Citation: Dudhani, R.V., Kyle, M., Dedeo, C., Riordan, M., Deshaies, E.M. A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage. J. Vis. Exp. (71), e4157, doi:10.3791/4157 (2013). AbstractObjective: To characterize and establish a reproducible model that demonstrates delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) in rats, in order to identify the initiating events, pathophysiological changes and potential targets for treatment.Methods: Twenty-eight male Sprague-Dawley rats (250 -300 g) were arbitrarily assigned to one of two groups -SAH or saline control. Rat subarachnoid hemorrhage in the SAH group (n=15) was induced by double injection of autologous blood, 48 hr apart, into the cisterna magna. Similarly, normal saline (n=13) was injected into the cisterna magna of the saline control group. Rats were sacrificed on day five after the second blood injection and the brains were preserved for histological analysis. The degree of vasospasm was measured using sections of the basilar artery, by measuring the internal luminal cross sectional area using NIH Image-J software. The significance was tested using Tukey/Kramer's statistical analysis.Results: After analysis of histological sections, basilar artery luminal cross sectional area were smaller in the SAH than in the saline group, consistent with cerebral vasospasm in the former group. In the SAH group, basilar artery internal area (.056 μm ± 3) were significantly smaller from vasospasm five days after the second blood injection (seven days after the initial blood injection), compared to the saline control group with internal area (.069 ± 3; p=0.004). There were no mortalities from cerebral vasospasm. Conclusion:The rat double SAH model induces a mild, survivable, basilar artery vasospasm that can be used to study the pathophysiological mechanisms of cerebral vasospasm in a small animal model. A low and acceptable mortality rate is a significant criterion to be satisfied for an ideal SAH animal model so that the mechanisms of vasospasm can be elucidated 7, 8 . Further modifications of the model can be made to adjust for increased severity of vasospasm and neurological exams. Video LinkThe video component of this article can be found at
Aortic dissection (AD) is a pathologic entity initiated from a tear in the intimal layer that allows blood flow between the intima and media, resulting in a separation of these layers into a true and false lumen. Subsequently, this flow within the false lumen encroaches on the true lumen flow and may cause malperfusion to vital organs or aortic rupture. On the basis of the anatomical location of the intimal tear, clinical presentation management may differ significantly. AD is classified as Stanford Type A or B based on the location of the intimal injury. In Stanford Type A, the site of injury is at the aortic root, which requires urgent surgical therapy. Type B are dissections that occur at or just distal to the takeoff of the left subclavian artery and in many situations can be managed medically by reduction in blood pressure.1,2 In type B dissections that fail medical management or develop malperfusion, endovascular treatment has been used and described.3 It provides a minimal invasive method; however, there are cases that may require open or a hybrid approach.3,4
Aortocoronary artery bypass grafts are time tested to be effective definitive therapy of symptomatic coronary artery disease since their inception in the 1960s. Over the years, multiple factors have affected the long-term outcome and patency rates of vein grafts. These can be divided into acute, subacute, and delayed categories. The most common causes, respectively, are thrombosis, intimal hyperplasia, and accelerated atherosclerosis. Numerous studies have analyzed postoperative angiographic images to evaluate these phenomena, and medical therapies have been instituted to prevent occlusion of these grafts. Besides these pathologic mechanisms, a surgeon and the surgeon's team must be aware of potential early reversible causes of coronary occlusion that are most often mechanical in nature. Graft kinking and external compression are known adverse events that may require early intervention to correct the underlying cause of graft occlusion. Here we present a case of graft occlusion by what we refer to as TOUGH syndrome: Thoracostomy tube Occluding Underlying coronary Graft causing Harm.
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