Ventilatory and cholinergic control of pulmonary surfactant in the rabbit

Oyarzún, M; Clements, John A.

doi:10.1152/jappl.1977.43.1.39

Cited by 121 publications

(36 citation statements)

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“…Smith (28) has shown that cultured cells similar to type I1 alveolar cells secrete increased amounts of phosphatidylcholine in response to acetylcholine and this effect may be blocked by atropine. In adult rabbits, increased pulmonary ventilation leads to increased alveolar Surfactant and this effect is mediated at least partially by the vagus nerve (23). In the present experiments, atropine blocked the effect of gas ventilation on net accumulation of alveolar surfactant after birth.…”

Section: Atropine O 3 U S I O N Me-rwrmentsupporting

confidence: 53%

Augmentation of Pulmonary Surfactant Secretion by Lung Expansion at Birth

et al. 1979

Pediatr Res

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SummaryTo study the effect of lung expansion at birth on surfactant secretion, we delivered by hysterotomy 11 litters of rabbit pups at 30 days of gestation and divided them into three groups that were killed: 1) after 30 min air-breathing, 2) after 30 min nitrogenbreathing, and 3) after 30 min tracheal occlusion. Each group was compared to a littermate group killed at birth. Groups 2) and 3) continued respiratory efforts for 30 min despite progressive asphyxia. Six additional litters were pretreated with atropine; at delivery one-half of each litter was killed, the remaining pups were subjected to 30 min of hypoxic gas breathing. After sacrifice, alveolar surfactant was recovered by saline lavage and estimated quantitatively on a surface-tension balance. Surfactant concentration at birth was 1.40 + 0.22 mg/g dry lung and increased to 1.86 f 0.19 (k SEM) after 30 min air-breathing (P < 0.01). Also, surfactant was increased in the nitrogen-breathing pups (from 1.61 , f 0.35 in littermate controls to 2.41 f 0.58, P < 0.03), but not to a significant degree in the occluded group (1.34 + 0.33 vs. 1.41 k 0.28), or the atropine pretreated breathing pups (1.77 + 0.29 vs. 1.89 + 0.25). SpeculationThe data indicate that lung expansion at birth enhances surfactant release from intracellular sites and suggest that the vagus nerve mediates this effect. It is possible that the effect of maternal atropine may have clinical significance in preterm infants.Studies with newborn rabbits have shown that the percent of acetone precipitable lecithin in pulmonary lavage (12), pulmonary stability (29), and pulmonary lavage phospholipid content (25) increase after birth. These findings indicate that immediately after birth the secretion of surfactant into the alveoli is increased over and above the fetal secretion rate. With the onset of breathing, augmented surfactant secretion may be due to mechanical, neuronal, or humoral factors. Both lower surface tension and increased saturated lecithin in alveolar wash result from constant air-expansion of excised adult dog lungs (8), a mechanical stimulus. In rabbits, fetal injection of pilocarpine or P-adrenergic stimulants (e.g., isoxsuprine) also result in increased alveolar surfactant (5,6,7,18,30). These pharmacologic effects suggest autonomic control of surfactant secretion.To determine the physiologic stimulus for increased alveolar surfactant after birth, we measured quantitatively the surfacebreathing and the occluded pups differentiate the effects of asphyxia with and without gas ventilation of the lungs. The findings in the atropine pretreated groups establish that neural factors mediate surfactant secretion at birth. MATERIALS AND METHODS ANIMAL PROCEDURESTwenty litters of New Zealand white rabbits were used. The gestation of each litter was known to be 30 days within 3 hr (term = 31 days). In 11 litters, the does were sacrificed immediately before laparotomy with an iv infusion of 300 mg pentobarbital. Within 2 min, all the pups of a litter were gently delivered within their amnioti...

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Section: Atropine O 3 U S I O N Me-rwrmentsupporting

confidence: 53%

Augmentation of Pulmonary Surfactant Secretion by Lung Expansion at Birth

et al. 1979

Pediatr Res

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“…Ventilation was assisted in four of five HMD animals and has been reported to increase PL recovered in airways lavage (21). However, this effect of ventilation is much too d l to account for the differences described here in PL in whole lung and SAM between normal and HMD lungs.…”

