Search PubMed⌕ Search

Biomedical subjects

J Hartiala

Publications and source records attributed to J Hartiala.

At least 55 records · Page 3Linked to original sources
PubMed1983

Development of the lipolytic activity in isolated perfused perinatal rabbit lungs and the influence of maternal cigarette smoke exposure on it.

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 28-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.

Animals↗
PubMed1982

The metabolism of arachidonic acid to an antiaggregatory compound in isolated lungs of fetal and neonatal rabbits.

The developmental pattern of fetal and neonatal rabbit lungs to generate an antiaggregatory compound from arachidonic acid (AA) was studied in isolated rabbit lungs, which were perfused with Krebs bicarbonate buffer. The antiaggregatory effect of the nonrecirculating perfusion effluent was tested by adding a small portion of the effluent to human platelet rich plasma (PRP) in a Born-type aggregometer before the aggregation was induced by ADP. The production of an antiaggregatory compound was minimal, when exogenous AA was not infused into the pulmonary circulation. When arachidonate (40 nmol/min) was infused into the pulmonary circulation of rabbits which were 1 day or 1 week old, the perfusion effluent significantly inhibited the ADP induced aggregation of PRP. Perfused lungs from fetal rabbits (gestation age 28-31 days) formed also an antiaggregatory compound from AA, but the antiaggregatory effect was not as great as 1 day after birth. It seems that neonatal rabbit lungs metabolize AA more to an antiaggregatory compound than late fetal lungs. The fact that the AA induced production of an antiaggregatory compound is inhibited by simultaneous infusion of indomethacin favours the hypothesis that this antiaggregatory compound could be PGI2.

Adenosine Diphosphate↗
PubMed1982

The metabolism of arachidonic acid in isolated rat lungs is not changed during cigarette smoke ventilation.

Cigarette smoke ventilation of isolated perfused rat lungs partially inhibited the pulmonary vascular pressor response to arachidonic acid. The amounts of metabolites of exogenous arachidonic acid in the perfusion effluent remained unchanged during smoke ventilation. The antiaggregatory effect of the effluent during pulmonary infusion of AA was not decreased by smoke ventilation. The cause of the previously reported increased platelet aggregation after smoking remains unclear.

Animals↗
PubMed1982

Exposure to carbon monoxide or to nicotine does not inhibit PGI2 formation by rat arterial rings incubated with human platelet-rich plasma.

The effects of nicotine and carbon monoxide on the production of PGI2 by rat arterial rings were studied. For PGI2 analysis, we used a bioassay based on platelet-rich plasma aggregation with ADP. Neither nicotine in the incubate nor pretreatment with carbon monoxide decreased PGI2-production as detectable in this bioassay system. Also, neither had a direct effect on the ADP-induced aggregability of human platelet-rich plasma. Consequently, these agents do not seem to be responsible for the temporary increase in platelet aggregability after cigarette smoking.

Adenosine Diphosphate↗
PubMed1981

The effect of cigarette smoke on the metabolism of arachidonic acid in isolated hamster lungs.

The effects of cigarette smoke on the metabolism of exogenous arachidonic acid (AA) were investigated in isolated hamster lungs. Arachidonate was injected into the pulmonary circulation and the metabolites were analysed from the nonrecirculating perfusion effluent by thin layer chromatography. After the pulmonary injection of 66 nmol of 14C-AA about 20% of the injected radioactivity appeared in the perfusion effluent mostly as metabolites in six minutes. When isolated lungs were ventilated with cigarette smoke during the perfusion, the amounts of PGF2 alpha, PGE2 and two unidentified metabolite groups increased in the lung effluent. In two other experimental series hamsters were exposed to cigarette smoke before the lung perfusion either once for 30 min or during one hour daily for ten consecutive days. Neither pre-exposures caused any changes in the amounts of arachidonate metabolites in the lung effluent.

Animals↗
PubMed1981

Effects of high oxygen tension on the metabolism of vasoactive hormones in isolated perfused rat lungs.

The effect of exposure of rats to high concentrations of oxygen (90-95%, normobaric) on the activation of angiotensin I to angiotensin II and on the inactivation of bradykinin, prostaglandin E2 (PGE2) and 5-hydroxytryptamine (serotonin) in the pulmonary circulation of isolated perfused rat lungs was investigated. After 36 h exposure, PGE2 survival in the pulmonary circulation increased and reached 3 times the control value after 48 h exposure. A decrease in the conversion of angiotensin I to angiotensin II was seen after 48 h exposure. No decrease in the inactivation of 5-hydroxytryptamine was seen until after 60 h exposure. At this time bradykinin inactivation was also decreased. The decrease in metabolism of angiotensin I and PGE2 following 48 h exposure to oxygen was reversed by a subsequent exposure to room air for 12 h. In these experiments, therefore, the earliest sign of oxygen toxicity was a decrease in PGE2 metabolism, a reaction associated with cells other than endothelial cells.

Angiotensin I↗
PubMed1981

The inactivation of prostaglandin E2 and 5-hydroxytryptamine in isolated perfused fetal and neonatal rabbit lungs.

