The role of inflammation in the pathogenesis of bronchopulmonary dysplasia.
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Animals↗
Biomedical subjects
E Bancalari
Publications and source records attributed to E Bancalari.
Effect of chestwall distortion on the measurement of pulmonary mechanics in preterm infants.
The purpose of this study was to determine the effect of chestwall distortion (CWD) on the measurement of pulmonary compliance (CL) and resistance (RL). Inductance plethysmography was used in 15 preterm infants to determine CWD as total compartmental displacement ratio (TCDR) and out of phase movement between ribcage and abdomen as phase shift (PS). Flow was measured by pneumotachography and esophageal pressure change (Pe) with a water-filled catheter. CL and RL were calculated by linear regression analysis. Seven infants (mean +/- SD: BW, 1,484 +/- 186 g, GA 32.4 +/- 2.2 weeks, age 8.7 +/- 4.7 days) had a breathing pattern characterized by episodes with a high degree of CWD, followed by periods with minimal CWD (distortion group). In this group lung function measurements were analyzed separately during periods with and without CWD. The remaining 8 infants (BW, 1,244 +/- 233 g, GA 30.4 +/- 2.4 weeks, age 7.4 +/- 3.1 days) always breathed with minimal CWD, and the measurements in this group (non-distortion group) were used as a reference for the values obtained in the distortion group. Measurements of TCDR, PS, CL, RL, and tidal volume (VT) obtained in the absence of CWD were not significantly different between distortion and non-distortion groups. The measurements obtained in the presence of CWD showed a significantly higher TCDR and PS, but CL and RL were not significantly different from the CL and RL measurements obtained in the distortion and non-distortion groups in the absence of CWD. The only significant effect of CWD was a reduction in VT.(ABSTRACT TRUNCATED AT 250 WORDS)
Birth Weight↗
Mechanisms for episodes of hypoxemia in preterm infants undergoing mechanical ventilation.
OBJECTIVE: To ascertain possible mechanisms implicated in the development of transient episodes of hypoxemia (oxygen saturation < 85%) frequently observed in preterm infants undergoing mechanical ventilation, even after the acute phase of respiratory failure has passed. STUDY DESIGN: Tidal flow, airway and esophageal pressure, and oxygen saturation were continuously recorded in 10 infants (mean +/- SD, birth weight 733 +/- 149 gm, gestational age 25.5 +/- 2.2 weeks, age 26.3 +/- 11.9 days) who had repeated episodes of hypoxemia without any evident cause. Measurements of minute ventilation (VE) inspiratory compliance (Ci), and inspiratory resistance (Ri) were compared before and during episodes of hypoxemia. RESULTS: All episodes of hypoxemia were preceded by an active exhalation that produced a mean decrease in end-expiratory lung volume of 6.4 +/- 2.8 ml/kg. The reduction in lung volume was immediately followed by a sudden decrease in tidal flow and volume, despite continuation of mechanical ventilation at the same rate and peak pressure. The resulting hypoventilation was associated with a drop in Ci to approximately one half and an increase in Ri to more than double the baseline values. Approximately 30 seconds after the beginning of hypoventilation, the arterial oxygen saturation reached a hypoxemic level (oxygen saturation < 85%)> CONCLUSION: Most hypoxemic episodes were triggered by an expiratory effort that produced a large decrease in lung volume. This reduction in lung volume probably leads to closure of small airways and the development of intrapulmonary shunts, which would explain the rapid development of hypoxemia.
Analysis of Variance↗
Changing trends in the epidemiology and pathogenesis of neonatal chronic lung disease.
