Cytochrome P450 down-regulation by serum from humans with a viral infection and from rabbits with an inflammatory reaction.

Serum from humans with an upper respiratory viral infection (HS(URVI)) and from rabbits with a turpentine-induced acute inflammatory reaction (RS(TIAR)) reduces the activity of hepatic cytochrome P450 (P450) following 4 h of incubation. The aim of the present study was to assess the effect of HS(URVI) and RS(TIAR) on P450 activity and expression following 24 h of incubation with hepatocytes from control (H(CONT)) and rabbits with a TIAR (H(INFLA)). RS(TIAR) incubated with H(CONT) for 24 h reduced P450 content and activity, and CYP3A6 by 45%, without changing CYP1A1 and 1A2; when incubated with H(INFLA), RS(TIAR) decreased P450 content and activity without affecting CYP1A1 or 1A2. HS(URVI) incubated for 4 h with H(CONT) decreased P450 activity without affecting the amounts of CYP1A1, 1A2, or 3A6, although when incubated for 24 h, P450 activity and CYP3A6 amount decreased. HS(URVI) incubated with H(INFLA) for 4 h reduced P450 content and activity, and incubated for 24 h reduced activity, P450 content, and amount of CYP1A1 and 1A2 proteins. The present study demonstrates that 1) the effect of RS(TIAR) and HS(URVI) depends upon the susceptibility of the hepatocyte, i.e., H(CONT) or primed H(INFLA); 2) P450 down-regulation is preceded by a decrease in P450 activity; 3) the nature of the inflammatory reaction determines the repercussions on P450 activity and expression; and 4) CYP3A6 is more vulnerable than CYP1A1 and 1A2 to the down-regulation provoked by an inflammatory challenge.

Vascular nurse as a smoking cessation specialist.

Cigarette smoking is a leading cause of disease and preventable death in the United States and is a major contributing factor to the development and progression of peripheral arterial disease. Vascular risk decreases immediately after smoking cessation and within 5-10 years reaches a level almost equivalent to that in nonsmokers. Despite the strong emphasis on smoking cessation, relapse frequently occurs. Smoking relapse is affected by physiologic and psychosocial factors. As a smoking cessation specialist, the vascular nurse can incorporate pharmacologic therapies and behavioral counseling into the treatment plan for patients with peripheral arterial disease. The role of a smoking cessation specialist enables the vascular nurse to assist patients in successfully overcoming these factors and maintaining abstinence.

Influence of lung volume on collateral resistance during methacholine-induced bronchospasm.

We tested the hypothesis that lung inflation in response to a bronchospasm could be beneficial by maintaining the lung collateral channels open. Six mild asthmatics were studied on 2 separate days. The first day we determined the methacholine dose response and measured collateral resistance (Rcoll) before and during the metacholine-induced bronchospasm and the effects of decreasing lung volumes on Rcoll. The lung volume changes were induced by applying progressively increasing positive extrathoracic pressures (PEP). The second day we measured the changes in end-expiratory lung volume (EELV) resulting from the inhaled methacholine and from the applied positive extrathoracic pressure. With the inhalation of methacholine, the FEV1 decrease ranged from 26-43% of the baseline values while Rcoll increased significantly in only three of the six subjects. EELV remained unchanged in one subject and increased by 1408, 990, 260, and 44 ml in four others. It was not measured in one subject. Decreasing EELV by PEP increased Rcoll in all subjects. By extrapolation of the lung volume-Rcoll relationship, we calculated that Rcoll would have increased by 18,227%, 6843%, 994%, 140%, and 128% if EELV had not increased in the five subjects in whom delta EELV was measured. We conclude that an increase in EELV in response to an induced bronchospasm helps maintain open and functional collateral pathways despite the bronchoconstriction.