PubMed · 7901918
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A E Tattersfield, P Wilding. 1993. Beta agonists and ventilation.. https://doi.org/10.1136/thx.48.9.877
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BACKGROUND: The left superior vena cava (LSVC) is the embryological precursor of the ligament of Marshall, which has been implicated in the initiation and maintenance of atrial fibrillation (AF). Rarely, the LSVC may persist and has been associated with some organized arrhythmias, though not with AF. We report 5 patients in whom the LSVC was a source of ectopy, initiating AF. METHODS AND RESULTS: In 5 patients (4 men; age, 46+/-11 years) with symptomatic drug-refractory AF, ectopy from the LSVC resulting in AF was observed after pulmonary vein isolation. The ectopics were spontaneous in 2 and induced by isoproterenol in the others and preceded P-wave onset by 67+/-13 ms. During multielectrode or electroanatomic mapping, venous potentials were recorded circumferentially at the proximal LSVC near its junction with the coronary sinus (CS), but at the mid-LSVC level, they were recorded only on part of the circumference. The LSVC was electrically connected to the lateral left atrium (LA) and through the CS to the right atrium, with 4.1+/-2.3 CS-LSVC and 1.6+/-0.5 LA-LSVC connections per patient. Catheter ablation in the LSVC targeting these connections resulted in electrical isolation in 4 of the 5 patients without complications. After 15+/-10 months, the 4 patients with successful isolation, including 1 who had successful reablation for LA flutter, remained in sinus rhythm without drugs. CONCLUSIONS: The LSVC can be the arrhythmogenic source of AF with connections to the CS and LA. Ablation of these connections resulted in electrical isolation.
To examine the changes in heat shock proteins (HSPs) and calcineurin (CaN), a calcium/calmodulin regulated protein phosphatase, in hypertrophied rat skeletal muscles, adult male Wistar rats were administered clenbuterol (CLB, 30 mg l(-1) in drinking water), a beta 2-agonist, for 4 weeks. Compared to controls, CLB-treated rats had significantly larger body (10%) and relative (to body weight) soleus (Sol, 16%), plantaris (Plt, 32%) and gastrocnemius (Gast, 27%) weights. Immunohistochemically classified fast fibers were hypertrophied in the Sol (64%), Plt (62%), and deep (d, 70%) and superficial (s, 44%) regions of the Gast, whereas slow fibers were hypertrophied only in the Plt (47%). The percentage of fast fibers in the Sol increased from 10% to 21%. The myosin heavy chain (MHC) isoform composition shifted from slow to fast in the Sol (increase in the percentage of type IIa MHC and de novo synthesis of type IIx MHC) and Gast-d (de novo synthesis of type IIb MHC) and to the faster isoforms in the Plt (increase in the percentage of type IIb MHC). Hsp72 and Hsp90 levels in CLB-treated rats were 52% and 50% lower in the Sol and 44 and 41% lower in the Gast-d, respectively, than in control rats. In control rats, the relative content of CaN was: Sol>Gast-d>Plt>Gast-s, and CLB treatment enhanced the CaN content by 1.4-, 1.2-, 5.0-, and 3.3-fold, respectively. These results indicate that the down-regulation of HSPs in the Sol and Gast-d was closely related to a decrease in the slow phenotype, and that the relative up-regulation of CaN among the muscles/regions was closely related to the selective hypertrophy of fast fibers in the CLB-treated rats.
BACKGROUND: The plasma interleukin (IL)-18 level is elevated in acute rejection after organ transplantation. Although beta2-adrenergic receptor (AR) agonists suppress the rejection of organ and tissue transplants, little is known about their action mechanisms. We examined the effects of endogenous catecholamines and beta2-AR agonists on the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, CD40, and CD40 ligand (CD40L) in human mixed lymphocyte reaction (MLR) and in an in vitro model of acute rejection in the presence or absence of IL-18. METHODS: ICAM-1, B7.1 B7.2, CD40, and CD40L expression on monocytes was measured by flow cytometry, and the production of interferon (IFN)-gamma and IL-12 was determined by enzyme-linked immunosorbent assay. Lymphocytes proliferation in MLR was measured by [3H]-thymidine uptake. The relevant AR subtypes were characterized using subtype-selective agonists and antagonists. RESULTS: beta2-AR agonists inhibited the expression of ICAM-1 and CD40 during MLR in the absence of IL-18. Among IL-18-induced expression of ICAM-1, B7.1, B7.2, CD40, and CD40L, beta2-AR agonists inhibited ICAM-1 and CD40 expression. beta2-AR agonists prevented the production of IFN-gamma and IL-12 in the presence of IL-18 but had no effect in the absence of IL-18. beta2-AR agonists inhibited lymphocyte proliferation in IL-18-treated MLR. CONCLUSIONS: We found that beta2-AR agonists strongly inhibited the expression of ICAM-1 and CD40, irrespective of the presence or absence of IL-18, which is different from that of histamine and prostaglandin E2.