OBJECTIVE: To assess the role of specific risk factors that may predispose preterm infants with mild or no initial respiratory distress syndrome to the development of chronic lung disease (CLD). STUDY DESIGN: Clinical data were collected prospectively from 119 ventilator-supported preterm infants with birth weights between 500 and 1000 gm, who survived more than 28 days and required fewer than 3 days of treatment with fraction of inspired oxygen > 25% during the first 5 days of life. Logistic regression analysis was used in a multivariate assessment of risk factors for CLD. RESULTS: Chronic lung disease occurred in 44 of the patients (37%). The analysis showed that low birth weight, patent ductus arteriosus (PDA), and sepsis were significant risk factors for CLD. The corresponding odds ratios for CLD and their 95% confidence intervals (CI) were as follows: 2.9 per 100 gm birth weight decrement (CI, 1.7 to 4.8); 6.2 (CI, 2.1 to 18.4) for PDA; and 4.4 (CI, 1.3 to 14.5) for sepsis. When sepsis and PDA occurred simultaneously, the odds ratio for CLD increased to 48.3 (CI, 6.3 to > 100) in comparison with infants without these conditions. Episodes of PDA were categorized as either early (occurring during the first week of life) or late (after the first week), and the respective odds ratios for CLD were 2.8 (CI, 0.8 to 9.4) and 21.1 (CI, 5.6 to 80) in comparison with infants without PDA. For the duration of symptomatic PDA, the odds ratio for CLD was 3.5 per week that the PDA remained open (CI, 1.9 to 6.5). CONCLUSION: CLD is a frequent sequela in very low birth weight infants with mild or no respiratory distress syndrome. In this population, the development of late episodes of PDA, usually in association with a nosocomial infection, seems to play a primary role in the pathogenesis of CLD.
Chronic Disease↗
Effects of epinephrine on the cardiorespiratory response to hypoxia in sedated newborn piglets with intact and denervated carotid bodies.
In order to evaluate the effects of epinephrine on the cardiorespiratory response to hypoxia in the neonate, 35 sedated, spontaneously breathing newborn piglets (mean +/- SD, age 5 +/- 0.8 days; weight 1.6 +/- 0.3 kg) with intact (ICB) or denervated (DCB) carotid bodies were studied before and during an infusion of saline or epinephrine (2.2 +/- 1.0 microgram/kg/min, i.v.). Cardiorespiratory measurements were performed while the animals breathed room air and after 10 min of hypoxia (FiO2 0.10) during saline or epinephrine infusion. During epinephrine infusion, the ICB animals had a sustained increase in minute ventilation during hypoxia while the control group showed a biphasic ventilatory response with depression during sustained hypoxia. After the chemodenervation, the ventilatory response to hypoxia was completely blunted in saline and epinephrine animals. In the ICB and DCB animals, the arterial blood pressure decreased significantly with hypoxia during epinephrine infusion, while cardiac output increased significantly in all ICB and DCB saline animals. The oxygen consumption (VO2) decreased significantly after 10 min of hypoxia in all groups except in the ICB epinephrine animals, in whom the VO2 did not change with hypoxia. In conclusion, the administration of epinephrine to newborn piglets reverses the depressed ventilatory response to hypoxia and this effect requires the activity of the peripheral chemoreceptors.
Animals↗
Cardiopulmonary effects of tumor necrosis factor-alpha in the piglet: influence of cyclooxygenase inhibition.
Tumor necrosis factor-alpha (TNF) is believed to play an important role in mediating many of the pathophysiologic changes accompanying bacterial sepsis. In order to characterize the cardiopulmonary responses to TNF in a young animal model and to determine to what extent these changes were secondary to cyclooxygenase byproducts, three groups of mechanically ventilated piglets received an infusion of either TNF, indomethacin followed by TNF (Indo+TNF) or neither (control). Compared to controls at 120 min, TNF resulted in the following changes beginning 30-60 min after the infusion began: mean pulmonary artery pressure (Ppa) increased from 1.7 +/- 0.3 to 4.4 +/- 0.7 kPa (13 +/- 2 to 33 +/- 5 mm Hg) (p < 0.001); cardiac output (CO) fell from 0.28 +/- 0.05 to 0.20 +/- 0.07 liters/kg/min (p < 0.01); mean arterial blood pressure (Psa) decreased from 9.5 +/- 1.2 to 7.9 +/- 1.9 kPa (71 +/- 9 to 59 +/- 14 mm Hg) as did pH from 7.49 +/- 0.04 to 7.13 +/- 0.17 (p < 0.001). Dynamic lung compliance (Cdyn) also decreased; however, pulmonary resistance (RI) remained unchanged. Thromboxane B2 (TxB2) rose in all animals at 60 min coincident with Psa elevation and was significantly blocked by Indo (p < 0.03). In the Indo+TNF group the early TNF-induced rise in Psa was blunted compared to the TNF group [2.9 +/- 1.2 vs. 3.6 +/- 0.8 kPa (22 +/- 3 vs. 27 +/- 6 mm Hg; p < 0.04)] as were the late decreases in pH and Psa (p < 0.04). There were no significant changes in Cdyn secondary to Indo. Although delayed, the hemodynamic changes observed with TNF infusion are similar to those reported for piglets receiving group B streptococci; however, in contrast to the latter the early changes secondary to TNF are only mildly effected by indomethacin. The significant improvement in the late occurring hypotension and acidosis suggests that TNF may act in part via the cyclooxygenase pathway as a mediator of the late hypotension associated with sepsis.
