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E Bancalari

Publications and source records attributed to E Bancalari.

At least 37 records · Page 2Linked to original sources

Effects of respiratory mechanical unloading on thoracoabdominal motion in meconium-injured piglets and rabbits.

Impaired pulmonary mechanics can cause chest wall distortion (CWD) so that work of breathing is dissipated in deforming the rib cage. We hypothesized that respiratory mechanical unloading as a technique of assisted mechanical ventilation would reduce CWD in animals with injured lungs. We studied five piglets and five adult rabbits to test across different ages and chest configurations. As a result of intratracheal meconium instillation, lung compliance decreased from 21 (median; range 17-35) to 9.5 (6.7-14) mL/kPa/kg in rabbits and from 26 (18-31) to 7.9 (4.9-11) in piglets. Airway resistance increased from 5.0 (4.6-6.1) to 6.9 (5.8-7.9) kPa/L/s in rabbits only. Respiratory inductive plethysmography was used to measure the phase shift between the rib cage and abdominal compartment movements and the total compartmental displacement ratio. We aimed at unloading at least three-fourths of lung elastance in all animals and 2.0 kPa/L/s of resistance in rabbits. Elastic unloading decreased the phase shift in all but one animal. It reduced the total compartmental displacement ratio from 1.27 (1.14-3.73) to 1.16 (1.02-1.82) in piglets and from 1.77 (1.45-5.24) to 1.37 (1.11-4.78) in rabbits. The inspiratory rib cage expansion increased, whereas abdominal expansion did not. The tidal esophageal pressure deflection decreased. Tidal volume increased, whereas respiratory rate remained unaffected so that the partial pressure of arterial CO2 decreased. Resistive unloading as an adjunct to elastic unloading further reduced CWD and induced a more rapid, shallower breathing. We conclude that respiratory unloading as a mechanical support to spontaneous breathing reduces CWD. We speculate that the decrease in CWD increases ventilatory efficiency for a given diaphragmatic effort.

Abdomen↗

Increased incidence of sighs (augmented inspiratory efforts) during synchronized intermittent mandatory ventilation (SIMV) in preterm neonates.

A reflex resulting in a deep, sigh-like inspiratory effort (augmented breath) is frequently triggered during synchronized mechanical ventilation in preterm infants. We studied the incidence of augmented inspiratory efforts and their effect on ventilation and lung compliance during conventional IMV and synchronized IMV (SIMV) in 15 preterm neonates (GA 26.7 +/- 1.5 wks (mean +/- SD), BW 925 +/- 222 g, age 1-8 days). Augmentation of spontaneous inspiratory effort was defined as an esophageal pressure deflection occurring coincident with a synchronized mechanical breath and exceeding the previous unassisted spontaneous effort by more than 50%. The incidence of augmented breaths was higher during SIMV (11.1 +/- 7.7%; P < 0.01) than during conventional IMV (5.1 +/- 6.1%). However, when the synchronized breaths were triggered late (200-300 msec) after the onset of inspiration, augmented breaths occurred no more frequently than during conventional IMV (6.0 +/- 4.7%). The incidence of augmented breaths correlated inversely with dynamic lung compliance (P = 0.014), but was not significantly influenced by a change in PEEP. Although inspiratory effort increased nearly three times during the augmented breaths, tidal volume increased only 12%. The change in tidal volume was limited because the augmented effort reached its maximal negativity only approximately 500 ms after the beginning of the synchronized, mechanical breath and at a time when the mechanical breath had already ended. For this reason the augmented effort did not contribute significantly to minute ventilation, but only prolonged inspiration. Dynamic lung compliance did not change significantly after an augmented breath. The results indicate that augmented inspiratory efforts are more common in preterm neonates ventilated with SIMV than with conventional IMV, but do not contribute significantly to ventilation.

Cohort Studies↗

Computer-controlled minute ventilation in preterm infants undergoing mechanical ventilation.

