摘要:

Ten anesthetized, tracheotomized, adult rabbits were used to test the validity of a method for calculation of total respiratory system compliance from resonant frequency (Cr). Reference values were obtained during constant flow inflation of the relaxed respiratory system by dividing the volume gain by the related difference in pressure at the airway opening (inflation method compliance, Ci). The animals were connected to a new type of servo-controlled infant ventilator. Besides volume-controlled mechanical ventilation at constant inspiratory flow rate and intermittent mandatory ventilation, there is a negative ventilator resistance mode integrated in this device for resistive unloading (Schulze A, Schaller P, Gehrhardt B, Mädler H-J, Gmyrek D: Pediatr Res 28:79-82,1990). To measure resonant frequency (fr), the respiratory system was totally unloaded for a short period by a negative ventilator resistance exceeding the combined resistances of the endotracheal tube and airways. This evoked a continuous oscillation at fr. By analogy with electrical circuit theory, Cr was calculated according to C=l/(4π2· I · fr2) where C is compliance and I is inertance. The inertance of the endotracheal tube is given and that of the bronchial tree was ignored assuming a much greater total cross-sectional area and therefore much lower inertance when compared with the endotracheal tube. Three pairs of Ci– Crvalues were obtained from each animal:1) during intact respiratory muscle activity;2) after pancuronium relaxation, and3) after surfactant depletion by saline washout. There was a significant linear correlation between Ciand Crvalues with the regression line lying close to the identity line (Cr=1.1 Ci– 0.74;r=0.97;p<0.0001). Ciincreased from 45.3 ± 9.4 to 47 ± 7.1 mL/kPa after pancuronium relaxation and dropped to 25.5 ± 5.2 after surfactant depletion. The corresponding Crvalues were 49.5 ± 11, 51 ± 8.2, and 27 ± 5.9 mL/kPa, respectively. The frvalue decreased from 274 ± 33.2 min-1before to 267 ± 21.4 after relaxation, and was 371 ± 39.5 min-1after injury.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