Section: Discussionmentioning

confidence: 64%

Lung Development in the Fetal Primate Macaca Nemestrina. III. HMD

Palmer

et al. 1979

Pediatr Res

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SummaryDelivery of M. nemestrina at 80% of normal gestation provides a population of neonates at high risk for hyaline membrane disease (HMD). The diagnosis of HMD was made by the presence of reticulogranular densities and air bronchograms on chest radiographs. Patchy atelectasis was seen in the lungs of animals assigned by clinical and radiographic criteria to the HMD group and not in the normal lungs of animals matched for gestational and postnatal age. Total phospholipid and phosphatidylcholine in whole lung, airway lavage fluid, and surface-active materials were lower in animals with HMD. Amniotic fluid L/S ratios were lower in the group that developed HMD. Pressure-volume measurements indicated decreased distensibility and unstable terminal air spaces in the HMD group. Alveolar-arterial oxygen pressure differences were greater in animals with HMD. There were no differences between HMD and normal groups in body weight, lung weight, percent dry lung weight, gestational age, and postnatal age at death. This primate species, subjected to premature delivery, is a suitable animal model of HMD in human neonates. Speculation An animal model of hyaline membrane disease (HMD) in a primate species is of interest to investigators of developmentally related pulmonary disorders. More complete knowledge of abnormalities in pulmonary function in HMD will contribute to development of both preventive and therapeutic measures and affords the opportunity to determine risks and benefits of such treatments to the fetus and newborn.

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“…Decreased compliance after periods up to 4 h of increased ventilation were attributed to altered surfactant function because extracts from these lungs exhibited increased minimal surface tensions (6)(7)(8)(9)(10). Increased alveolar surfactant phospholipids were found by Oyarzun and Clements (8, 9) after hyperventilation of adult rabbits for periods up to 4 h. They postulated that increased secretion of tissue pools occurred followed by inactivation.…”

Section: Resultsmentioning

confidence: 99%

“…Oyarzun and Clements (8, 9) measured alveolar surfactant phospholipids in hyperventilated adult rabbits and found that alveolar surfactant increased during the first 2 h but substantially decreased after 4 h of increased tidal volume ventilation. They speculated that secretion was stimulated by hyperventilation, thereby increasing alveolar surfactant pools at the expense of tissue pools (8,9). Similar conclusions were drawn by Wyszogrodski et al from their study of hyperventilated adult cats (10).…”

Section: Perinatal Research Laboratories Department Of Pediatrics Hmentioning

confidence: 99%

Surfactant Metabolism during Hyperventilation of Newborn Lambs with Atrial Right to Left Shunts

et al. 1989

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ABSTRACT. We studied the effect on surfactant metabolism of 8 h of mechanical ventilation at tidal volumes of 13 2 0.3 ml/kg and very high tidal volumes of 28 f 1.5 ml/kg, with and without added COz, in the presence of an atrial right to left shunt in 4-to 8-day-old lambs. Similarly aged, spontaneously breathing lambs were used as controls. Right to left atrial shunts were created by inflating a balloon in the right atrium after a Rashkind atrial septostomy, thus creating a stable, easily controlled atrial shunt. Radiolabeled surfactant phospholipid precursors were used to probe incorporation into and secretion of surfactant phosphatidylcholine, whereas intratracheally administered labeled natural surfactant was used to evaluate alveolar clearance. Protein leak from the vascular space to the lungs was measured using radioactive iodine-labeled albumins. At the end of the 8-h study period, tissue association of alveolar surfactant was significantly increased to 63% in the mechanically hyperventilated lambs as compared to 44% in those lambs mechanically ventilated but not hyperventilated (p < 0.05) and to 39% in the spontaneously breathing control animals (p < 0.05). No increased surfactant secretion or decreased compliance was detected with hyperventilation. However, the lambs had very large surfactant-saturated phosphatidylcholine pool sizes, and a large portion (50%) was already in the alveolar pool, even in the spontaneously breathing lambs. Precursor incorporation into saturated phosphatidylcholine was similar in all groups, and very low and comparable protein leaks were seen in the different groups of lambs. These experiments did not detect any adverse effects of 8 h of mechanical ventilation, large atrial shunts or mechanical hyperventilation on the surfactant system of newborn lambs. (Pediatr Res 25:83-88,1989) In neonates with persistent pulmonary hypertension, hyperventilation has been considered an essential part of the ventilatory support ( I ) . Suprasystemic pulmonary arterial pressures cause right to left shunts at the patent foramen ovale and ductus arteriosus levels which result in progressive hypoxemia. The goal of hyperventilation is to attain a critically low P a c o~ and alkaline pH which may promote reversal of the right to left shunt by decreasing pulmonary artery pressures to less than systemic levels (1). However, infants often become less responsive to the same

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Ventilatory and cholinergic control of pulmonary surfactant in the rabbit

Cited by 121 publications

References 0 publications

Augmentation of Pulmonary Surfactant Secretion by Lung Expansion at Birth

Augmentation of Pulmonary Surfactant Secretion by Lung Expansion at Birth

Lung Development in the Fetal Primate Macaca Nemestrina. III. HMD

Surfactant Metabolism during Hyperventilation of Newborn Lambs with Atrial Right to Left Shunts

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