INTRODUCTION: Computer-controlled minute ventilation (CCMV) continuously adjusts the ventilator rate to changes in spontaneous respiratory drive and pulmonary mechanics to maintain a preset total minute ventilation. HYPOTHESIS: We hypothesized that CCMV would maintain ventilation and oxygenation with fewer mechanical breaths than conventional intermittent mandatory ventilation in very low birth weight infants. METHODS: Very low birth weight infants in clinically stable condition who were undergoing mechanical ventilation were enrolled. The number of mechanical breaths, total and mechanical expiratory minute ventilation, mean airway pressure, oxygen hemoglobin saturation by pulse oximetry, and transcutaneous partial carbon dioxide and partial oxygen tensions were obtained during intermittent mandatory ventilation and CCMV (45 to 60 minutes) and compared by paired t test. RESULTS: Fifteen infants were studied. Birth weight (median, range) was 700 gm (550 to 1205 gm), gestational age 26 weeks (23 to 34 weeks), age 21 days (3 to 50 days). When switched from intermittent mandatory ventilation to CCMV, the number of mechanical breaths was reduced (15 +/- 2.8 to 8.6 +/- 2.9 breaths per minute, p < 0.001), leading to lower airway pressure (3.97 +/- 1.00 to 3.45 +/- 1.00 cm H2O, p < 0.001) and lower expiratory minute ventilation generated by the mechanical ventilator (116 +/- 31 to 65 +/- 28 ml/min per kilogram, p < 0.001), while total expiratory minute ventilation remained unchanged. Mean transcutaneous partial carbon dioxide and oxygen tensions, oxygen hemoglobin saturation, and the time spent within different oxygen hemoglobin saturation ranges did not differ between both ventilatory modes. CONCLUSION: CCMV maintained adequate ventilation and oxygenation with lower mechanical ventilatory support than IMV. CCMV may reduce barotrauma and chronic lung disease during long-term use.

Down-Regulation↗

Randomized, multicenter trial of inhaled nitric oxide and high-frequency oscillatory ventilation in severe, persistent pulmonary hypertension of the newborn.

BACKGROUND: Although inhaled nitric oxide (iNO) causes selective pulmonary vasodilation and improves oxygenation in newborn infants with persistent pulmonary hypertension, its effects are variable. We hypothesized (1) that the response to iNO therapy is dependent on the primary disease associated with persistent pulmonary hypertension of the newborn (PPHN) and (2) that the combination of high-frequency oscillatory ventilation (HFOV) with iNO would be efficacious in patients for whom either therapy alone had failed. METHODS: To determine the relative roles of iNO and HFOV in the treatment of severe PPHN, we enrolled 205 neonates in a randomized, multicenter clinical trial. Patients were stratified by predominant disease category: respiratory distress syndrome (n = 70), meconium aspiration syndrome (n = 58), idiopathic PPHN or pulmonary hypoplasia (excluding congenital diaphragmatic hernia) ("other": n = 43), and congenital diaphragmatic hernia (n = 34); they were then randomly assigned to treatment with iNO and conventional ventilation or to HFOV without iNO. Treatment failure (partial pressure of arterial oxygen [PaO2] < 60 mm Hg) resulted in crossover to the alternative treatment; treatment failure after crossover led to combination treatment with HFOV plus iNO. Treatment response with the assigned therapy was defined as sustained PaO2 of 60 mm Hg or greater. RESULTS: Baseline oxygenation index and PaO2 were 48 +/- 2 and 41 +/- 1 mm Hg, respectively, during treatment with conventional ventilation. Ninety-eight patients were randomly assigned to initial treatment with HFOV, and 107 patients to iNO. Fifty-three patients (26%) recovered with the initially assigned therapy without crossover (30 with iNO [28%] and 23 with HFOV [23%]; p = 0.33). Within this group, survival was 100% and there were no differences in days of mechanical ventilation, air leak, or supplemental oxygen requirement at 28 days. Of patients whose initial treatment failed, crossover treatment with the alternate therapy was successful in 21% and 14% for iNO and HFOV, respectively (p = not significant). Of 125 patients in whom both treatment strategies failed, 32% responded to combination treatment with HFOV plus iNO. Overall, 123 patients (60%) responded to either treatment alone or combination therapy. By disease category, response rates for HFOV plus iNO in the group with respiratory syndrome and the group with meconium aspiration syndrome were better than for HFOV alone or iNO with conventional ventilation (p < 0.05). Marked differences in outcomes were noted among centers (percent death or treatment with extracorporeal membrane oxygenation = 29% to 75%). CONCLUSIONS: We conclude that treatment with HFOV plus iNO is often more successful than treatment with HFOV or iNO alone in severe PPHN. Differences in responses are partly related to the specific disease associated with PPHN.

