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Triple-tracer autoradiography was used to measure topographic changes in local cerebral blood flow, cerebral tissue pH, and local cerebral glucose utilization in hyperglycemic and normoglycemic rats, all of which had undergone occlusion of the middle cerebral artery. More severe and extensive reduction of all three variables was observed in the hyperglycemic than in the normoglycemic rats. In seven normoglycemic rats, significant reduction in local cerebral blood flow (p< 0.025) was observed in the ischemic but not in the contralateral nonischemic side at the lateral portion of the caudate nucleus and the neocortex. Tissue pH was significantly lower (p < 0.025) only at the lateral portion of the caudate nucleus in the ischemic side. No significant differences in local cerebral glucose utilization were observed when the two hemispheres were compared. In the ischemic hemisphere of five hyperglycemic rats, the caudate nucleus and the neocortex exhibited significant reduction (p< 0.025) in local cerebral blood flow, tissue pH, and local cerebral glucose utilization. Even in the nonischemic hemisphere of the hyperglycemic rats, local cerebral blood flow in the caudate nucleus and the neocortex was significantly reduced (p< 0.025) compared with the normoglycemic rats. No significant change in tissue pH or local cerebral glucose utilization was observed throughout the nonischemic hemisphere of the hyperglycemic compared with the normoglycemic rats. Tissue pH was systematically lower in the hyperglycemic than in the normoglycemic rats. The threshold level of local cerebral blood flow for tissue pH reduction was 49 ml/100 g/min with a 95% confidence interval of 46-54 ml/100 g/min in normoglycemic rats (37% of control) and 63 ml/100 g/min with a 95% confidence interval of 58-70 ml/100 g/min in hyperglycemic rats (47% of control). The threshold level of local cerebral blood flow for local cerebral glucose hyper metabolism was 20 ml/100 g/min with a 95% confidence interval, of 20-24 ml/100 g/min in normoglycemic rats (15% of control) and 30 ml/100 g/min with a 95% confidence interval of 30-49 ml/100 g/min in hypergfycemic rats (22% of control). (Stroke 1988;19:764-772)

Time-dependent changes in the lumped and rate constants in a bilateral middle cerebral artery (MCA) occlusion in cats were evaluated. These variables were measured in 11 cats after a sham operation, in five after a 1-h occlusion, in two after a 2-h occlusion, in five after a 4-h occlusion, and in four after a 16-h occlusion. The time course of the cerebral tissue radioactivity [Ci* (t)] was monitored by external coincidence counting during a programmed infusion of [18F]2-fluorodeoxyglucose (FDG). Arterial plasma concentration [Cp* (t)] of tracer was kept constant during the first 45 min. Comparison of k2* and k3* in the sham-operated group, estimated by external coincidence counting, and by the ratio of extraction fractions of glucose and [18F]2-FDG, demonstrated no significant difference between these rate constants in these two groups of animals. The rate and lumped constants were also estimated from Ci* (t) and Cp* (t), as well as from the ratio of extraction fractions of glucose and [18F]2-FDG, respectively, in the MCA occlusion group. Significant decrease in k3* was observed after 1 h of occlusion (20% lower than in the sham operation, p less than 0.05); in k1* decrease occurred within 4 h of occlusion (21% lower than in the sham operation, p less than 0.05). However, decrease in k2* was observed only after 16 h of occlusion (26% lower than in the sham operation, p less than 0.05). Namely, decrease of rate constants occurred first in k3* then in k1* and k2*.(ABSTRACT TRUNCATED AT 250 WORDS)

Seafood/fish intake has been regarded as a protective factor for coronary heart disease (CHD), while smoking is a strong risk factor. To examine whether associations between smoking and risk of CHD are modified by seafood/fish intake, we studied 72,012 Japanese men and women aged 45-74 years who completed 2 food frequency questionnaires, 5 years apart, during the period 1995-2009. After 878,163 person-years of follow-up, 584 incident cases of CHD (101 fatal and 483 nonfatal), including 516 myocardial infarctions, were documented. There was a clear dose-response association between smoking and CHD risk among subjects with a low seafood/fish intake (<86 g/day) but not among those with a high seafood/fish intake (≥86 g/day). Compared with never smokers, the multivariable hazard ratios in light (1-19 cigarettes/day), moderate (20-29 cigarettes/day), and heavy (≥30 cigarettes/day) smokers were 2.39 (95% confidence interval (CI): 1.60, 3.56), 2.74 (95% CI: 1.90, 3.95), and 3.24 (95% CI: 2.12, 4.95), respectively, among low seafood/fish eaters and 1.13 (95% CI: 0.64, 1.99), 1.29 (95% CI: 0.95, 2.04), and 2.00 (95% CI: 1.18, 3.51), respectively, among high seafood/fish eaters. Compared with heavy smokers with a low seafood/fish intake, light smokers with a high seafood/fish intake had substantially reduced risk of CHD (hazard ratio = 0.57, 95% CI: 0.32, 0.98). High seafood/fish intake attenuated the positive association between smoking and risk of CHD.