No abstract

Isolated heart muscle preparations were used to investigate the onset and development of myocardial inotropic dysfunction during endotoxin shock in guinea pigs. Left atrial muscles were removed from separate groups of animals at increasing time intervals after administration of either 4 mg/kg purified Escherichia coli endotoxin (shock groups) or an equivalent volume of isotonic saline (control groups). Peak developed contractile tension (CT) and maximal rate of tension development (+dT/dtmax) were significantly depressed in shock tissues as early as 2 h postendotoxin (P less than 0.01), with the magnitude of the contractile deficit progressively increasing during 4, 6, and 12 h postendotoxin. Contractility remained significantly depressed (P less than 0.001) at 16 and 24 h postendotoxin but progressively recovered toward control levels during 16, 24, 48, and 72 h postendotoxin. Shock-induced myocardial dysfunction was characterized by altered contractile responsiveness to low-Ca2+ medium (0.5 mM), gentamicin (4 mM), and hypoxia; altered inotropic reactivity to these interventions followed similar temporal development as the postendotoxin changes in basal contractile parameters. Left ventricular papillary muscles obtained at 16 h postendotoxin corroborated the shock-induced contractile depression observed in atria. These studies provide evidence for early and progressive intrinsic myocardial dysfunction in endotoxin shock and demonstrate that this dysfunction can be unmasked through the study of in vitro atrial and ventricular heart muscle preparations isolated from in vivo shocked animals.

Atrial muscle isolated from guinea pigs subjected to Escherichia coli endotoxin shock was used to study the myocardial changes associated with this experimental disease state. Isometric contractile tension and its first derivative (dT/dt) consistently were depressed by about 45% in muscle from the shock group (P less than 0.001), but contraction time intervals of the shock tissues were not significantly altered. The inotropic deficit of shock was completely antagonized by high concentrations of Ca2+ (greater than 4.5 mM). However, the maximal positive inotropic response to increased frequency of stimulation (0.1-2.2 Hz) only partially antagonized shock-induced cardiac depression. Heart muscle from shocked animals exhibited increased sensitivity to the negative inotropic effects of Mn2+, low Ca2+, and gentamicin; recovery from the depressant actions of these agents was prolonged 3.6- to 4.8-fold in shock. However, the negative inotropic potency of slow Ca2+ channel blockers, D 600 and nifedipine, was unaffected by shock. Similarly, studies with an isoproterenol-activated slow Ca2+ channel technique demonstrated equivalent inotropic responses of shock and control heart muscle. Present data provide evidence for a disruption of myocardial Ca2+ metabolism associated with endotoxin-induced inotropic depression of the heart but suggest that slow Ca2+ channels of the sarcolemma remain functional in this disease state.

Three unusual features were observed in a patient with chronic relapsing polyneuropathy: myokymia, muscle hypertrophy, and prolonged contraction in response to muscle percussion. Low nerve conduction velocity and conduction block were demonstrated in all motor nerves tested, indicating a demyelinating peripheral neuropathy. Myokymia was caused by spontaneous motor unit activity which was shown to originate in peripheral nerves, since it persisted after nerve block and was abolished by regional curarization. Muscle hypertrophy was attributed to increased peripheral nerve activity, and the prolonged contraction of muscle in response to direct percussion was attributed to irritability of intramuscular nerve terminals.

. and Surg., Salt Lake City, Utah. ~osit'ional therapy for gastroesophageal re-flux was evaluated by extended pH monitoring of the esophagus during the postprandial period in 28 normal and 45 reflux patients. Frequency of reflux (F), percent time the esophagus was pH<4 (%) and mean duration of reflux (MD) were determined while awake, asleep, su ine, sitting, and prone on a board with the head elevated g 30 . In normals, position or state of alertness did not affect reflux. Compared to normals, the increased % in reflux patients while awake (p<.001) was mainly related to increased F (p<.001) and normal MD; while asleep the increased % (p<.05) was related to normal F and prolonged MD (p<.05). Reflux patients have less % while on the board than while sitting or supine, both awake and asleep (p<.05). MD while asleep on the board was less than supine (p=.05), but F was unchanged; while awake, F was less on the board (p=.02) than supine, but MD was unchanged. These data demonstrate that alertness and position affect gastroesophageal reflux only in abnormal patients. The major determinant of increased acid exposure to the esophagus in reflux patients varies with the state of alertness, being mainly frequency of reflux while awake and prolonged duration while asleep. The prone Urinary urea nitrogen (UUN) excretion as an index of protein catabolism was assayed in 32 children (2m to 15y, median 6y)(50% mechanically ventilated) during an ICU course of 1 to 10 days (median 3d). Mean daily UUN excretion was 171 i 89 mglkg (4.38 rt 2.22 gm/m2), with greater excretion within 24 hours of ICU admission than subsequently. Average daily nitrogen balance per child was -146 f 82 mg/kg (-3.73 k 2.04 gm/m2), and was independent of caloric intake.Average daily UUN excretion per child was well described by regression equations for weight (mg = 219.76(kg) -1.74(kg)2, r2 = 0.908), height (mg = 4.07(cm) + 0.25(cm)2, r2 = 0,917), and meter squared body surface area (mg = 4421,5(BSA), r2=0.903). Excretion data in mechanically ventilated versus spontaneously breathing children, and in 4 diagnostic subgroups (sepsis 6, Reye syndrome 7, elective surgery 7, and,miscellaneous 12) was evenly distributed about regression lines for length, weight, and body surface area. Increased UUN excretion accompanied isoproterenol infusion and prednisone administration, Decreased excretion accompanied insulin infusion and high blood levels of barbiturates.This study documents the magnitude and time course of protein catabolism in critically ill children and suggests rarely considered drug effects, It confirms progressive protein depletion at per kg rates of UUN excretion comparable to critically ill adults with wide individual variability but little variation between diagnostic subgroups. To assess the state of nutrition of patients3talized at CMC, objective data were obtained by physical and biochemical measurements. Anthropometrics, body weight, and clinical observations were made by the CMC Nutrition Support Team on 74 of the total inpatient census of 77 ...