻ 0.05, respectively). Conclusions: Transplantation of HGF gene-modified MSCs induces powerful neuroprotection on spinal cords against ischemia-reperfusion injury and is more therapeutically efficient than transplantation of MSCs only. P ARAPLEGIA remains a major devastating and unpredictable complication after surgical repair of descending and thoracoabdominal aortic aneurysms. This complication is attributed primarily to temporary or permanent intervention of the blood supply of spinal cords. Regardless of the progress with surgical techniques and pharmacologic interventions, the incidence of paraplegia is still high at 6.6 -8.3% in patients with extent II thoracoabdominal aortic aneurysms. 1,2Hepatocyte growth factor (HGF) was originally found from plasma and serum as a molecule that could stimulate DNA synthesis in rat and human hepatocytes.3 HGF has been identified as a potential angiogenetic factor. 4 Moreover, HGF also plays a role as a neurotrophic and survival factor to maintain the structure and function of the nervous system. 5 HGF has been reported to induce versatile neuroprotective effects both in vitro and in vivo. 6 In our previous report, transfer of human HGF gene has been shown to attenuate the neurologic injury caused by spinal cord ischemia, as evidenced by the improvement of hind-limb motor function and the protection of the motor neurons. Address correspondence to Dr. Jiang: Department of Anesthesiology, First Affiliated Hospital, China Medical University, Shenyang, P. R. China, 110001. jiangsophie@hotmail.com. Information on purchasing reprints may be found at www.anesthesiolo...
In this study, we present a successful endovascular therapy using a small-diameter stent graft for a 73-year-old man who developed asymptomatic pseudoaneurysm of the brachiocephalic artery. An 8F sheath was placed in the brachial artery, and a stiff guidewire was advanced to the descending aorta. The stent graft was delivered to the brachiocephalic artery via the brachial approach. After the initial dilatation, the stent graft was post-dilated to maximum diameter. Final digital subtraction angiography confirmed no endoleak. We believed that endovascular for a brachiocephalic pseudoaneurysm using a small-diameter stent graft might be a minimally invasive and simple method useful in clinical practice.
Background Acute kidney injury (AKI), which may progress to end-stage kidney disease (ESKD), is a potential complication of aortic dissection. Notably, in all reported ESKD cases secondary to aortic dissection, imaging evidence of static obstruction of the renal arteries always shows either renal artery stenosis or extension of the dissection into the renal arteries. Case presentation We present the case of a 58-year-old man with hypertension who was diagnosed with a Stanford type B aortic dissection and treated with medications alone because there were no obvious findings indicative of dissection involving the renal arteries. He had AKI, which unexpectedly progressed to ESKD, without any radiological evidence of direct involvement of the renal arteries. Thus, we failed to attribute the ESKD to the dissection and hesitated to perform any surgical intervention. Nevertheless, the patient’s hormonal levels, fractional excretion values, ankle brachial indices, and Doppler resistive indices seemed to indirectly suggest kidney malperfusion and implied renal artery hypo-perfusion. However, abdominal computed tomography imaging only revealed progressive thrombotic obstruction of the false lumen and compression of the true lumen in the descending thoracic aorta, despite the absence of anatomical blockage of renal artery perfusion. Later, signs of peripheral malperfusion, such as intermittent claudication, necessitated surgical intervention; a graft replacement of the aorta was performed. Post-operatively, the patient completely recovered after 3 months of haemodialysis, and the markers that had pre-operatively suggested decreased renal bloodstream normalised with recovery of kidney function. Conclusions To the best of our knowledge, this is the first report of severe AKI, secondary to aortic dissection, without direct renal artery obstruction, which progressed to “temporary” ESKD and was resolved following surgery. This case suggests that only coarctation above the renal artery branches following an aortic dissection can progress AKI to ESKD, despite the absence of radiological evidence confirming an obvious anatomical blockage. Further, indirect markers suggestive of decreased renal blood flow, such as ankle brachial indices, renal artery resistive indices, urinary excretion fractions, and hormonal changes, are useful for evaluating concomitant AKI and may indicate the need for surgical intervention after a Stanford type B aortic dissection.
Prophylactic administration of edaravone exerted a significant protective effect against postoperative neurologic dysfunction after antegrade selective cerebral perfusion in a canine model with old cerebral infarction.
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