SUMMARY A 58-year-old man with hypertensive cardiovascular disease and atrial flutter underwent electrophysiologic studies, including multiple intra-atrial recordings and atrial stimulation. Although the surface ECG suggested the presence of atrial flutter, intra-atrial recordings demonstrated the presence of (1) sinus-like rhythm localized to an area of approximately 5 mm in and around the region of the sinus node, which was protected by entrance block; (2) flutter and/or fibrillation of the remaining parts of the right atrium; (3) fibrillation of the left atrium; and (4) transient degeneration of flutter into fibrillation at right atrial sites, with predominant flutter activity. Although a major part of the right atrium was in flutter and/or fibrillation, we could assess sinus node function by overdrive stimulation of the area of sinus node activity. Sinus node function studies revealed an underlying sick sinus syndrome.THE DIAGNOSIS of atrial arrhythmias is essentially based on the analysis of the configuration, timing, and rate of P waves on the surface ECG. However, recent studies in selected patients have demonstrated dissimilar atrial rhythms with direct intra-atrial recordings otherwise not discernible on the surface ECG."3 In this paper we report the electrophysiologic findings in a patient in whom the ECG revealed atrial flutter and intra-atrial recordings demonstrated the presence of sinus-like rhythm in and around the region of the sinus node, flutter and/or fibrillation of the remaining parts of the right atrium and fibrillation of the left atrium. We also assessed sinus node function, although a major part of the right and left atria were in flutter and/or fibrillation. Assessment of sinus node function revealed an underlying sick sinus syndrome.Case Report A 58-year-old man with hypertensive cardiovascular disease was admitted to the Medical Service of the Brooklyn Veteran's Administration Medical Center for uncontrolled hypertension, congestive heart failure and atrial flutter of recent onset. A 12-lead ECG suggested the presence of atrial flutter at a rate of 240 beats/min, with a ventricular response of 120 beats/min and poor R-wave progression from V1 to V3 ( fig. 1). Chest x-ray film showed cardiomegaly and pulmonary congestive changes. Echocardiogram revealed left atrial and left ventricular enlargement. The patient's hypertension and congestive heartfailure responded promptly to medical therapy. He was then referred to the cardiology service for elective electrical conversion of the atrial flutter after medical conversion with digitalis and quinidine had failed. Electrophysiologic StudiesThe patient underwent electrophysiologic studies to convert the atrial flutter by overdrive atrial stimulation. The procedure was explained to the patient, who gave signed consent. The electrophysiologic studies were performed after withholding digitalis and quinidine for 2 days. Serum digoxin level was 0.5 ng/ml on the day of the study. Two quadripolar #6FUSCI catheters with 10-mm interelectrode distance ...

Breathing at volumes lower than functional residual capacity (FRC) can induce changes in nonasthmatic airways consistent with the behaviour of asthmatic airways. This study investigated the chronic effect of breathing at volumes lower than FRC on the contractility of airway smooth muscle and myosin light chain kinase (MLCK) content and activity.Sheep of three age groups (neonate, adolescent and adult) had their FRC reduced by y25% for 4 weeks using a leather corset. Contractile responses to carbachol were then recorded in isolated tracheal strips and bronchial rings. MLCK content and activity were assessed by immunoblotting.The rate of stress generation increased in the bronchial smooth muscle of both adult and adolescent but not neonatal corseted sheep: adolescent corseted versus control, 65.0¡4.1 versus 103.4¡7.0 s (to reach 50% maximum stress), respectively; and adult corseted versus control, 57.0¡6.4 versus 93.4¡8.2 s, respectively. This was not due to increases in either bronchial or tracheal smooth muscle amount or MLCK content and activity.The present results indicate that chronic breathing at low lung volumes increases the rate of stress generation in airway smooth muscle. Excessive airway narrowing resulting from airway smooth muscle (ASM) contraction in response to physical and chemical stimuli is a characteristic of asthma. Breathing at volumes lower than functional residual capacity (FRC) can induce changes in nonasthmatic airways that are consistent with the behaviour of asthmatic airways. Animal studies have shown the marked influence of lung volume on ASM function [1][2][3], and in some clinical situations in which patients chronically breathe at lower lung volumes, this has been suggested as being responsible for changes in airway symptoms. This is the case in obese patients in whom there is an increased prevalence of wheezing [4-6] and airway hyperresponsiveness [7,8].The key regulator of the enzymatic pathway involved in smooth muscle contraction is myosin light chain kinase (MLCK), a dedicated protein kinase, with myosin as its only physiological substrate. MLCK regulates smooth muscle contraction by controlling the activity of actomyosin adenosine triphosphatase (ATPase) and in turn the rate of cross-bridge cycling [9,10]. In smooth muscle, it has been shown that the activity of actomyosin ATPase can be viewed mechanically as an index of shortening velocity [11,12]. A number of physiological studies have been performed using sensitised ASM as a model of asthmatic muscle. These studies have shown that sensitised ASM exhibits increased maximal shortening capacity and increased early shortening velocity [13,14]. Further investigations revealed that these observed changes in the contractile response of ASM were a result of an increase in both the amount and activity of MLCK present in the muscle [15][16][17].Another proposed mechanism for the effect of lung volume is ASM plasticity, in which the organisation of the contractile apparatus of the smooth muscle cell is modified to adapt to ...

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Isocaloric feeding of diets varying in lipid content to albino hairless mice has shown that their susceptibility to skin tumorigenesis induced by simulated solar UV light was not affected by the level of polyunsaturated fat, 5% or 20%. However a qualitative effect of dietary lipid was demonstrated. Mice fed 20% saturated fat were almost completely protected from UV tumorigenesis when compared with mice fed 20% polyunsaturated fat. Multiple latent tumours were detected in the saturated fat-fed mice by subsequent dietary replenishment, suggesting that a requirement for dietary unsaturated fat exists for the promotion stage of UV-induced skin carcinogenesis.