The release of surfactant in rat lung by brief periods of hyperventilation

Nicholas, Terence E.; Barr, Heather A.

doi:10.1016/0034-5687(83)90137-8

Cited by 81 publications

(38 citation statements)

References 20 publications

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“…Animal studies have demonstrated that hyperventilation will lead not only to a leakage of proteins, but also to a release into the alveolar space of pulmonary surfactant [31]. Initially, the surfactant inhibiting effect of the invading proteins will be dominant, but as the concentration of surfactant is increased it is likely that it will regain its ability to adsorb quickly, and the monolayer that forms at the air-liquid interface will then exert a high surface pressure.…”

Section: Discussionmentioning

confidence: 99%

Surfactant function affected by airway inflammation and cooling: possible impact on exercise-induced asthma

Enhörning¹,

Hohlfeld

Krug

et al. 2000

Eur Respir J

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Pulmonary surfactant maintains patency of narrow conducting airways. An inflammation, with a leakage of plasma proteins into the airway lumen, causes surfactant to lose some of this ability. Will a lowering of temperature aggravate the deteriorating effect of an inflammation?Calf lung surfactant extract (CLSE) with proteins added was studied with a capillary surfactometer (CS) at temperatures of 25±428C. BALB/c mice were infected with respiratory syncytial virus (RSV). Six days later the lungs were lavaged and the surfactant in the lavage fluid was studied with the CS at temperatures of 25±428C. Lavage fluid from allergen challenged asthmatics was examined for its content of surfactant inhibitors at reduced temperatures.It was shown that CLSE with proteins gradually lost its ability to maintain patency as the temperature was lowered. Lavage fluid from the RSV infected mice showed a similar dysfunction at low temperatures. Lavage fluid from the airways of human asthmatics, when challenged with antigen but not with saline, contained agents inhibiting surface activity, particularly at reduced temperatures.Airway inflammation causes surfactant to lose its ability to maintain patency, particularly as the temperature is reduced. That might be a reason for the increased airway resistance observed in asthma patients hyperventilating in cold weather. Eur Respir J 2000; 15: 532±538.

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Section: Discussionmentioning

confidence: 99%

Surfactant function affected by airway inflammation and cooling: possible impact on exercise-induced asthma

Enhörning¹,

Hohlfeld

Krug

et al. 2000

Eur Respir J

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“…This has been reported in both unanaesthetized (Nicholas et al, 1982a, Power et al, 1986 and anaesthetized animals (Oyarzun & Clements, 1978;Klass, 1979;Nicholas & Barr, 1983); both stimulatory and inhibitory factors 'Author for correspondence may be involved in vivo (Nicholas & Barr, 1983). In the isolated perfused lung of the rat, release is directly related to the Vt value, once Vt exceeds the normal resting value (Nicholas & Barr, 1981); surfactant can even be released by a single simulated deep breath (Nicholas et al, 1982b).…”

Section: Introductionmentioning

confidence: 80%

“…Whereas salbutamol consistently releases a limited amount of surfactant and this in turn can be blocked by propranolol, the release induced by an, increased Vt was much larger and could not be blocked (Nicholas & Barr, 1981). We suggested that two pools of tissue surfactant exist: a large pool that turns over slowly and is released in response to type II cell distortion, and a small pool that turns over rapidly and is under sympathetic nervous control (Nicholas et al, 1982a;Nicholas & Barr, 1983). In the present paper we have further examined the possible role of the Padrenergic, cholinergic and prostaglandin systems in control of release of surfactant in unanaesthetized resting rats and in rats with hyperpnoea induced by altering the inspired gas.…”

Section: Introductionmentioning

confidence: 92%

“…The presence oftwo pools oftissue surfactant Previously we proposed that the alveolar compartment is supplied by two pools of tissue surfactant (Nicholas et al, 1982a;Nicholas & Barr, 1983;Power et al, 1986;1987). The first is relatively small, turns over rapidly and is under the control of the sympathetic nervous system.…”

Section: Control Ofsurfactant In Hyperpnoeic Ratsmentioning

confidence: 99%

“…Importantly, it is not affected by tetrodotoxin (Nicholas & Barr, 1981), indicating that intrapulmonary neurones are not required for this response. We suggested that surfactant is released in response to direct distortion of the type II cell (Nicholas et al, 1982a;Nicholas & Barr, 1983).…”

Section: Introductionmentioning

confidence: 96%

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Control of alveolar surfactant in rats at rest and during prolonged hyperpnoea: pharmacological evidence for two tissue pools of surfactant

Barr

Nicholas

Power

1988

British J Pharmacology

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Propranolol, atropine and indomethacin (i.p.) affect neither the amount (PLalv), nor the specific activity (PLalvsp.act.) of alveolar surfactant‐type phospholipids lavaged from the lungs of unanaesthetized rats, either at rest or made hyperpnoeic for 24 h with 5%CO2/13%O2/82%N2. Whereas salbutamol (280 μg kg−1 body weight, i.p.) consistently increased PLalv and PLalvsp.act., pilocarpine (1.5, 3, 10 and 50 mg kg−1, i.p.) and labetalol (1 and 5 mg kg−1, i.p.) had no effect. The dose of pilocarpine reported by others to release surfactant (150 mg kg−1) induced marked salivation, diarrhoea, chromodacryorrhoea and a three‐fold increase in tidal volume. In the isolated perfused lung of the rat, salbutamol (1.5 μm) consistently increased PLalvsp.act, whereas pilocarpine (0.1 and 1 μM) had no effect on these variables. In the isolated perfused lung, the maximum amount of surfactant that could be released by salbutamol (0.5 mM) was smaller than that which could be released in response to an increase in tidal volume (peak inflation pressure 28 cmH2O). When the concentration of salbutamol in the isolated perfused lung was adjusted to produce the same increase in PLalv as did a single simulated deep breath, the PLalvsp.act was significantly increased by salbutamol, but not by the simulated deep breath. We conclude, that neither the autonomic nervous system nor the prostaglandin system is essential for the release of surfactant at rest or during hyperpnoea. Furthermore, we suggest that two pools of surfactant, with different release mechanisms, exist in lung tissue.

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