Administration, Inhalation↗

Necrotizing enterocolitis in full-term or near-term infants: risk factors.

A retrospective case-control study of necrotizing enterocolitis (NEC) affecting infants weighing > 2,000 g at birth was performed to determine those factors which could contribute to the development of NEC. Twenty-four infants met the criteria of definite NEC. For each case the next 2 healthy newborns were matched as controls. When compared with the control group, NEC infants had a significantly higher frequency of prolonged rupture of membranes, chorioamnionitis, Apgar score < 7 at 1 and 5 min, respiratory problems, congenital heart disease, hypoglycemia, and exchange transfusions. Only 3 infants with NEC were healthy newborns with an unremarkable perinatal course before NEC. There were no differences in the frequency of preeclampsia, maternal diabetes, maternal drug abuse, meconium-stained amniotic fluid and polycythemia. These results indicate that most of these more mature infants have a predisposing factor before developing NEC.

Case-Control Studies↗

Intrasubject variability of repeated pulmonary function measurements in preterm ventilated infants.

This study set out to describe the variability and assess the reproducibility of repeated pulmonary function measurements in ventilated preterm infants. We measured tidal volume (VT), lung compliance (CL), and resistance (RL) in 16 infants (mean +/- SD: birthweight 1222 +/- 343 g) during spontaneous breathing and during mechanical ventilation, suppressing breathing efforts by mild hyperventilation. CL and RL were calculated from the equation of motion using linear regression analysis (LR), and by the Mead and Wittenberger method (MW). Flow and transpulmonary pressure were recorded for at least two consecutive periods, after which the esophageal tube was removed and replaced 1 hour later for a second set of recordings. The mean percent change (% delta) between the initial and the repeated measurements with their respective 95% confidence intervals were calculated. Reproducibility was assessed by the intraclass correlation coefficient (ICC) (total agreement = 1, good reproducibility > or = 0.75). The mean % delta between initial and repeat measurements during spontaneous breathing ranged from 11% to 14% for CL and VT, and from 22% to 32% for RL. The variation for RL was even higher when the analysis was done separately for the inspiratory and expiratory phase. CL and VT had good reproducibility (ICC > 0.9), while RL was significantly less reproducible (ICC < 0.75). Measurements obtained from mechanical breaths had less variability than from spontaneous breaths, ranging from 8% to 15% for CL and VT, and from 13% to 21% for RL. Reproducibility assessed by the ICC was good for most measurements during mechanical breaths. The variability and reproducibility of measurements were similar for both methods of analysis during mechanical ventilation, but during spontaneous breathing variability was larger with the MW method than with LR analysis. We concluded that VT and CL were reproducible during spontaneous and mechanical breathing. However, RL measurements were reproducible only during mechanical ventilation. The high variability of RL in spontaneously breathing preterm infants may reduce the clinical usefulness of this measurement for individual patients.

Humans↗

Patient-triggered ventilation: a comparison of tidal volume and chestwall and abdominal motion as trigger signals.