Animals↗
Influence of chest wall distortion and esophageal catheter position on esophageal manometry in preterm infants.
The purpose of this study was to determine the effect of chest wall distortion on esophageal manometry by measuring simultaneous esophageal pressure changes at two sites in preterm infants. Fourteen infants were studied (mean +/- SD; birth weight, 1340 +/- 260 g; age, 8.5 +/- 4 d). Esophageal pressure was measured through two water-filled catheters, one placed just above the cardia (Pes1) and the other at the level of the carina (Pes2). Chest wall distortion was measured by inductance plethysmography, and inspiratory and expiratory flow by pneumotachography. No significant differences were found between the peak to peak esophageal pressure changes measured through the lower and higher catheters during both airway occlusion (18.7 +/- 4.4 versus 18.3 +/- 2.6 cm H2O) and spontaneous breathing (9.4 +/- 1.8 versus 9.0 +/- 1.8 cm H2O), although half of the infants had significant chest wall distortion. Mean pulmonary compliance and resistance measures calculated from the two pressures for individual infants showed small differences consistent with the difference between Pes1 and Pes2. For the whole group of 14 infants, however, these differences were not significant. The pressure changes from the lower and higher measuring sites for each breath were analyzed using linear regression. The weighted average of the mean slopes of the 14 infants was significantly different from 1.0 (mean +/- SD: 0.92 +/- 0.10, range: 0.75-1.10; p < 0.05). In some of the infants, the slopes for different breaths were not consistent, but varied from breath to breath.(ABSTRACT TRUNCATED AT 250 WORDS)
Airway Resistance↗
Effect of an interleukin-1 receptor antagonist on the hemodynamic manifestations of group B streptococcal sepsis.
IL-1 is purported to be a proximal mediator in the cascade leading to septic shock. To characterize its hemodynamic effects and to ascertain whether its blockade would ameliorate the deleterious consequences of sepsis, an IL-1 receptor antagonist (IL-1ra) was administered to 16 anesthetized, mechanically ventilated piglets that received a continuous infusion of group B streptococci (GBS) (7.5 x 10(7) colony-forming units/kg/min). Systemic (Psa), pulmonary artery (Ppa), and wedge (Pwp) pressures and cardiac output were measured pre-GBS and every 30 min during GBS infusion. After 15 min of bacterial infusion the control group received normal saline, whereas the treatment group received a bolus of IL-1ra (40 mg/kg) followed by a continuous infusion of IL-1ra (60 micrograms/kg/min). In comparing IL-1ra-treated animals with controls from the 15-min GBS baseline to the succeeding septic study period (45-120 min), the following treatment effects were noted (120-min values shown): mean Psa remained elevated in treatment compared with control animals (12.7 +/- 2.5 versus 9 +/- 3.5 kPa; p < 0.001) as did CO (0.21 +/- 0.07 versus 0.13 +/- 0.08 L/min/kg; p < 0.001). Pwp decreased in the treatment compared to the control group over the study period (1 +/- 0.3 versus 1.6 +/- 0.7 kPa; p < 0.02). Mean Ppa and mean Pra were not different between groups over time. Median length of survival was significantly longer (p = 0.04) in treated (226 min) compared with control animals (150 min). These data suggest that IL-1 plays an important role in GBS sepsis and septic shock, and that IL-1ra may in part ameliorate the cardiovascular alterations associated with GBS sepsis in the neonate.
Animals↗
Comparison of the effects of acetazolamide and aminophylline on apnea incidence and on ventilatory response to CO2 in preterm infants.
