ABSTRACT
The authors attempted to simultaneously measure cardiac output by thermodilution (COtd), thoracic bioimpedance (CObi), and suprasternal Doppler ultrasound (COdopp) in 68 patients. Subgroups separately compared included patients whose lungs were mechanically ventilated, patients undergoing cardiac surgery, aortic surgery, patients with dysrhythmias, and patients with sepsis. The authors also studied the value of the ventricular ejection time (VET) in evaluating the agreement of CObi and COdopp with COtd. Simultaneous CObi and COtd were available in a total of 56 patients (416 data sets) with an overall correlation coefficient r = 0.61, regression slope (m) of 0.52, intercept (y) of 2.46, and mean (CObi-COtd) difference (bias) of -0.67 +/- 1.72 (SD) l/min. Simultaneous COdopp and COtd were available in 59 patients (446 data sets) with an overall r = 0.51, m of 0.53, y of 2.05, and bias of -0.79 +/- 1.95 l/min. CObi agreed most closely with COtd in patients whose lungs were mechanically ventilated, who had not undergone cardiac or aortic surgery, and with VET difference less than 40 ms (16 patients, 99 data sets; r = 0.74; m = 0.97; y = 0.15; bias = -0.02 +/- 1.53 l/min). COdopp agreed most closely with COtd in patients whose lungs were mechanically ventilated, who had not undergone cardiac or aortic surgery, and in sinus rhythm with VET difference less than 40 ms (10 patients, 45 data sets; r = 0.82; m = 0.98; y = -0.07; bias = -0.82 +/-1.03 l/min). VET by radial artery can help evaluate the reliability of CObi and COdopp.
Subject(s)
Cardiac Output , Aorta/surgery , Arrhythmias, Cardiac/physiopathology , Cardiac Surgical Procedures , Cardiography, Impedance , Humans , Infections/physiopathology , Respiration, Artificial , Statistics as Topic , Thermodilution , UltrasonographyABSTRACT
Actinomycin D (ACT-D), an inhibitor of transcription, was added to chick muscle cultures to study its effect on the synthesis of acetylcholine receptor (ACHR) and acetylcholinesterase (ACHE, EC 3.1.1.7). Doses of ACT-D (1.85-18.5 nM), which inhibited uridine incorporation up to 80%, increased ACHR, ACHE, and creatine kinase (CK, EC 2.7.3.2) levels without affecting general cell protein. Degradation of ACHR was slower in ACT-D treated cultures than controls, resulting in a twofold increase in receptor half-life. Uridine incorporation was inhibited by ACT-D in both mononucleated cells and myotubes and [3H]uridine nuclear grain distribution were shifted to values lower than controls. The results indicate that posttranscriptional effects of ACT-D increase levels of ACHR, ACHE, and CK and that decreased degradation could account for the increase in the number of surface ACH receptors.
Subject(s)
Acetylcholinesterase/biosynthesis , Dactinomycin/pharmacology , Muscles/metabolism , Receptors, Cholinergic/biosynthesis , Animals , Autoradiography , Cells, Cultured , Chick Embryo , Creatine Kinase/biosynthesis , Dose-Response Relationship, Drug , Muscles/embryology , RNA/biosynthesisSubject(s)
Chickens , Muscular Dystrophy, Animal/drug therapy , Phenytoin/therapeutic use , Poultry Diseases/drug therapy , Acetylcholinesterase/metabolism , Animals , Butyrylcholinesterase/metabolism , Male , Muscles/enzymology , Muscles/pathology , Muscular Dystrophy, Animal/enzymology , Muscular Dystrophy, Animal/pathology , Poultry Diseases/enzymologyABSTRACT
Chicks affected with hereditary muscular dystrophy were injected twice daily with 20 milligrams of diphenylhydantoin per kilogram of body weight on days 1 to 40 after hatching. The righting ability of dystrophic chicks treated with diphenylhydantoin was improved compared to that of untreated dystrophic chicks, and acetylcholinesterase activity was reduced to normal levels in the posterior latissimus dorsi muscles.