Patient-triggered synchronized ventilation requires reliable and early detection of the infant's inspiratory effort. Several trigger methods have been developed that frequently lack the sensitivity to detect inspiration in small preterm infants (trigger failure), or show a high rate of breaths triggered by artifacts in the respiratory signal (autotrigger). The purpose of this study was to determine the effectiveness of the following trigger signals: abdominal movement sensed by a newly developed induction technique, chestwall motion detected by changes in transthoracic impedance, and tidal volume measured by anemometry at the endotracheal tube connector. Ten preterm infants (birth weight, 580-1,424 g; median weight, 943 g; study weight, 535-1,415 g; median weight, 838 g; gestation age, 26-32 weeks, median gestational age, 28 weeks, study age, 1-50 days, median study age, 11 days) were included in the study. A Sechrist SAVI ventilator was triggered by one of three signals: chestwall or abdominal movement, or tidal volume generated by the infants. Response time between beginning of inspiratory flow, the occurrence of the trigger signal (signal delay), and the onset of the triggered breath (trigger delay) were determined for each of the three signals. The signal response time was -13.5 msec (95% CI, -33 to -2 msec) for the abdominal movement signal, indicating that it started before inspiratory flow; 0.0 msec for the volume signal; and 44.0 msec (95% CI, 29-73 msec) for the chestwall signal (P < 0.002); this long delay was secondary to chestwall distortion and a subsequent delay in outward ribcage movement in many infants. The trigger delay for the abdominal signal was 90.0 msec (95% CI, 55-104 msec), 135.5 msec (95% CI: 82-186 msec) for the volume signal, and 176.5 msec (95% CI: 165-232 msec) for the chestwall signal, indicating that there was a difference in the rise time of signal voltage between the three methods (P < 0.01). The rate of autotriggered breaths was 3.2% (95% CI, 0.3-9.3%) when using the abdominal signal, 0.55% (95% CI, 0.0-2.1%) for the tidal volume signal, and 11.25% (95% CI, 0.5-27.8%) for the chestwall signal (P < 0.05). The incidence of trigger failure was low with all three signals and was not significantly different between the techniques. In summary, the chestwall signal had a long trigger delay and was highly susceptible to false triggering. It is, therefore, not a reliable trigger signal for synchronized mechanical ventilation in preterm infants. In contrast, tidal volume and abdominal movement signals had an acceptable trigger delay and a low rate of autotriggering, making them useful clinical trigger signals.

Confidence Intervals↗

Effect of leak around the endotracheal tube on measurements of pulmonary compliance and resistance during mechanical ventilation: a lung model study.

We studied the effect of leaks around the endotracheal tube (ETT) on the measurement of pulmonary mechanics during mechanical ventilation. We also evaluated the influence of different ventilator settings on the magnitude of leak. An adjustable leak was created at the end of the ETT in a lung model with constant compliance. Flow, tidal volume, and pressure changes were measured above and below the leak. Compliance (Ci) and resistance (Ri) during inspiration were determined by linear regression analysis (LRA) using the equation of motion and the Mead and Wittenberger method (MWM). The ventilatory change that influenced the degree of leak most was prolongation of inspiratory time (Ti). The presence of a leak around the ETT resulted in an overestimation of the Ci and Ri values, which was proportional to the size of the leak. This overestimation was also influenced by the method used to determine Ci and Ri. Because the contribution of the leak to the fidal volume progressively increases as inspiration continued, methods of analysis that depended mainly on measurement points at the end of inspiration showed a larger deviation from the true Ci and Ri values than methods mainly influenced by measurement points at the beginning of inspiration. Because of this, shortening of inspiration, or analysis of points at the beginning of inspiration reduces the error in the measurements of Ci and Ri when a leak is present. Breaths with a large leak should be excluded from any analysis of pulmonary mechanics.

Airway Resistance↗

Influence of different methods of synchronized mechanical ventilation on ventilation, gas exchange, patient effort, and blood pressure fluctuations in premature neonates.

We studied the effects of two methods of synchronized mechanical ventilation [synchronized intermittent mandatory ventilation (SIMV) and assist/control (A/C)] on ventilation, gas exchange, patient effort, and arterial blood pressure (ABP) fluctuations. SIMV and A/C were applied in random order in 12 preterm neonates (gestational age, 29.7 +/- 2.3 weeks; birth weight, 1,217 +/- 402 g). We measured total (Vetot) and mechanical (Vemech) minute ventilation, spontaneous (Vtspont) and ventilator supported (Vtmech) tidal volume, transcutaneous oxygen saturation (SpO2), transcutaneous PO2 (TcPO2), and PCO2, (TcPCO2), mean airway pressure (Paw), phasic esophageal pressure deflections (Pe) as an estimate of inspiratory effort, mean arterial blood pressure (ABP), and beat-to-beat ABP fluctuations. The measurements obtained during conventional intermittent mandatory ventilation (IMV) were compared with the recordings during SIMV and A/C. To make the measurement conditions comparable and to prevent hyperventilation, peak inspiratory pressure was reduced during the A/C mode so that Vetot remained in the same range as during the IMV mode. Whereas Vetot was similar in all three conditions by study design, Vemech was larger during SIMV and A/C than during IMV. Vtmech increased during SIMV and by study design was smaller during A/C than during IMV. Pe decreased during SIMV and A/C compared with IMV, and Paw was higher during A/C than during IMV or SIMV. Beat-to-beat ABP fluctuations were reduced during SIMV and A/C compared with IMV and showed a close positive correlation with Pe changes. We conclude that SIMV increases Vemech and reduces Pe compared with IMV, resulting in smaller intrathoracic and ABP fluctuations. During A/C, a substantial portion of the spontaneous respiratory effort is shifted to the ventilator, resulting in a further decrease in Pe and ABP fluctuations.

