RESUMEN
The purpose of this study was to review the positive angiographic findings in patients with polyarteritis nodosa (PAN). The authors reviewed the angiograms of 56 consecutive patients (25 women and 31 men; age range, 18-81 years; mean age, 55 years) with PAN and arterial abnormalities consistent with necrotizing vasculitis. Aneurysms were present in 27 patients and segments of ectasia were present in seven patients, for a total of 34 (61%) of 56 patients with aneurysmal lesions. The remaining 22 (39%) patients had arterial lesions that were occlusive: luminal irregularity, stenosis, or occlusion. All but one of the patients with an aneurysm also had occlusive lesions. Therefore, 55 (98%) of the 56 patients were found to have occlusive lesions. Skeletal muscle arteries were affected in 18 patients, nine in the extremities. The most frequent finding in patients with PAN was occlusive arterial lesions. Although the presence of aneurysms increases specificity for the diagnosis of PAN, many patients have only occlusive lesions. Involvement of skeletal muscle arteries was common.
Asunto(s)
Angiografía , Poliarteritis Nudosa/diagnóstico por imagen , Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Studies were designed to examine aspects of phosphorylation and dephosphorylation in rat lung cells in response to hyperoxic exposure. Protein kinase and phosphatase activities were measured in preparations of lungs from normoxic rats, hyperoxia-exposed rats (95% O2 for 60h), and rats recovering in room air for 1 and 3 days. Protein kinase C (PKC) activity immediately postexposure was significantly lower than in normoxic controls (normoxia 127.1 +/- 13 vs. hyperoxia 101.5 +/- 6 pmol/min mg-1) and continued to decline during the recovery period (85.3 +/- 4 and 78.2 +/- 6 pmol/min mg-1 at 1 and 3 days recovery, respectively). The PKC activity did not translocate from cytoplasm to the membranes. In contrast, PKA activity did not change in response to hyperoxia exposure or recovery. Protein phosphatase activity was decreased significantly by hyperoxia exposure (normoxia 30.7 +/- 3 vs. hyperoxia 21.9 +/- 1 pmol/min microgram-1) but returned to normoxic control levels by 1 and 3 days (24.1 +/- and 31.5 +/- 1 pmol/min microgram -1, respectively). Protein phosphatase activity was inhibited by okadaic acid (Ki = 1 nM) and calyculin A (Ki = 0.61 pM), indicating a type 2A protein phosphatase. Enzyme activities in cultured type II alveolar cells paralleled those observed in whole lung preparations. Decreased enzyme activities in the lung may be located to the development of acute lung injury during hyperoxic exposure.