Accuracy of the volume and pressure displays of high frequency oscillators.

OBJECTIVE: To determine the effect of frequency on the accuracy of volume and pressure displays of high frequency oscillators. METHODS: The effect of frequency on the displayed volume of the Stephanie, Dräger Babylog 8000 Plus, and SLE 5000 oscillators was assessed. A sine wave pump delivered a constant tidal volume at frequencies of 5-15 Hz to the patient manifold of the oscillators. The displayed volumes at each frequency were compared with the delivered volume. The effect of frequency on displayed pressure was assessed by connecting the oscillator's patient manifold to a lung model; three types of oscillator were studied (SensorMedics 3100A, SLE 5000, and Stephanie). Airway pressure was measured from the manifold using a pressure transducer and non-compliant tubing; the pressure measuring system had a flat frequency response to 30 Hz. RESULTS: The SLE 5000 volume display overread the delivered volume (by about 5%), but was not affected by frequency. At 5 Hz, the Dräger Babylog 8000 Plus and the Stephanie underread the delivered volume (by about 20%). Increasing frequency resulted in a greater discrepancy between the delivered and displayed volume with the Stephanie, but a smaller discrepancy with the Dräger Babylog 8000 Plus. Altering frequency had a small effect (maximum difference 6%) on the relation between the displayed and delivered pressure for all three oscillators. CONCLUSION: Frequency affects the accuracy of displayed volumes and, to a lesser extent, displayed pressures of high frequency oscillators. The results emphasise that data displayed by new devices should not be uncritically accepted.

Effect of posture on respiratory function and drive in preterm infants prior to discharge.

Our objective was to determine the effect of posture on respiratory function and drive in prematurely born infants immediately prior to discharge. Twenty infants (6 oxygen-dependent), median gestational age 29 weeks (range, 25-32), were studied at a median postconceptional age (PCA) of 36 weeks (range, 33-39). On 2 successive days, infants were studied both supine and prone; each posture was maintained for 3 hr. The order on each day in which postures were studied was randomized between infants. At the end of each 3-hr period, tidal volume (Vt), inspiratory (Ti) and expiratory (Te) time, respiratory rate, and minute ventilation were measured. In addition, respiratory drive was assessed by measuring the pressure generated in the first 100 msec of an imposed airway occlusion (P(0.1)), and respiratory muscle strength was assessed by recording the maximum inspiratory pressure (Pimax) generated against an occlusion which was maintained for at least five breaths. Overall, tidal volume was higher (P < 0.05), but respiratory rate (P < 0.05), P(0.1) (P < 0.05), and Pimax (P < 0.05) were lower in the prone compared to the supine position. There were no significant differences in Ti or Te between the two postures. In oxygen-dependent infants only, minute volume was higher in the prone position (P < 0.05). In conclusion, posture-related differences in respiratory function are present in prematurely born infants studied prior to neonatal unit discharge.

Perforation complications of percutaneous central venous catheters in very low birthweight infants.

OBJECTIVE: To prospectively survey perforation complications of consecutively inserted percutaneous central venous catheters (PCVC) in very low birthweight (VLBW) infants over a 2 year period. METHODOLOGY AND RESULTS: Three serious perforation complications were encountered in a series of 100 consecutive PCVC. One infant (birthweight 685 g) developed pericardial effusion and fatal cardiac tamponade during the use of a polyurethane PCVC. At autopsy, the pericardial sac contained 8 mL fluid with a glucose concentration of 109 mmol/L and the catheter tip was embedded in the right ventricular wall. The second infant (birthweight 1380 g) showed pleural effusion and transient immobility of the right diaphragmatic leaf after perforation of a similar PCVC into the right pleural cavity. The third perforation, causing subcutaneous oedema, occurred in a 655 g infant who had a silastic PCVC. CONCLUSIONS: The data suggest a 3% incidence for PCVC-associated symptomatic perforation complications and a 1% incidence for fatal perforations, despite a policy of careful placement. The data also indicate that perforation complications occur regardless of the size or material of the PCVC. Proper visualization of the PCVC and vigilant attention to its location is required to prevent these rare but potentially fatal complications.

Neonatal Type I diabetes associated with maternal echovirus 6 infection: a case report.

