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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraoperative monitoring is essential for providing safe and effective care during open surgery. In this paper, numerical simulation is performed to track the flow and heat transfer of carotid arteries with and without atherosclerotic plaque in a real physiological system during surgery, in which the heat transport is first considered to couple to the blood flow due to the temperature dependence of the blood viscosity. The impacts of the operating room temperature and hematocrit (H) on the viscosity, velocity, temperature, wall shear stress (WSS), pressure drop and oscillation are investigated. The results demonstrate that the presence of plaque in the carotid artery induces a greater blood flow velocity, pressure drop, WSS, and oscillation, as well as a smaller viscosity and temperature variations. A decreasing ambient temperature leads to a decrease in the temperature and an increase in the low-WSS area, which implies a greater risk of hypothermia and atherosclerosis. As H increases, the high-WSS areas substantially expand; when H varies from 65% to 80%, WSSave increases by 70.02% and 68.57% for the arteries with and without plaque, respectively, which indicates a higher risk of vascular injury. The results obtained can serve as a guideline regarding the selection of an operating room temperature for carotid disease patients with distinct hematocrits.
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PMID:Numerical investigations of temperature and hemodynamics in carotid arteries with and without atherosclerotic plaque during open surgery. 3271 71

Sudden myocardial ischaemia causes an acute coronary syndrome. In the case of ST-elevation myocardial infarction (STEMI), this is usually caused by the acute rupture of atherosclerotic plaque and obstruction of a coronary artery. Timely restoration of blood flow can reduce infarct size, but ischaemic regions of myocardium remain in up to two-thirds of patients due to microvascular obstruction (MVO). Experimentally, cardioprotective strategies can limit infarct size, but these are primarily intended to target reperfusion injury. Here, we address the question of whether it is possible to specifically prevent ischaemic injury, for example in models of chronic coronary artery occlusion. Two main types of intervention are identified: those that preserve ATP levels by reducing myocardial oxygen consumption, (e.g. hypothermia; cardiac unloading; a reduction in heart rate or contractility; or ischaemic preconditioning), and those that increase myocardial oxygen/blood supply (e.g. collateral vessel dilation). An important consideration in these studies is the method used to assess infarct size, which is not straightforward in the absence of reperfusion. After several hours, most of the ischaemic area is likely to become infarcted, unless it is supplied by pre-formed collateral vessels. Therefore, therapies that stimulate the formation of new collaterals can potentially limit injury during subsequent exposure to ischaemia. After a prolonged period of ischaemia, the heart undergoes a remodelling process. Interventions, such as those targeting inflammation, may prevent adverse remodelling. Finally, harnessing of the endogenous process of myocardial regeneration has the potential to restore cardiomyocytes lost during infarction.
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PMID:Targeting myocardial ischaemic injury in the absence of reperfusion. 3305 4


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