The data indicate that sensory and motor neocortex and hippocampal neurons are selectively vulnerable to neurologic injury after HCA as indicated by elevated levels of TUNEL-positive cells in these brain regions. It is noteworthy that evidence of significant neuronal injury is observed in the acute state. The absence of morphological evidence of apoptosis or necrosis with high levels of TUNEL-positive cells, strongly suggests activation of the apoptotic mechanisms at this early stage. These findings are compatible with data showing morphological evidence of apoptosis in these regions after a more prolonged period in a chronic animal model. The mechanisms underlying neuronal injury, and potential neuroprotective strategies remain to be elucidated.
To evaluate the thrombogenicity of transvenous silicone and polyurethane pacemaker leads, 9 of 12 anesthetized Yorkshire pigs (27-32 kg) were implanted with silicone (n = 5) or polyurethane (n = 4) pacemaker leads via a femoral vein. The remaining three pigs served as controls. All 12 pigs were injected with autologous indium-111 labeled platelets (300-420 muCi) 24 hours before anesthesia induction. The pigs were monitored for 3 hours under a gamma camera. Radioactivity in blood and lead segments was measured with a gamma counter. Platelet deposits were denser on silicone leads (441.58 +/- 915.0 to 2.19 +/- 2.07) than on polyurethane leads (1.21 +/- 1.33 to 0.27 +/- 0.14) (P > 0.05). Denser platelet deposits were detected at the tip of all leads. Density of platelet deposits declined from tip to distal segments in silicone leads. The percentage of injected platelet radioactivity in the lungs of pigs with either silastic leads (12.9 +/- 2.3%) of polyurethane leads (10.1 +/- 2.2%) was higher than in the controls (4.6 +/- 0.5%) (P < 0.05). This difference indicates thrombus formation and embolization in the lungs early after lead implantation. Thrombogenicity of polyurethane leads may be lower than that of silicone leads.
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