AIMS/HYPOTHESIS: Neonatal diabetes mellitus is rare, and it has not been associated with beta-cell autoimmunity. Enteroviral infections during pregnancy have been implicated as a risk factor for the later development of Type I (insulin-dependent) diabetes mellitus. We now report of a baby girl who was born severely growth-retarded with neonatal insulin-deficient diabetes, and look for evidence of intrauterine enteroviral infections and beta-cell targeted autoimmunity. METHODS: Diabetes-associated autoimmunity was studied by measurement of several types of islet cell reactive autoantibodies. The infant's T-cell responses to insulin and enterovirus antigens were recorded and enterovirus antibodies were measured both from the mother and the child. RESULTS: Several types of diabetes-associated autoantibodies were detected postnatally, including insulin autoantibodies, conventional islet cell autoantibodies and glutamic acid decarboxylase antibodies, whereas no autoantibodies were observed in the mother. The infant's T-cells showed reactivity to insulin and purified enterovirus particles. Based on serological studies, the pathogenetic process could have been triggered by an echovirus 6 infection during pregnancy. The patient's diabetes has been permanent, although there were signs of endogenous insulin production for several months. Exocrine pancreatic insufficiency was diagnosed at the age of 1 year. CONCLUSION/INTERPRETATION: These observations suggests that enteroviral infections may induce beta-cell autoimmunity even in utero.

Apparently new syndrome of short stature, lumbar malsegmentation, and minor facial anomalies in two brothers.

We describe a previously unrecognized syndrome in two brothers with short stature, webbed neck, unusual face, moderate malsegmentation of the lumbar spine, and unilateral Legg-Perthes-Calvé type "disease" of the hip. Autosomal recessive inheritance is proposed, although we cannot exclude the possibility of an X-linked recessive or an autosomal dominant condition with germinal mosaicism.

Protection of the reperfused heart by L-propionylcarnitine.

The effects of L-propionylcarnitine on mechanical function, creatine phosphate and ATP content, and lactate dehydrogenase leakage were studied in isolated perfused rat hearts exposed to global no-flow ischemia for 30 min followed by reperfusion for 20 min. Five and 10 mM L-propionylcarnitine resulted in a 100% recovery of left ventricular-developed pressure, whereas the recovery was only 40% in the hearts perfused without this agent. Ischemia-reperfusion caused a 85% loss of creatine phosphate and a 77% loss of ATP, which was prevented by 10 mM L-propionylcarnitine. Five millimolar L-propionylcarnitine protected the heart from the loss of creatine phosphate but not from the loss of ATP. Ten millimolar L-propionylcarnitine failed to improve the postischemic left ventricular-developed pressure, when it was added to the perfusate only after ischemia. L-propionylcarnitine alleviated the decrease of coronary flow in the reperfused hearts. Lactate dehydrogenase leakage was aggravated in the beginning of the reperfusion period by 10 mM L-propionylcarnitine. This adverse effect was, however, transient. L-Propionylcarnitine provides protection for the postischemic reperfused heart in a dose-dependent manner. The optimal time for administration is before the ischemic insult. High doses of this compound may perturb cell membrane integrity. Moreover, the present data point to an intracellular, metabolic, and perhaps anaplerotic mechanism of action of L-propionylcarnitine in cardiac ischemia-reperfusion injury.

Transmural distribution of calcium accumulation and glucose uptake in the calcium paradox in the rat left ventricle.

The calcium paradox was induced in the isolated perfused rat heart and the transmural distributions of glucose uptake and calcium accumulations were determined using 2-deoxy-D-[3H]glucose and 45Ca2+ as tracers. The regional distribution of coronary flow was measured using radiolabelled microspheres. A significant transmural gradient was observed in left ventricular glucose uptake both in the control and the calcium paradox hearts: subendocardial and subepicardial glucose uptake rates were 5.70 +/- 0.65 mumol/min/g protein (mean +/- S.E.M.) and 4.29 +/- 0.35 mumol/min/g protein (P less than 0.05) in the control hearts, and 8.64 +/- 0.79 mumol/min/g protein and 4.09 +/- 0.71 mumol/min/g protein (P less than 0.01) in the paradox hearts. This increase in subendocardial glucose uptake in the calcium paradox was also significant (P less than 0.05), while the average left ventricular calcium accumulation was about 10-fold in the paradox hearts compared to the controls mumol x 10(-1)/min/g protein in the subendocardium and 14.02 +/- 0.93 mumol x 10(-1)/min/g protein in the subepicardium (P less than 0.001). The subendocardium received initially 30% more perfusion than subepicardium (P less than 0.01), but the subendocardial flow during the calcium depletion and replenishment periods was only 40% of that in the subepicardium (P less than 0.001) and the average myocardial flow was reduced by c. 60% (P less than 0.001). The data show clear transmural differences in the alterations associated with the calcium paradox. This suggests that the calcium paradox induced myocardial injury is unevenly distributed across the left ventricular wall, this uneven distribution possibly being due to regional differences in the damage of mitochondrial energy production.