Acetazolamide (ACTZ) reduces sleep apnea in adults exposed to high altitude and augments the ventilatory response to CO2. In order to determine the effect of ACTZ on the ventilatory response to CO2 and the incidence of apnea in preterm infants, 7 infants (BW, 1070 +/- 191 g; postnatal age, 9 +/- 7 days) were randomized to receive ACTZ (5 mg/kg/dose Q6h for 36 hr) and 7 infants (BW, 1092 +/- 292 g; post-natal age, 5 +/- 2 days) received aminophylline (AMINO; 8 mg/kg bolus then 2.5 mg/kg Q12h for 36 hr). Minute ventilation (VE), end-tidal CO2 (PETCO2), ventilatory response to CO2, number of apneic episodes (> or = 15 sec duration), and arterial blood gases were measured before and 24-36 hr after starting therapy. In the AMINO group there was a significant decrease in apnea frequency from 6 +/- 1 to 2 +/- 2 episodes over an 8 hr epoch (P < 0.05), while no significant change was observed in the ACTZ group. The end-tidal CO2 decreased significantly from 44 +/- 7 to 38 +/- 6 mmHg in the AMINO group and from 47 +/- 5 to 36 +/- 5 mmHg in the ACTZ (P < 0.05), which lead to a shift to the left of the CO2-response curve in both groups. The slope of the CO2 response curve did not change significantly in the AMINO group and decreased in the ACTZ group. There was a significant decrease of pH from 7.43 to 7.26 in the ACTZ group, whereas in the AMINO group pH increased from 7.38 to 7.44.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetazolamide↗
Effect of dopamine on hypoxic ventilatory response of sedated piglets with intact and denervated carotid bodies.
To determine whether the neonatal hypoxic ventilatory depression is in part produced by an increased endogenous dopamine release that can depress the activity of central and peripheral chemoreceptors, 31 sedated and spontaneously breathing newborn piglets [age 5 +/- 1 (SD) days; weight 1.7 +/- 0.4 kg] were randomly assigned to an intact carotid body or a chemodenervated group. Minute ventilation (VE), arterial blood pressure, and cardiac output (CO) were measured in room air before infusion of saline or the dopamine antagonist flupentixol (0.2 mg/kg i.v.) and 15 min after drug infusion and were repeated after 10 min of hypoxia (inspiratory O2 fraction = 0.10). VE increased significantly after 10 min of hypoxia in the piglets that received flupentixol independent of whether the carotid bodies were intact or denervated. However, the increase in VE was largest and sustained throughout the 10 min of hypoxia only in the intact carotid body flupentixol group. As expected, the initial increase in VE with hypoxia was abolished by carotid body denervation. Changes in arterial blood gases, CO, and mean arterial blood pressure with hypoxia were not different among groups. These results demonstrate that flupentixol reverses the late hypoxic decrease in VE, acting through peripheral and central dopamine receptors. This effect is not related to changes in cardiovascular function or acid-base status.
Acid-Base Equilibrium↗
Effects of GABA receptor blockage on the respiratory response to hypoxia in sedated newborn piglets.
Brain gamma-aminobutyric acid (GABA) levels increase during hypoxia, which may modulate the ventilatory response to hypoxia. To test the possibility that the depressed neonatal ventilatory response to hypoxia may be related to increased central nervous system GABA activity, 26 sedated spontaneously breathing newborn piglets (age 5 +/- 1 day, wt 1.7 +/- 0.4 kg) were studied. Minute ventilation (VE), oxygen consumption, heart rate, arterial blood pressure, and arterial blood gases were measured in room air and after 1, 5, and 10 min of hypoxia (inspired O2 fraction 0.10) before drug intervention. Immediately after these measurements, an infusion of saline or the GABA alpha-receptor blocker (bicuculline, 0.3 mg/kg iv) or beta-receptor blocker (CGP-35348, 100-300 mg/kg iv) was administered while animals were hypoxic. All measurements were repeated at 1, 5, and 10 min after initiation of the drug infusion. Basal VE was similar among groups. During hypoxia, VE increased significantly in the animals that received either a GABA alpha- or beta-receptor blocker but not in those receiving saline. Changes in arterial Po2, oxygen consumption, heart rate, and arterial blood pressure were similar among groups before and after saline or GABA antagonist infusion. These results suggest that the decrease in ventilation during the biphasic ventilatory response to hypoxia in the neonatal piglet is in part mediated through the depressant effect of GABA on the central nervous system.
Animals↗
Validation of cardiac output measurements with noninvasive Doppler echocardiography by thermodilution and Fick methods in newborn piglets.
