We can speculate about the role of seven cabin-related risk factors: low humidity, hypoxia, diuretic effect of alcohol, insufficient fluid intake, smoking, "coach" position, and immobilization. In travelers with patient-related risk factors, the cabin-related risk factors are superimposed and may increase the risks for air travel-related acute venous thromboembolism. Active prophylaxis is recommended.

In this rat gracilis muscle microcirculation model, the increase in pedicle arterial leukocyte and neutrophil concentrations following ischemia-reperfusion injury was significantly reduced to sham levels by HBO treatment. This observed reduction was not attributable to HBO-induced pulmonary sequestration, which did not significantly change with HBO administration. Further investigation is required to elucidate the mechanisms of action of HBO in ameliorating ischemia-reperfusion injury in this model.

The low flow state that results from ischemia and reperfusion injury is a potentially reversible process that is important in numerous clinical situations. However, the point in time during the course of reperfusion where tissue injury becomes irreversible is unknown. This experiment evaluated the continuum of tissue damage in skeletal muscle after ischemic insult by quantifying the number of flowing capillaries and percentage muscle necrosis in a male Wistar rat skeletal muscle model. A gracilis muscle flap was raised on the vascular pedicle of 39 male Wistar rats and examined at 832x using intravital videomicroscopy. The numbers of flowing capillaries in five consecutive high-power fields were counted for baseline values. The flap was then subjected to 4 hours of global ischemia (except in sham animals, n = 7) by placing a microvascular clamp on the pedicle artery and vein. Upon reperfusion, flowing capillaries were counted in the same five high-power fields at intervals of 5, 15, 30, and 60 minutes, then at 2 to 8 (1-hour intervals), 24, and 48 hours. The gracilis muscle was then harvested at these intervals during reperfusion and assessed for viability. Compared with baseline, flowing capillaries from the ischemia and reperfusion group (mean +/- SEM) decreased significantly in the first 8 hours of reperfusion (7.7 +/- 0.2 to 3.2 +/- 0.3, p < 0.001) with minimal change noted from 8 to 48 hours. Percentage muscle necrosis increased progressively in ischemia and reperfusion preparations from 1 to 7 hours of reperfusion (16.5 +/- 2.6 percent to 38.9 +/- 1.2 percent, p < 0.001). No significant change in muscle necrosis in the ischemia and reperfusion group was noted between 7 and 48 hours. Sham preparations showed no change in the number of flowing capillaries through 3 hours of reperfusion, with a slight decrease at 24 hours. This rat gracilis microcirculation skeletal muscle model demonstrates a heterogeneous reperfusion injury. The decrease in flowing capillaries correlated with the increase in percentage necrosis and appeared to stabilize at the 7- to 8-hour interval. This finding may have important implications for the timing of interventions aimed at minimizing tissue damage from ischemia-reperfusion.

Purposes: To evaluate the natural history of the carotid artery in patients who have undergone endarterectomy of the opposite carotid artery, study its relation to new neurologic events by clinical follow-up and serial duplex scanning, review the literature for management guidelines at present, and evaluate the impact on these guidelines from recently published prospective, randomized trials. Methods: A retrospective study of 275 consecutive patients who underwent carotid endarterectomy (CEA) from December 1985 through December 1992.Results: Of 275 patients, 115 were excluded (lost to follow-up, preoperative contralateral carotid occlusion, perioperative death or stroke) leaving 160 patients as the final study group. Progression of contralateral stenosis from <50% to 50-79% occurred in 13/113 patients (11.5%), all asymptomatic; from 50-79% to 80-99% in 10/38 patients (26.3%), (two symptomatic-one transient ischemic attack [TIA] and one stroke-<50% to 80-99% in one patient who was asymptomatic); no patient progressed to total occlusion. All nine patients with an initial contralateral stenosis 80-99% remained asymptomatic (Abstract continued) prior to subsequent CEA. Neurologic events referable to the contralateral carotid distribution occurred in 10 patients of 160 (6.3%) at a mean of 12.8 months after initial surgery, six TIAs and four strokes, none of which was heralded by TIA. Thus 24 patients showed progression of stenosis, with two (8.3%) manifesting symptoms. Of the other 136 patients without progression of stenosis, eight (5.9%) developed symptoms. Conclusions: Our data and a review of the literature does not support an aggressive approach to the contralateral carotid artery stenosis. Based on NASCET and ACAS, however, new guidelines for management are suggested.

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