Transmural distribution of left ventricular glucose uptake in spontaneously hypertensive rats during rest and exercise.

The transmural distribution of glucose uptake was studied in the left ventricle of 6-month-old male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) during rest and swimming (20 min) using the 2-deoxyglucose method. The baseline mean arterial pressure was 128 +/- 8 (n = 8) in the WKY and 188 +/- 22 mmHg (n = 8) in the SHR (P less than 0.001). This pressure remained constant in the resting groups, whereas the product of mean arterial pressure and heart rate was initially 45 x 10(3) +/- 3 x 10(3) and 63 x 10(3) +/- 4 x 10(3) mmHg beats min-1 in the swimming WKY and SHR and increased by 34-48 x 10(3) mmHg beats min-1 during the swimming period. Total glucose uptake was 3.9 +/- 1.2 mumol min-1 g-1 protein in the resting WKY rats and 1.4 +/- 0.4 mumol min-1 g-1 protein (P less than 0.001) in the swimming ones, the corresponding values for the resting and swimming SHR being 4.8 +/- 1.4 mumol min-1 g-1 protein and 3.2 +/- 1.2 mumol min-1 g-1 protein (P less than 0.01). Glucose uptake was 30% greater in the subendocardium (ENDO) of the resting WKY than in the subepicardium (EPI) (P less than 0.01), but this gradient disappeared during swimming. Glucose uptake in the resting SHR was greatest in the middle layer of the ventricular wall, with no difference between ENDO and EPI, whereas during swimming the glucose uptake was distributed evenly across the left ventricular wall. The blood lactate/pyruvate ratio increased only transitorily during the first minutes in the swimming SHR, while their plasma free fatty acid concentration was 1.2-1.3 mM initially and decreased by 32% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Transmural distribution of biochemical markers of total protein and collagen synthesis, myocardial contraction speed and capillary density in the rat left ventricle in angiotensin II-induced hypertension.

The effect of angiotensin II-induced hypertension on selected biochemical parameters was studied in Sprague-Dawley rats. Angiotensin II infusion at rates of 41.7 micrograms h-1 kg-1 and 12.5 micrograms h-1 kg-1 for 2, 5, 10 and 15 days elevated the systolic blood pressure from 143 +/- 7 mmHg to 215-230 mmHg (P less than 0.001) and 185-195 mmHg (P less than 0.001), respectively. The left ventricular weight/body weight ratio increased 10-14% (P less than 0.05) and 23-32% (P less than 0.001) after 2-15 days in rats treated at the lower and higher infusion rates, respectively. Prolyl 4-hydroxylase (PH) activity, a marker of collagen synthesis, was evenly distributed in the left ventricle. PH activity increased by about 100% in both subendocardial and subepicardial layers of the left ventricular wall after angiotensin II infusion for 10 days at 41.7 micrograms h-1 kg-1, but remained unaltered at 12.5 micrograms h-1 kg-1. No change was observed in hydroxyproline concentration. Myosin isoenzymes (V1-V3), which reflect myocardial contractility, were unevenly distributed in the left ventricular wall: the proportion of the fast-turnover isoenzyme (V1) was smaller in the subendocardial layer than in the subepicardial layer. The proportion of V1 decreased after treatment in both layers. Alkaline phosphatase activity, a marker of capillary density, was evenly distributed transmurally in the left ventricular wall. Angiotensin II caused a slight decrease in this activity in both myocardial layers. The results suggest that the elevation of blood pressure leads to transmurally evenly distributed changes in biochemical parameters reflecting collagen synthesis, capillary density and contractile properties of the myocardium.