Since cardiac output measured by the noninvasive pulsed Doppler technique has not been well correlated to results from the invasive thermodilution or Fick methods in neonates, the three methods were evaluated in 6 sedated newborn piglets (age < or = 7 days, weight 1.5 +/- 0.7 kg) in room air and after 10 min of hypoxia. Doppler velocities were measured in the ascending aorta, and the aortic root diameter was measured in early diastole. A Swan-Ganz catheter in the left pulmonary artery sampled mixed venous blood for central venous O2 content and measured cardiac output by thermodilution. Oxygen consumption was measured by the open-circuit technique and used to determine cardiac output by the Fick method. In room air, values obtained by pulsed Doppler, thermodilution and Fick methods (0.270 +/- 0.05, 0.246 +/- 0.05 and 0.241 +/- 0.05 liters/kg/min, respectively) were similar, with a correlation coefficient (r) between Doppler and thermodilution values of 0.89, Doppler and Fick values of 0.82 and thermodilution and Fick values of 0.88. Although hypoxia sometimes produced larger differences between paired values, correlation coefficients remained high (Doppler echocardiography vs. thermodilution, r = 0.96; Doppler vs. Fick methods, r = 0.92; thermodilution vs. Fick method, r = 0.95). The mean +/- SD of the percent difference between values obtained by Doppler echocardiography and thermodilution was 4.2 +/- 14.4% in room air and 12.8 +/- 14.4% in hypoxia, whereas differences in values obtained by Doppler and Fick methods was 6 +/- 14.9% in room air and 14.7 +/- 8.5% with hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of amino acid infusion on the ventilatory response to hypoxia in protein-deprived neonatal piglets.
Several amino acids (AA) act as neurotransmitters and mediate the ventilatory response to carbon dioxide and hypoxia in adult human beings and animals. To evaluate the influence of AA on the neonatal ventilatory response to hypoxia, 29 newborn piglets less than 5 d old were randomly assigned to a control diet or protein-free diet for 7-10 d. Minute ventilation, arterial blood pressure, oxygen consumption, and arterial blood gases were measured in sedated, spontaneous breathing piglets while they breathed room air and at 1, 5 and 10 min of hypoxia (fraction of inspired oxygen concentration--0.10) before and after 4 h of AA (Trophamine, 3 g/kg, i.v.) or 10% dextrose infusion. The administration of AA solution in protein-deprived piglets resulted in a significant increase in minute ventilation after 10 min of hypoxia (26 +/- 19%) in comparison with their ventilatory response before AA infusion (10 +/- 12%; p < 0.02). Similar increase in the ventilatory response to hypoxia was observed in the control diet group after AA infusion (23 +/- 17% versus 11 +/- 11%; p < 0.05). Changes in arterial blood pressure, oxygen consumption, and arterial blood gases during hypoxia were similar before and after AA infusion. The ventilatory response to hypoxia in both protein-free and control diet animals were similar before and after the 10% dextrose infusion. These results stress the importance of nutritional factors in the neonatal control of breathing.
Acid-Base Equilibrium↗
Electroencephalography in congenital malformations of the central nervous system.
We studied clinical and EEG features of 36 cases with congenital malformations of the CNS. Patients were followed at the outpatient clinic of Hospital Cayetano Heredia and of Hogar Clinica San Juan de Dios in Lima-Peru, from January 1984 to June 1992. Eighty percent of the patients had convulsive syndromes and mental retardation. The most frequent malformation was agenesis of corpus callosum, and it was not possible to find a "typical" EEG pattern. The second were porencephalic cysts, with a good clinical-EEG correlation. There were two typical cases of schizencephaly, one of hemimegalencephaly with good prognosis, and one of holoprosencephaly. The results are compared to those obtained for a series we previously reported. Data discussed take into account reports on the subject registered in the literature. It is concluded that EEG is an useful method to evaluate possible CNS malformations in developing countries.
Adolescent↗
Changes in ventilation and oxygen consumption during acute hypoxia in sedated newborn piglets.