Blood Pressure↗

Decreased ventilatory response to hypoxia in sedated newborn piglets prenatally exposed to cocaine.

OBJECTIVE: Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets. METHODS: Cocaine hydrochloride, 1.0 or 2.0 mg/kg given intramuscularly, or saline solution was administered daily to pair-fed pregnant sows during the last month of gestation. Thirteen cocaine-exposed piglets (mean +/- SD: age, 4.4 +/- 1.3 days; weight, 2.10 +/- 0.10 kg) and 15 saline solution-exposed piglets (age, 4.6 +/- 1.1 days; weight, 2.32 +/- 0.42 kg) were studied under chloral hydrate sedation. Minute ventilation (VE), arterial blood pressure (BP), heart rate (HR), oxygen consumption (VO2), and arterial blood gases were measured in room air. During hypoxia (fraction of inspired oxygen = 0.10), the values for VE, BP, and HR were obtained at 1, 5, and 10 minutes, VO2 was calculated during the last 5 minutes, and arterial blood gas samples taken after 10 minutes. RESULTS: Basal VE did not differ between saline solution- and cocaine-exposed animals. The increase in VE at 1 minute of hypoxia was also similar. However, at 5 and 10 minutes of hypoxia, VE was significantly lower in the cocaine group than in the saline group (6% +/- 9% and 4% +/- 10% vs 15% +/- 13% and 21% +/- 14%; p < 0.02). Mean baseline BP and the initial increase in BP during hypoxia were not different between groups. However, BP remained increased throughout hypoxia only in the saline solution-exposed animals (p < 0.05). Changes in HR, VO2, arterial oxygen tension, and base excess during hypoxia were similar between groups. CONCLUSIONS: These results show a decrease in the ventilatory response to hypoxia in newborn piglets prenatally exposed to cocaine. This change is most likely to be centrally mediated because the initial hypoxic hyperventilation was not modified by the intrauterine cocaine exposure. This decrease in ventilation cannot be explained by changes in metabolic rate or in cardiovascular or acid-base status.

Animals↗

Influence of infection on patent ductus arteriosus and chronic lung disease in premature infants weighing 1000 grams or less.

OBJECTIVES: To test the hypotheses that (1) infection increases ductal dilatory prostaglandins and inflammatory mediators that may influence the closure of a patent ductus arteriosus (PDA), increasing the incidence of late episodes of PDA (after 7 days) and the rate of closure failures, and (2) the concurrence of PDA and infection increases the risk of chronic lung disease (CLD). METHODS: One hundred fourteen premature infants (birth weight, 500 to 1000 gm) were prospectively assessed for PDA and infection. Serum levels of 6-ketoprostaglandin F1 alpha and tumor necrosis factor alpha were measured routinely in all infants and when PDA or infection was present. Multivariate assessment of risk factors for PDA closure failure and for CLD was done by logistic regression, and expressed as an odds ratio and as 95% confidence intervals. RESULTS: Late PDA episodes were more frequent in infants with infection than in those without infection. A temporally related infection (<5 days between both diagnoses) was associated with an increased risk of PDA closure failure (odds ratio, 19.1 (confidence interval, 4 to 90)). In addition to birth weight and the severity of initial respiratory failure, PDA and infection increased the risk of CLD (odds ratio, 11.7 (confidence interval, 1.7 to 81) for PDA; odds ration, 3.1 (confidence interval, 1 to 11) for infection). Furthermore, when both factors were temporally related, they further increased the risk of CLD (odds ratio, 29.6 (confidence interval, 4.5 to >100)). Infants with infection and those with PDA had higher levels of 6-ketoprostaglandin F1 alpha than did control subjects. Levels of tumor necrosis factor alpha were also elevated in infants with infection and in those with late PDA. CONCLUSIONS: Infection adversely influences PDA outcome by increasing the risk of late ductal reopening and PDA closure failures. Increased levels of prostaglandins and tumor necrosis factor alpha in infants with infection may explain the poor PDA outcome. The concurrence of PDA and infection potentiates their negative effects on the risk of CLD.