To evaluate the effect of an elevation in systemic arterial pressure upon pulmonary blood flow and arterial oxygenation during right ventricular hypertension (RVH), we acutely studied 13 1-d-old piglets. Catheters were positioned in the pulmonary artery, both atria, and the aorta for hemodynamic measurements. An electromagnetic probe was positioned in the main pulmonary artery for pulmonary blood flow measurement. Systemic and regional blood flow were measured with the radiolabeled microsphere technique. A balloon-mounted catheter was advanced in the aorta and maintained at the lower thoracic level. After induction of RVH (pulmonary artery banding), a significant decrease in arterial O2pressure from 54.4 ± 1.6 to 10.6 ± 0.4 kPa (p< 0.01), a 30% reduction in systemic arterial pressure, and a 44% decrease in pulmonary blood flow were observed. During RVH, partial inflation of the aortic balloon to restore the systemic arterial pressure to its initial value led to an increase in arterial O2pressure to 23.5 ± 3.1 kPa (p< 0.01). Full inflation of the balloon further increased the arterial O2pressure to 32.6 ± 2.9 kPa (p< 0.01). Aortic balloon inflation increased pulmonary blood flow in 11 and systemic O2delivery in nine of the 13 animals. RVH was associated with a significant increase in cerebral and right ventricular myocardial free-wall blood flow and a decrease in renal and bowel blood flow and O2delivery (p<0.01). Aortic balloon inflation during RVH did not change either the cerebral or myocardial free-wall blood flow, but further significantly decreased renal and bowel blood flow and O2delivery. In conclusion, an elevation in systemic arterial pressure significantly reduces foramen ovale shunt and increases pulmonary blood flow and systemic O2delivery in the newborn pig with RVH. This finding may prove useful in the clinical management of hypoxemic infants with persistent pulmonary hypertension syndrome.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1αproduction, and cerebral metabolic rate of oxygen (CMRO2) during hypercapnia and during hypercapnia at increased mean airway pressure (Pāw), both before and after treatment with indomethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Pāw was increased from 3 ± 2 to 16 ± 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Pāw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin F1αincreased from 9 ± 1 to 15 ± 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 ± 1 ng/min/100 g when hypercapnia was coupled with an increase in Pāw. CMRO2was not changed by either hypercapnia or increased Pāw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Pāw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hypercapnic hyperemia requires brain prostanoid production and that when Pāw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The purpose of this project was to study the role of lipid peroxidation in oxygen-induced lung injury in the newborn lamb. It was our hypothesis that injury to the microvascular bed of the lung by oxygen would coincide with a burst of peroxidative activity and would be accompanied by an increased rate of excretion of ethane and pentane in expired gas. We measured vascular pressures, the rate of lung lymph flow and concentrations of ethane and pentane in exhaled gas in 10 newborn lambs that breathed >95% oxygen continuously. Our marker for oxygen-induced lung injury was an increase in the permeability of the microvascular bed of the lung to protein (an increase in the rate of lung lymph flow accompanied by an increase in the protein concentration in lymph). Although all 10 lambs demonstrated an abrupt increase in microvascular permeability to protein within 48 to 96 h of exposure to >95% oxygen, the rates of ethane and pentane excretion remained unchanged throughout the entire experimental period. Lung tissue concentrations of glutathione decreased by 40% in the oxygen-exposed lambs and the concentrations of glutathione disulfide increased 85% relative to air-breathing controls. Activities of glutathione reductase and superoxide dismutase were lower in the lungs of the oxygen- exposed lambs than in controls, whereas the activities of glutathione peroxidase and catalase were not changed. We conclude that, in the lamb, changes in the rates of excretion of ethane and pentane do not correlate with the timing of injury to the microvascular bed of the lung.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Superoxide anion generation during severe asphyxia and reventilation was assessed in newborn pigs. Using closed cranial windows over the parietal cortices, superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction was determined during asphyxia/ reventilation. Asphyxia was induced by turning off the respirator and occluding the endotracheal tube. In each animal, 2.4 mM NBT dissolved in artificial cerebrospinal fluid was placed under one window and under the opposite window, NBT (2.4 mM) plus SOD (60 U/mL) dissolved in artificial cerebrospinal fluid was used. A significant increase in SOD-inhibitable NBT reduction was observed in asphyxiated piglets (14.67 ± 4.5 pmol/mm2· 20 min) when compared with control piglets (2.82 ± 1.1 pmol/mm2-20 min). In another group in which the animals were treated with indomethacin (5 mg/kg i.v.) before asphyxia/reventilation, there was minimal SOD-inhibitable NBT reduction. Our results indicate that superoxide anion is generated on the cerebral cortex during asphyxia/reventilation via the prostaglandin endoperoxide synthase pathway.