Cigarette smoke affects lipolytic activity in isolated rat lungs

Hartiala, Jaakko; Viikari, Jorma; Hietanen, Eino; Toivonen, Heikki; Uotila, Pekka

doi:10.1007/bf02534227

Cited by 7 publications

(14 citation statements)

References 28 publications

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“…Second, circulating tri glycerides are reported to be the dominant precursors of lung phospholipids [10], al though phosphatidylcholine can be synthe sized in smaller amounts also from glucose and acetoacetate [25], Exposure of pregnant rabbits to cigarette smoke did not result in significant changes in the lung lipolytic activity of their litters. This result is similar to our earlier results in adult rats, in which pre-exposure to cigarette smoke did not influence lung lipolytic activ ity [15]. It has earlier been shown by other groups that exposure to cigarette smoke does also not influence palmitate uptake or phos pholipid synthesis either in dog [7] or in rat [12] lungs.…”

Section: Discussionsupporting

confidence: 82%

“…Smoking during pregnancy is known to be associated with retarded fetal growth and with other complications [18]. We have earlier reported that LPL activity in adult rat lungs is inhibited during cigarette smoke inhalation [ 15], Changes in the activity of lung enzymes measured in vitro do not necessarily indicate physiological importance, because other fac tors (e.g. distribution of blood flow) may be equally important for the metabolic pro cesses.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, the lungs contain lipoprotein lipase (LPL) en-zyme, which catalyzes the release of fatty acids from triglycerides and from very low density lipoproteins [9,16,20]. Based on their location in the circulation, on their large capillary endothelial area [23], and on their high activity of the endothelial LPL [9,16,20], it is not surprising that the lungs are a potent organ for lipolysis [15]. The role of pulmonary LPL in relation to surfactant syn thesis is further supported by the experimen tal evidence that fatty acids from circulating triglycerides can be incorporated into pulmo nary phospholipids in the isolated perfused lungs [10].…”

Section: Introductionmentioning

confidence: 99%

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Development of the Lipolytic Activity in Isolated Perfused Perinatal Rabbit Lungs and the Influence of Maternal Cigarette Smoke Exposure on It

Simberg¹,

Hartiala²,

Hietanen³

1983

Neonatology

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The ability of the lungs to release fatty acids from circulating triglycerides or lipoproteins for its own phospholipid synthesis may be one of the factors which limit the rate of surfactant formation. Therefore, the development of the lipolytic activity of lungs obtained from late fetal and neonatal rabbits has been studied and the results correlated to the phospholipid content of lungs of similar ages. Isolated lungs were perfused with a medium which contained cold and radioactive triglyceride, and the release of fatty acids into the perfusion medium was analyzed by both colorimetric and radiochemical methods. The phospholipids of the postmitochondrial supernatant fractions of the lungs were extracted and quantified by measuring inorganic phosphorus. Finally, the influence of maternal cigarette smoke exposure on the lipolytic activity of the lungs of their litters were studied. A high lipolytic activity in the lungs of 2 8-day-old fetuses was detected. The activity decreased towards birth, and was lowest on the first day after birth (about 20% of that observed in 28-day-old fetuses). However, it increased again during the first week after birth. Exposure of the mothers to cigarette smoke during the last 10 days before delivery did not affect the pulmonary lipolytic activity of the offspring. Although the lung phospholipid content increased 3.6-fold from 28 days of fetal life to 1 week after birth, it remained unchanged on the days when the lung lipolytic activity was lowest. We conclude that changes in lung lipolytic activity influence lung phospholipid synthesis, and consequently influence also surfactant formation in the lungs.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Development of the Lipolytic Activity in Isolated Perfused Perinatal Rabbit Lungs and the Influence of Maternal Cigarette Smoke Exposure on It

Simberg¹,

Hartiala²,

Hietanen³

1983

Neonatology

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“…The air flow was directed with unidirectional valves (v). The suction removes the smoke from a lighted cigarette (Hartiala et al 1980) and pushes it into the jacket (about 20 ml) containing the tissue. The tissue was continuously superfused with Krebs bicarbonate buffer.…”

Section: Methodsmentioning

confidence: 99%

“…Larson & Silvette 1975). We have earlier reported that nicotine inhibits the contractile responses of rat colons t o angiotensin 11 and, depending on the dose, either inhibits or enhances the responses of hamster stomach strips t o prostaglandin EZ (Toivonen et al 1980). In the present work we investigated, if similar changes could be detected with cigarette smoke or with some of its compounds.…”

mentioning

confidence: 96%

Cigarette Smoke Inhibits Contractile Responses of Rat Isolated Colon to Angiotensin II

Toivonen

Nienstedt

Uotila

1981

Acta Pharmacologica et Toxicologica

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Abstracr:The contractile response of isolated superfused rat colons to angiotensinII was inhibited almost totally when cigarette smoke was in contact with the serosal surface of the colon. Filtration of visible particles from the smoke diminished but did not abolish this inhibitory action. An inhibitory factor was also retained by the filter papers. One inhibitor, which was dissolved in Krebs buffer, behaved like nicotine. Carbon monoxide and dioxide were effective inhibitors but only at higher concentrations than they are present in cigarette smoke. Removal of carbon dioxide from cigarette smoke did not abolish the inhibitory action. Neither of the gases nor nicotine alone could fully mimic the action of cigarette smoke. It is possible that the inhibitory action ofcigarette smoke was due to combined action of these compounds. It is, however, also possible, that cigarette smoke contains still other inhibitory compounds. Cigarette smoke probably had its effect directly on the smooth muscle cells, but activation of inhibitory nerves could not be excluded.

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Lipoproteins and Lipoprotein Lipase

Hamosh

1985

Comprehensive Physiology

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The sections in this article are: History Lipoproteins Chylomicrons Very‐Low‐Density Lipoproteins Low‐Density Lipoproteins High‐Density Lipoproteins Lipoprotein Lipase History of Lipoprotein Lipase Distribution of Lipoprotein Lipase Regulation of Lipoprotein Lipase Activity Ontogeny of Lipoprotein Lipase Characteristics of Lipoprotein Lipase Mechanisms of Hydrolysis of Circulating Triglycerides Characteristics of Lipolytic Activity of Lipoprotein Lipase Lipoprotein Lipase in Lung Tissue Distribution and Regulation of Activity Lung Lipoprotein Lipase in Disease Origin Functions

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Cigarette smoke affects lipolytic activity in isolated rat lungs

Cited by 7 publications

References 28 publications

Development of the Lipolytic Activity in Isolated Perfused Perinatal Rabbit Lungs and the Influence of Maternal Cigarette Smoke Exposure on It

Development of the Lipolytic Activity in Isolated Perfused Perinatal Rabbit Lungs and the Influence of Maternal Cigarette Smoke Exposure on It

Cigarette Smoke Inhibits Contractile Responses of Rat Isolated Colon to Angiotensin II

Lipoproteins and Lipoprotein Lipase

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