Chronic Disease↗

Effect of N-methyl-D-aspartate-receptor blockade on hypoxic ventilatory response in unanesthetized piglets.

The central excitatory amino acid (EAA) neurotransmitter glutamate has been shown to mediate the ventilatory response to hypoxia through N-methyl-D-aspartate (NMDA) receptors in anesthetized adult animals. To determine the role of the EAA glutamate in the neonatal ventilatory response to hypoxia, 19 unanesthetized chronically instrumented piglets were studied. Minute ventilation (VE), oxygen consumption (VO2), arterial blood pressure (ABP), heart rate (HR), and blood gases were measured in room air (RA) and after 1, 5, and 10 min of hypoxia (inspired oxygen fraction = 0.10) before and after an infusion of saline or CGS-19755, a competitive NMDA-receptor blocker (10 mg/kg i.v.). Nine control piglets [age 6 +/- 1 (SD) days; weight 2.02 +/- 0.40 kg] and 10 CGS-19755-treated animals (age 6 +/- 1 days; weight 1.90 +/- 0.66 kg) were studied during quiet sleep and in a thermoneutral environment. There was a marked decrease in the VE response to hypoxia after the administration of CGS-19755. The ventilatory response to hypoxia was not modified by saline infusion. Changes in ABP and arterial PO2 during hypoxia were similar between groups, whereas the decrease in arterial PCO2 was significantly less after CGS-19755 administration. The increase in HR with hypoxia was eliminated by the NMDA-receptor blocker administration. VO2 decreased with hypoxia in both groups, but this decrease was more marked after the NMDA-receptor blockade. These results suggest that the central EAA glutamate mediates, at least in part, the hypoxic hyperventilation in unanesthetized newborn piglets.

Animals↗

Effects of the cyclooxygenase inhibitor ibuprofen on retinal and choroidal blood flow during hyperoxia in newborn piglets.

PURPOSE: The effect of the cyclooxygenase inhibitor ibuprofen (IB) on choroidal (ChBF) and retinal (RBF) blood flow during hyperoxia was examined in 21 spontaneously breathing newborn piglets. METHODS: ChBF and RBF were measured using radiolabelled microspheres before and 30 min after either saline or IB (30 mg/kg, i.v.) infusion in room air and subsequently, after 90 min of hyperoxia (O2). RESULTS: The basal RBF and ChBF did not change after IB infusion. However, during hyperoxia a significant decrease in RBF was observed in the IB group (54 +/- 5 to 37 +/- 3 ml/min/100 g, p < 0.02) and in the control group (54 +/- 3 to 37 +/- 5 ml/min/100 g, p < 0.02). Also, ChBF decreased in the IB group (2,635 +/- 446 to 1,670 +/- 199 ml/min/100 g, p < 0.02) and in the control group, (2,997 +/- 346 to 2,014 +/- 246 ml/min/100 g,p < 0.02) during hyperoxia. CONCLUSIONS: Despite cyclooxygenase inhibition with IB, RBF and ChBF decreased to the same extent as in the control group following exposure to O2. These data suggest that hyperoxia decrease RBF and ChBF through mechanisms and/or mediators other than the cyclooxygenase by-products of arachidonic acid metabolism.

Animals↗

Effects of chloral hydrate on the cardiorespiratory response to hypoxia in newborn piglets.