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The proto-oncogene c-erbA and its analogues are genes that encode thyroid hormone receptors. In rats, at least two loci have been identified by their homology to c-erbA. Each locus can produce at least two distinct mRNA species via RNA processing. However, one of those transcripts, r-erbAα-2, does not yield a triiodothyronine (T3)- binding protein when translated invitro. Proper development of the rat brain is thyroid hormone-dependent during the perinatal period and there is a documented increase in brain nuclear T3-binding capacity during that time. By hybridizing cDNA probes specific to various rat erbA-like transcripts with RNA extracted from developing rat brain, we sought changes in thyroid hormone receptor mRNA levels that correspond with changes in T3-binding capacity in rat brain during the perinatal period. Three mRNA of the erbA family showed variations in relative abundance during brain development. Oddly, r-erbAα-2, a variant that does not code for a T3-binding protein, was the most abundant erbA-like RNA to correlate with the reported changes in T3-binding capacity. The message for rat rerbAα-1 that encodes a functional T3 receptor also varies with T3-binding capacity but at a level that is at least 8- fold lower than the r-erbAα-2 message. The level of rat erbAβ-l message also varies in rat brain during the perinatal period but not in a way that correlates with changes in T3-binding capacity.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Low-dose estrogen therapy significantly increases radioimmunoassayable serum hGH concentrations in the prepubertal hypogonadal female. In this study, we have examined the effects of short- and long-term low-dose ethinyl estradiol therapy on the endogenous production rates and metabolic clearance rates of hGH. We used deconvolution mathematical modeling to provide quantitative estimates of individual secretory parameters and to calculate subject-specific hGH metabolic clearance rates, by using all serum hGH concentrations and their variances considered simultaneously. Nine girls with Turner's syndrome (mean age 7.7 ± 0.5 y) were studied on three separate nights by drawing blood every 20 min from 2200 to 0800 h before (I), after 1 wk (II), and 5 wk (III) of 100 ng/kg/d ethinyl estradiol therapy orally. We found that the endogenous hGH production rate more than doubled in all patients studied after 5 wk of ethinyl estradiol therapy (194 ± 22 (I), 290 ± 43 (II), and 412 ± 66 (III) µg/L/12 h;p< 0.05 for I and III). The half-life of endogenous hGH was not altered in the estrogen treatment paradigm with a mean of 19 ± 1.6 min in study I and 18 ± 1.2 min in both studies II and III. Our results suggest that even prepubertal concentrations of gonadal steroids in the hypogonadal female may be physiologically relevant to the maintenance of normal somatotrope secretory function.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The energy intake, expenditure, and deposition of 40 breast-fed and formula-fed infants were investigated at 1 and 4 mo of age to explore possible differences in energy utilization between feeding groups. Energy intake was calculated from 5-d test-weighing records or pre- and postweighing of formula bottles, in combination with bomb calorimetry of the milks. Total daily energy expenditure (TDEE) was determined by the doubly labeled water method. Sleeping metabolic rate (SMR) and minimal observable energy expenditure were measured by indirect calorimetry. Activity was estimated as the difference between TDEE and SMR. Energy deposition was estimated from dietary intake and TDEE. Energy intakes were significantly higher for the formula-fed than breast-fed infants at 1 mo (118 ± 17 versus 101 ± 16 kcal/kg/d) and 4 mo (87 ± 11 versus 72 ± 9 kcal/kg/d) (p < 0.001). TDEE averaged 67 ± 8 and 64 ± 7 kcal/kg/d at 1 mo and 73 ± 9 and 64 ± 8 kcal/kg/d at 4 mo for the formula-fed and breast-fed infants, respectively, and differed between feeding groups ((p< 0.04). SMR and minimal observable energy expenditure (kcal/min) were higher among the formula- fed infants at 1 and 4 mo (p< 0.005). The energy available for activity and the thermic effect of feeding did not differ between feeding groups. Rates of weight gain (g/d) and energy deposition (kcal/kg/d) tended to be greater among the formula-fed infants at 1 and 4 mo ((p< 0.06). Differences in weight gain, energy deposition, SMR, minimal observable energy expenditure, and TDEE partially accounted for the discrepancy in energy intake observed between breast-fed and formula-fed infants. The response to the varying levels of energy intake in infancy appear to be mediated through growth and basal-energy-requiring processes, but not through physical activity.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Six pregnant rats were made mildly hyperglycemic by intraperitoneal injection of streptozotocin on d 5 of gestation. Four control rats were injected with citrate buffer. Thirty pups born to experimental dams who had increased birth weight (birth weight >1.7 SD of mean birth weight of pups from control dams) maintained accelerated growth through 10 wk of age. At 10 wk, oral glucose tolerance tests showed higher glucose and insulin levels than the controls (n= 37). In addition to the higher body weight, the experimental rats also had higher fat weight to body weight ratios. Adipocytes of epididymal fat from obese males and periovarian fat from obese females had higher lipid content with significantly larger cell size than the adipocytes of the controls. The adipocytes of macrosomic rats showed attenuated response to insulin-stimulated glucose conversion to total lipid and fatty acid when compared with the responses seen in the adipocytes of the control rats. Interestingly, although the insulin-stimulated glucose conversion to CO2was similar in macrosomic and control males, the response in the macrosomic female was blunted when compared with that of the control females. Insulin receptor binding capacities of the macrosomic rats were lower than those of the controls, which is consistent with a phenomenon of down-regulation. However, the receptor affinities were higher in the experimental animals than in controls. Therefore, a postreceptor defect may account for the abnormality in glucose metabolism in the obese rats. In conclusion, the abnormal response to oral glucose loading in these experimental obese, hyperinsulinemic rats is due to peripheral tissue insulin resistance that is probably postreceptor in nature.

ISSN:0031-3998    

出版商:OVID    

年代:1990

数据来源: OVID