By Anish Bhardwaj, Nabil J. Alkayed, Jeffrey R. Kirsch, Richard J. Traystman
Because the 3rd best reason behind loss of life within the usa, stroke bills for one in each fifteen deaths and is the main reason for incapacity within the state. Compiled by way of a well known editorial workforce, this reference bridges the space among uncomplicated technological know-how and sufferer care protocols, and collects forty three expertly written chapters that diversity from laboratory-based examine on animal types to the development, mechanisms, remedy, and analysis of illnesses equivalent to subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), focal ischemic stroke, and international cerebral ischemia.
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Extra info for Acute Stroke: Bench to Bedside (Neurological Disease and Therapy)
82. Nagai H, Noda S, Mabe H. Experimental cerebral vasospasm. Part 2: Effects of vasoactive drugs and sympathectomy on early and late spasm. J Neurosurg 1975; 42:420 – 428. 83. Allen GS, Bahr AL. Cerebral arterial spasm: part 10. Reversal of acute and chronic spasm in dogs with orally administered nifedipine. Neurosurgery 1979; 4:43 – 47. 84. Kistler JP, Lees RS, Candia G, Zervas NT, Crowell RM, Ojemann RG. Intravenous nitroglycerin in experimental cerebral vasospasm. A preliminary report. Stroke 1979; 10:26–29.
Foley PL, Caner HH, Kassell NF, Lee KS. Reversal of subarachnoid hemorrhage-induced vasoconstriction with an endothelin receptor antagonist. Neurosurgery 1994; 34:108 –112; discussion 112–103. 66. Roux S, Loffler BM, Gray GA, Sprecher U, Clozel M, Clozel JP. The role of endothelin in experimental cerebral vasospasm. Neurosurgery 1995; 37:78–85; discussion 85–76. 67. Wanebo JE, Arthur AS, Louis HG, et al. Systemic administration of the endothelin-A receptor antagonist TBC 11251 attenuates cerebral vasospasm after experimental subarachnoid hemorrhage: dose study and review of endothelin-based therapies in the literature on cerebral vasospasm.
To induce vasospasm, a number of techniques have been used that lead to the development of delayed-onset, sustained arterial narrowing. These techniques can be grouped into 3 general categories: (i) puncture of an artery (endovascularly or under direct vision), (ii) surgical exposure of an artery and placement of an autologous blood clot obtained from another vessel, and (iii) injection of blood obtained from a peripheral vessel into the subarachnoid space. A disappointing feature common to all animal models of SAH and vasospasm is the lack of vasospasm-related ischemic, neurologic deficits (28), most likely secondary to an abundance of collateral blood flow in smaller vertebrates.
Acute Stroke: Bench to Bedside (Neurological Disease and Therapy) by Anish Bhardwaj, Nabil J. Alkayed, Jeffrey R. Kirsch, Richard J. Traystman