To assess the effects of chloral hydrate (CH) on the cardiorespiratory response to hypoxia in the neonate, 17 newborn piglets were chronically instrumented 48-72 h before study and randomly assigned to a CH group (100 mg/kg, i.p.) or saline group. The animals were intubated and studied under quiet sleep which was determined by behavioral states, and continuous electro-oculographic and electroencephalographic monitoring. Minute ventilation (VE), tidal volume, respiratory rate, arterial blood gases (ABG), oxygen consumption (VO2), arterial blood pressure (ABP) and heart rate (HR) were measured before and after CH or saline administration during room air and after 10 min of hypoxia (fraction of inspired oxygen concentration = 0.10). Cardiorespiratory response to hypoxia was similar before and after saline infusion. Basal VE and the ventilatory response to hypoxia were similar before and after CH administration. In contrast, the basal ABP decreased significantly (p < 0.05) after CH administration, but the ABP response to hypoxia was similar before and after CH. A significant increase in both basal HR and HR with hypoxia was observed after CH administration. In addition, VO2 and ABG were not modified by CH treatment during normoxia and hypoxia. These data demonstrate that a sedative dose of CH does not significantly modify the ventilatory response to hypoxia in newborn piglets. However, CH produced some changes in the cardiovascular system which should be considered when using it in infants with hemodynamic derangements.

Animals↗

Patient-triggered ventilation in neonates: comparison of a flow-and an impedance-triggered system.

We conducted a study with the objective of comparing the performance of two different systems for patient-triggered ventilation in neonates (impedance versus flow/volume-triggered) by measuring response time, autotrigger and trigger failure rates, ventilation, and gas exchange. The two ventilator systems were applied in random order in 10 preterm neonates (median gestational age: 30.5 wk; range: 27 to 34 wk; body weight: 1,266 g; range: 840 to 2,240 g) using identical ventilator settings. The median (range) response time was 169 (98 to 305) ms for the impedance system and 115 (79 to 184) ms for the flow/volume system (p < 0.01). The longer and more variable response time of the impedance system was secondary to a phase lag of the impedance signal caused by chest wall distortion. Although 13.1 (0.2 to 29.4)% of mechanical breaths were autotriggered with the impedance system, there were no autotriggered breaths using the flow/volume system (p < 0.01). The rate of trigger failures was not significantly different with the two systems, at 1.2 (0 to 4.4)% (impedance) versus 3.1 (0 to 6.4)% (flow/volume). Minute ventilation was smaller with the impedance system (p < 0.001), because of the larger number of breaths triggered late in inspiration or during expiration. We conclude that the flow/volume-triggered system is less prone to autotriggering and has a shorter and more consistent response time than the impedance-triggered system. The impedance-triggered system is more susceptible to artifacts and chest wall distortion.

Female↗

Effects of ATP-magnesium chloride on the cardiopulmonary manifestations of group B streptococcal sepsis in the piglet.

Low dose ATP-MgCl2 is reported to cause selective pulmonary vasodilation during hypoxic and thromboxane mimetic-induced constriction. In addition, it has been shown to increase cardiac output and improve cellular function during circulatory shock. Based on these properties we hypothesized that ATP-MgCl2 might ameliorate the cardiopulmonary manifestations of sepsis secondary to group B streptococci (GBS). We studied 14 anesthetized, mechanically ventilated piglets who received a continuous infusion of GBS (7.5 x 10(7) colony-forming units/kg/min) and were randomly assigned to a treatment group that received a continuous infusion of ATP-MgCl2 at 0.6 mumol/kg/min or a control group that received normal saline as placebo. Comparison of the hemodynamic measurements, pulmonary mechanics, and arterial blood gases over the first 120 min of ATP-MgCl2 infusions with those of the control group revealed the following: GBS infusion caused significant increases in mean pulmonary artery pressure, pulmonary vascular resistance (PVR), mean systemic arterial blood pressure, systemic vascular pressure (SVR), and PVR/SVR ratio with decreases in cardiac output and stroke volume. ATP-MgCl2 caused significant reduction in mean pulmonary artery pressure (p < 0.001), PVR (p < 0.0001), mean systemic arterial blood pressure (p < 0.003), SVR (p < 0.01), and PVR/SVR ratio (p < 0.03) with improvement in cardiac output (p < 0.001) and stroke volume (p < 0.01). The partial pressure of arterial O2 (p < 0.04), and pH (p < 0.001) were higher and the partial pressure of arterial CO2 (p < 0.02) lower in ATP-MgCl2-treated animals. Also dynamic lung compliance was higher (p < 0.001) and pulmonary airway resistance lower (p < 0.001) in treated animals. Median survival in control animals was 153 min, whereas all treated animals survived to 240 min (p < 0.001). These data demonstrate that ATP-MgCl2 ameliorates the deleterious cardiopulmonary manifestations of GBS sepsis and results in improved survival in a young animal model.