The purpose of this study was to evaluate the relationship between changes in minute ventilation (VE) and oxygen consumption (VO2) in response to acute hypoxia in the newborn piglet. Twenty-five (mean +/- SD; age, 4.7 +/- 1.1 d; weight, 1451 +/- 320 g) sedated, spontaneously breathing newborn piglets were studied. VE was measured by pneumotachography, and VO2 was measured by the open-circuit technique. Measurements were performed while the animals breathed room air and repeated after 10 min of hypoxia, which was induced by breathing 10% oxygen. Although the mean VE values during hypoxia displayed a typical biphasic ventilatory response, the individual pattern of this ventilatory response to hypoxia was variable. Thirteen animals sustained VE above baseline after 10 min of hypoxia, whereas the 12 remaining animals decreased VE after 10 min of hypoxia to values below their room air baseline. The VO2 values did not differ between groups during normoxia, and a similar decrease in VO2 occurred in both groups after 10 min of hypoxia. Furthermore, no correlation was observed between changes in VE and VO2 during hypoxia either in absolute values or in the percent change from room air baseline. Arterial PO2 decreased similarly in both groups, but PACO2 decreased significantly only in the group that sustained VE above baseline after 10 min of hypoxia. These data demonstrate that in this animal model the hypoxic ventilatory depression is not determined by the decrease in VO2 that occurs during hypoxia.
Animals↗
Effect of early initiation of intravenous lipid administration on the incidence and severity of chronic lung disease in premature infants.
OBJECTIVE: To investigate whether intravenous administration of lipid nutrition (Intralipid) within 12 hours of birth to ventilator-dependent premature infants would decrease the incidence or severity, or both, of chronic lung disease. METHOD: We randomly assigned 133 infants to Intralipid or control groups, using two weight strata: 42 Intralipid versus 37 control subjects in the 600 to 800 gm stratum, and 28 Intralipid versus 26 control subjects in the 801 to 1000 gm stratum. The Intralipid group received 20% Intralipid at < 12 hours after birth, starting at a dose of 0.5 gm/kg and increasing to a maximum of 1.5 gm/kg, maintained through day 7. Control infants received no lipid until after day 7. Neither group received enteral feedings until after day 7. RESULTS: No significant differences in mortality rates were present in the total population (23/70 = 32.9% vs 16/63 = 25.4%; p = 0.35, Intralipid vs control); however, the mortality rate increased significantly in 600 to 800 gm infants receiving Intralipid versus the control infants (20/41 = 47.5% vs 9/37 = 24.3%; p = 0.032). No significant differences were found in the number of infants in whom chronic lung disease developed (requiring oxygen for > or = 28 days), proportion requiring oxygen for > or = 60 days, number of survivors without chronic lung disease, or total oxygen and ventilation requirements. However, 600 to 800 gm infants receiving Intralipid had significantly more pulmonary hemorrhage, and greater numbers of infants receiving Intralipid in both weight categories required supplemental oxygen at day 7. The incidence of other complications of prematurity, time required to regain birth weight, and duration of hospital stay did not differ between groups. CONCLUSION: Intralipid administration initiated at < 12 hours after birth failed to protect very low birth weight premature infants from chronic lung disease. Some of the results raise questions about possible deleterious effects of Intralipid when administered early in the first week of life.
Chronic Disease↗
Metabolic, hemodynamic, and ventilatory responses to respiratory load in sedated neonatal piglets.
Some neonatal species fail to develop the expected degree of hypercapnia during hypoventilation with mechanical loads. We studied 13 spontaneously breathing, sedated piglets (1-9 days old), grouped by age as young (< or = 3 day old) or old (> 3 day old). Baseline measurements of minute ventilation, arterial blood pressure (BP), cardiac output, and O2 consumption were repeated after continuous (inspiratory and expiratory) flow-resistive loading of 330 cmH2O.l-1 x s for 10 min. Older animals [n = 6, age 6.6 +/- 1.9 (SD) days, wt 1.99 +/- 0.5 kg] increased metabolic rate (9.8 +/- 1.4 to 10.5 +/- 1.3 ml.min-1 x kg-1, P < 0.01), whereas younger animals (n = 7, 2.6 +/- 0.6 days, 1.37 +2- 0.3 kg) invariably decreased metabolic rate with loading (9.7 +/- 1.6 to 7.9 +/- 2.6 ml.min-1 x kg-1); changes were different between groups (P < 0.02). Although ventilation decreased with loading in both groups (P < 0.01), younger animals showed a relatively greater fall from baseline values (38 vs. 27%). Despite differences in the degree of hypoventilation, arterial CO2 tension increased similarly in both groups (21%). BP increased (P < 0.01) with loading in older but not younger animals. We conclude that the decreased metabolic rate and limited hemodynamic response in younger piglets reflect an accomodative response to hypoventilation in contrast to that of older animals, which display an adult pattern of increased metabolic rate and BP with loaded breathing.
Anesthesia↗