Background. Optimal treatment practices and factors associated with in-hospital mortality in spontaneous pneumothorax (SP) are not fully understood. We evaluated prevalence, clinical characteristics, and in-hospital mortality among Japanese patients with primary or secondary SP (PSP/SSP). Methods. We retrospectively reviewed and stratified 938 instances of pneumothorax in 751 consecutive patients diagnosed with SP into the PSP and SSP groups. Factors associated with in-hospital mortality in SSP were identified by multiple logistic regression analysis. Results. In the SSP group (n = 327; 34.9%), patient age, requirement for emergency transport, and length of stay were greater (all, p < 0.001), while the prevalence of smoking (p = 0.023) and number of surgical interventions (p < 0.001) were lower compared to those in the PSP group (n = 611; 65.1%). Among the 16 in-hospital deceased patients, 12 (75.0%) received emergency transportation and 10 (62.5%) exhibited performance status (PS) of 3-4. In the SSP group, emergency transportation was an independent factor for in-hospital mortality (odds ratio 16.37; 95% confidence interval, 4.85–55.20; p < 0.001). Conclusions. The prevalence and clinical characteristics of PSP and SSP differ considerably. Patients with SSP receiving emergency transportation should receive careful attention.
We tested the efficacy of preischemic and postischemic systemic treatment with 30,000 units polyethylene glycol-conjugated superoxide dismutase in a reperfusion model of focal cerebral ischemia. Forty-one anesthetized cats underwent 2 hours' occlusion of the left middle cerebral artery and both common carotid arteries followed by 4 hours of reperfusion. Cats were blindly assigned to one of three groups: treatment with vehicle (10% polyethylene glycol in saline, n=17), pretreatment with drug 3 hours before ischemia (n=12), and posttreatment with drug at the time of reperfusion (n=12). Size of the ischemic injury was calculated from 2,3,5-triphenyltetrazolium chloride staining. Injury in the caudate nucleus was significantly reduced with pretreatment (28 ±6% of ipsilateral caudate volume, mean±SEM) compared with the vehicle (56 ±8%). Posttreatment did not significantly ameliorate caudate injury (46 ±10%). Between the first and second hours of ischemia ipsilateral caudate blood flow determined using microspheres increased significantly from 11±4 to 16±5 ml/min/100 g with pretreatment, but blood flow remained constant throughout ischemia with vehicle (8 ±2 ml/min/100 g) and posttreatment (10±3 ml/min/100 g). The size of cortical injury (vehicle, 17±5%; pretreatment, 11 ±3%; posttreatment, 17±5% of hemispheric volume) did not differ significantly among groups. Somatosensory evoked potential recovery did not differ among groups. We conclude that pretreatment with conjugated superoxide dismutase can ameliorate the extent of injury in an end-artery region, such as the caudate nucleus, in a reperfusion model of focal ischemia. Because posttreatment was less effective and pretreatment led to increased blood flow during ischemia, superoxide dismutase may operate via a vascular mechanism during ischemia. (Stroke 1991^2:1193-1200) O xygen radicals may contribute to reperfusion injury, depending on the severity and duration of ischemia. 1 In heart and intestines, intravenous administration of free radical scavenger enzymes such as superoxide dismutase (SOD) can ameliorate damage.2 -3 In brain, positive evidence for protection with administration of these enzymes after global ischemia is less compelling, 4 -5 although improved cerebral oxygen consumption has been reported in postasphyxic lambs.6 However, with focal ischemia, Liu et al 7 reported a 24% amelioration of Received November 12, 1990; accepted May 22, 1991. infarct volume after 24 hours' occlusion of the middle cerebral artery (MCA) combined with 90 minutes' occlusion of both common carotid arteries in rats pretreated with polyethylene glycol (PEG)-conjugated SOD and catalase. Conjugation with PEG extends the half-life of circulating SOD beyond 1 day. 2 Similar reductions in infarct size have been reported after pretreatment with liposome-entrapped SOD in rats with permanent occlusion of the right MCA and right carotid artery plus 1 hour's occlusion of the left carotid artery. 8 We examined the efficacy of PEG-SOD in a model of focal ischemia that permits full rep...
To enhance the consistency of the ischemic insult caused by reversible transorbital middle cerebral artery occlusion, we investigated the variability of somatosensory evoked potential amplitudes and regional cerebral blood flow in 26 anesthetized cats using four procedures to induce transient ischemia. These procedures included 60 minutes of left middle cerebral artery occlusion with or without left common carotid artery occlusion and 120 minutes of left middle cerebral artery occlusion with or without bilateral common carotid artery occlusion. Blood flow in the left middle cerebral artery territory was markedly and consistently reduced to <20 ml/min/100 g with simultaneous occlusion of the left middle cerebral artery and both common carotid arteries. The standard deviation of blood flow with this procedure (5.4) was less than that with the other three procedures (13-25). The amplitudes of ipsilateral somatosensory evoked potentials were decreased to approximately 20% of control during ischemia with all four procedures. During reperfusion, amplitudes recovered more slowly, to half of control, after both procedures involving 120 minutes of ischemia. After 120 minutes of reperfusion, the range of amplitudes was smallest in the group exposed to middle cerebral artery occlusion with bilateral common carotid artery occlusion. The degree of recovery of the somatosensory evoked potentials correlated with residual blood flow in both the ipsilateral middle cerebral artery territory and in the white matter during ischemia. We conclude that the most consistent model of focal ischemia and reperfusion in cats in which there is partial recovery of somatosensory evoked potentials is occlusion of one middle cerebral artery and both common carotid arteries for 120 minutes. (Stroke 1990:21:908-916)
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