Adenosine Triphosphate↗

Effects of treatment with pentoxifylline on the cardiovascular manifestations of group B streptococcal sepsis in the piglet.

Pentoxifylline (PTXF) is a methylxanthine derivative which modifies leukocyte function and inhibits tumor necrosis factor (TNF)-alpha release. As TNF-alpha is considered a proximal mediator in the cascade leading to septic shock, we evaluated the ability of PTXF to attenuate the cardiovascular manifestations of sepsis secondary to an infusion of group B beta-hemolytic streptococci (GBS). Fifteen anesthetized, mechanically ventilated piglets (weight, 2815 +/- 552 g) were randomly assigned to a treatment group which received a continuous infusion of PTXF (5 mg/kg/h) beginning 30 min after GBS (7.5 x 10(8) colony-forming units/kg/min) administration was started or to a control group which received GBS plus saline as placebo. Comparison of the hemodynamic measurements and arterial blood gases over the first 120 min of bacterial infusion for treatment and control groups revealed the following statistically significant differences (120-min values presented): cardiac output was significantly higher in the PTXF group (0.159 +/- 0.035 versus 0.09 +/- 0.026 L/kg/min; p < 0.05) as was stroke volume (0.54 +/- 0.11 versus 0.27 +/- 0.126 mL/kg/beat; p < 0.01). Pulmonary and systemic vascular resistances remained lower in the PTXF-treated animals (167 +/- 45 versus 233 +/- 69 mm Hg/L/kg/min; p < 0.03) and (427 +/- 162 versus 828 +/- 426 mm Hg/L/kg/min; p < 0.03, respectively). Median survival time was significantly longer in the PTXF group (180 versus 120 min; p < 0.05). In an additional group of animals, PTXF administration before GBS infusion revealed no attenuation in the rise of TNF-alpha, accompanying sepsis. These data demonstrate that treatment with PTXF may ameliorate some of the deleterious hemodynamic manifestations of GBS sepsis and result in improved survival in a young animal model without significantly modifying plasma TNF-alpha levels.

Animals↗

Effects of dexamethasone on retinal and choroidal blood flow during normoxia and hyperoxia in newborn piglets.

Our purpose was to study the effect of dexamethasone (DEX) on choroidal (ChBF) and retinal blood flow (RBF) during normoxia and hyperoxia. Eighteen spontaneously breathing newborn piglets were examined. ChBF and RBF were measured using radiolabeled microspheres while the piglets were in normoxia before (RA1) and 45 min after either saline or DEX (2 mg/kg) infusion (RA2), and after 90 min of hyperoxia (O2) (Pao2 40-60 kPa). Vitreous prostanoids (prostaglandins F1 alpha and E2 and thromboxane B2) and leukotrienes (leukotriene B4) measurements were obtained during normoxia after either placebo or DEX infusion in an additional 22 piglets. Vitreous prostanoids were also studied after 90 min of hyperoxia. We found that RBF increased significantly after DEX infusion (p < 0.02). There was no change in RBF from RA1 to RA2, before and after saline infusion. RBF decreased significantly during hyperoxia in both groups (p < 0.03). ChBF did not change significantly between RA1 and RA2 in any of the groups. ChBF decreased significantly during hyperoxia in both groups (p < 0.03). Vitreous prostanoids and leukotrienes were reduced significantly after DEX infusion (p < 0.05). Prostanoids were similar in the two groups during hyperoxia. We concluded that DEX increases RBF significantly, but not ChBF. RBF and ChBF decreased in both groups during hyperoxia. Therefore, the metabolites of arachidonic acid do not seem to be involved as mediators of hyperoxic vasoconstriction.

Animals↗