A STUDY OF INFLATABLE CUFFS ON ENDOTRACHEAL TUBES: Pressures exerted on the trachea

A simple method of measuring the pressure exerted by the cuffof an endotracheal tube on the trachea is described and hasbeen used to measure the pressures exerted by 16 commerciallyavailable cuffs on the wall of a model trachea. The Shiley,Portex soft-seal, Kamen-Wilkinson (Bivona Fome) tubes had thelowest tracheal wall pressures. Using this method in vivo thechanges in tracheal wall pressure exerted by a low-pressurecuff during percussion and vibration physiotherapy, and whenthe patient "fights the ventilator", were recorded.     

High resolution protein mapping in fibroblast cell lines and hair roots from patients with genetic disease*

Protein patterns of cultured fibroblasts and hair root lysates from healthy controls and patients with genetic diseases (Duchenne muscular dystrophy, Friedreich's ataxia, Marie's ataxia, Lesch-Nyhan syndrome, maple syrup urine disease, and trisomy 13, 18 and 21) were obtained with two-dimensional electrophoresis. The analysis of these patterns in 39 gels by visual comparison revealed differences in the presence and absence of 20 specific protein spots. However, this variability, which has been observed in healthy controls as well as in patients, could not provide a diagnosis for a specific genetic disease. Only in one case - trisomy 18 - was an additional spot observed, which was not present in any of the other gels.     

Magnetic Resonance Imaging and Signal-Averaged Electrocardiography in Patients with Repetitive Monomorphic Ventricular Tachycardia and Otherwise Normal Electrocardiogram

Early or localized forms of arrhythmogenic right ventricular dysplasia (ARVD) have been proposed as the arrhythmogenic substrate of repetitive monomorphic ventricular tachycardia (RMVT) originating in the right ventricular outflow tract in patients without any underlying cardiac abnormality on clinical examination and echocardiography. To further examine this hypothesis, magnetic resonance imaging (MRI) and signal-averaged electrocardiography (SAECG) were performed on 23 patients with RMVT and normal 12-lead standard ECG of conducted sinus beats. MRI was performed using ECG-gated turbo spin-echo images of the heart in order to detect signs of early or localized forms of ARVD, such as localized wall thickness reductions, signal intensity increase indicating adipose tissue infiltrates, and regional bulgings or aneurysms. MRI was normal in 22 (96%) of 23 study patients. In the remaining patient (4%), MRI demonstrated signal intensity increase in the intraventricular septum but not in the right ventricular outflow tract. Time-domain analysis of the SAECG was normal in 21 (91 %) of 23 patients and revealed ventricular late potentials in 2 study patients (9%). Frequency-domain analysis of the SAECG was normal in 22 (96%) of 23 patients and revealed ventricular late potentials in one study patient (4 %). We conclude that normal MRI findings of the heart and absence of ventricular late potentials in the SAECC in most patients with RMVT and otherwise normal ECG do not support the hypothesis that early or localized forms of ARVD create the arrhythmogenic substrate in the majority of these patients.     

Secondary hypertriglyceridaemia in patients with parenchymal liver disease

Hypertriglyceridaemia occurring in patients with liver disease has been studied by measuring hepatic triglyceride lipase (H-TGL) and plasma lipoprotein lipase (LPL) by selective precipitation of H-TGL with specific antibodies. Lipid analysis, determination of lecithin-cholesterol-acyltransferase (LCAT) activity, and liver function tests were performed in parallel in fifty patients with acute hepatitis, twenty patients with chronic active or persistent hepatitis and fifty with cirrhosis of the liver. Total post-heparin lipolytic activity (PHLA) decreased with the severity of liver dysfunction. This decrease was due to low H-TGL and only to some degree to low LPL activity. With improvement over several weeks of hospitalization, hypertriglyceridaemia disappeared with a concomitant increase of H-TGL and LPL. It is concluded that impaired triglyceride metabolism in liver disease is at least partly caused by diminished plasma hepatic TGL activity.