Vascular air embolism is a potentially life-threatening event that is now encountered routinely in the operating room and other patient care areas. The circumstances under which physicians and nurses may encounter air embolism are no longer limited to neurosurgical procedures conducted in the "sitting position" and occur in such diverse areas as the interventional radiology suite or laparoscopic surgical center. Advances in monitoring devices coupled with an understanding of the pathophysiology of vascular air embolism will enable the physician to successfully manage these potentially challenging clinical scenarios. A comprehensive review of the etiology and diagnosis of vascular air embolism, including approaches to prevention and management based on experimental and clinical data, is presented. This compendium of information will permit the healthcare professional to rapidly assess the relative risk of vascular air embolism and implement monitoring and treatment strategies appropriate for the planned invasive procedure.
Background and Purpose-We have previously shown that 17-estradiol reduces infarction volume in female rats. The present study determined whether single injection or chronic implantation of estrogen confers neuroprotection in male animals with middle cerebral artery occlusion (MCAO) and whether there is an interaction with endogenous testosterone. Methods-Male Wistar rats were treated with 2 hours of reversible MCAO. In protocol 1, acute versus chronic estrogen administration was examined in groups receiving the following: Premarin (USP) 1 mg/kg IV, immediately before MCAO (Acute, nϭ13, plasma estradiolϭ171Ϯ51 pg/mL); 7 days of 25 g (E25, nϭ10, 10Ϯ3 pg/mL) or 100 g 17-estradiol (E100, nϭ12, 69Ϯ20 pg/mL) by subcutaneous implant; or saline (SAL, nϭ21, 3Ϯ1 pg/mL). Laser-Doppler flowmetry was used to monitor the ipsilateral parietal cortex throughout the ischemic period and early reperfusion. At 22 hours of reperfusion, infarction volume was determined by 0 2,3,5-triphenyltetrazolium chloride staining and image analysis. In protocol 2, rats were castrated to deplete endogenous testosterone and then treated with estradiol implants: castration only (CAST, nϭ13, estradiolϭ5Ϯ2 pg/mL), sham-operated (SHAM, nϭ10, 4Ϯ2 pg/mL), estradiol implant 25 g (CASTϩE25, nϭ16, 7Ϯ2 pg/mL) or 100 g (CASTϩE100, nϭ14, 77Ϯ14 pg/mL). Results-Cortical infarct volumes were reduced in all estrogen-treated groups: Acute (21Ϯ4% of ipsilateral cortex), E25 (12Ϯ5%), and E100 (12Ϯ3%) relative to SAL (38Ϯ5%). Caudate infarction was similarly decreased: Acute (39Ϯ7% of ipsilateral striatum), E25 (25Ϯ7%), and E100 (34Ϯ6%) relative to SAL (63Ϯ4% Key Words: estrogen Ⅲ cerebral ischemia Ⅲ neuroprotection Ⅲ stroke Ⅲ testosterone Ⅲ rats R ecent evidence emphasizes striking sex-linked differences in brain damage after experimental stroke. We have shown previously that female rats sustain approximately one third of the total tissue infarction observed in agematched males during middle cerebral artery occlusion (MCAO).1 Furthermore, both endogenous and exogenous estrogens improve tissue damage after stroke and brain injury in female animals.1-4 Estrogen may act both by vascular mechanisms to enhance residual ischemic blood flow and by direct neuroprotection of neurons and glia in female brain, [5][6][7][8][9] but effects in the male brain are unclear. The major male reproductive steroid, testosterone, has not been studied in experimental cerebral ischemia and remains an alternative to estrogen as the source of sex differences in stroke. Like estrogen, testosterone is a vasodilator of some vascular beds, 10,11 possibly by a common mechanism involving vascular smooth muscle potassium channels.9 -11 The purpose of the See Editorial Comment, page 1670present study was to determine whether estrogen administered to adult male Wistar rats confers protection after MCAO and whether there is a potential interaction between exogenous estrogen and native testosterone. Materials and MethodsThis study was conducted in accordance with the National Institutes of Health guid...
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