The inactivation of prostaglandin E2(PGE2) and 5-hydroxytryptamine (5-HT) was studied in isolated perfused lungs from fetal and neonatal rabbits. PGE2 inactivation was considerable already at the 28th day of fetal life, as only 11% of injected substrate survived passage through the pulmonary circulation. However, the inactivation increased significantly during the last 3 prenatal days (4% survival) and remained at this level when analyzed one week postnatally. In contrast to PGE2-metabolism, 5-HT inactivation was relatively stable during the studied fetal period (47-49% inactivation), but was decreased significantly on the 7th day postnatally when compared to newborn litters. The results indicate that pulmonary prostaglandin and amine metabolism reach maturity at different times during the perinatal period.

Age Factors↗
PubMed1980

Cigarette smoke affects lipolytic activity in isolated rat lungs.

Isolated perfused rat lungs liberated fatty acids at a rate of 15 mumol/hr during perfusion of triglyceride-rich medium through the pulmonary vascular bed. About 80% of this activity seemed to result from lipoprotein lipase and 20% to hormone-sensitive lipase. Ventilation of the lungs with cigarette smoke instead of air during the perfusion reduced fatty acid liberation by 23%. Pre-exposure of rats to cigarette smoke for either 1 or 10 days did not cause significant changes in lung lipolytic activity compared to sham-exposed controls.

Animals↗
PubMed1980

Demonstration of PGI2 production by isolated perfused rat lungs with platelet aggregation test.

Platelet aggregation test was used for PGI2 measurements. The use of 6 % CO2 in air stabilized human platelet rich plasma (PRP) so that it could be used for up to 7 hours in these measurements. The PGI2 caused inhibition of aggregation in response to ADP was concentration dependent in the range of 0.5 ng/ml to 50 ng/ml. Isolated perfused rat lungs released spontaneously 190 ng/min PGI2 and about 3 % of infused arachidonic acid potassium salt (equivalent to 25 microgram/min arachidonic acid) was converted to PGI2.

Adenosine Diphosphate↗
PubMed1980

The metabolism of arachidonic acid in isolated hamster, rat and guinea pig lungs.

The perfusion effluent from isolated rat lungs caused relaxations of superfused strips of bovine (BBBCA) and pig (PCA) coronary arteries. The effluent from hamster lungs had similar effect on BCA. Bolus injections of arachidonate (AA, 10-20 microgram) into rat lungs caused further relaxations of superfused BCA and contractions of rat stomach strip (RSS). AA injections into guinea pig lungs resulted in dose dependent contractions of BCA and PCA. Similar dose dependent contractions of PCA and RSS were seen in hamster experiments, however the responses of BCA varied with the AA dose. Infusion of AA (5-25 microgram/min) into guinea pig lungs resulted in dose dependent contractions of superfused PCA and BCA. In hamster experiments AA infusion (5 microgram/min) caused a small relaxation of BCA, but had no effect on PCA. When 14C-AA was injected into the pulmonary circulation, the amounts of metabolites were greater in the perfusion effluent from hamster than from rat lungs. In rat lungs 6-oxo-PGF1 alpha was one of the main metabolites. In contrast, in hamster lungs this metabolite represented only a small part of the total metabolite formation. Thromboxane B2 was one of the main metabolites formed in hamster lungs and its rate of formation increased greatly with increasing AA doses. The results indicate that the metabolite pattern of arachidonate in isolated rat lungs is different from that in hamster and guinea pig lungs. The total rate of AA metabolism in rat lungs is smaller than in hamster lungs.

Animals↗
PubMed1979

Effects of cigarette smoke on the metabolism of vasoactive hormones in rat isolated lungs.

1. The effects of exposure of rats to cigarette smoke have been studied on the metabolism of vasoactive hormones in isolated lungs from these animals. 2. Rats were exposed for 1 h per day to cigarette smoke for 1 day or for 10 days. 3. Angiotensin I conversion was increased after 1 day's exposure but after 10 days' exposure conversion returned to normal. 4. Inactivation of prostaglandin E2 was decreased after 1 day's exposure. After 10 days' exposure there was a further decrease which could not be attributed to smoke alone. 5. The inactivation of 5-hydroxytryptamine and bradykinin remained unchanged after both short and longer exposures to smoke. 6. The metabolic activity of the lung towards some vasoactive hormones in the pulmonary circulation is affected by exposure of the animal to cigarette smoke and such changes may be relevant to the initiation of cardiovascular changes consequent upon cigarette smoking.

Angiotensin I↗
PubMed1979

Developmental pattern of pulmonary lipoprotein lipase in growing rats.

The developmental pattern of pulmonary lipoprotein lipase (LPL) activity was measured in growing male and female rats from the neonatal period to the adult age. The pulmonary phospholipid content showed a sharp increase at term from premature low level. At the same time the LPL activity increased markedly showing thereafter a decrease at 1 week of age and increasing thereafter to the adult age. Also the phospholipid content was low at 1 week of age. Thus the pulmonary phospholipid content and LPL activity change in the same way during the development indicating possibly that the LPL by supplying free fatty acids for the phospholipid biosynthesis may be one of the rate-limiting enzymes in the pulmonary surfactant synthesis.

Age Factors↗
PubMed1979

Absorption and metabolism of intratracheally instilled cortisol and beclomethasone dipropionate in the isolated perfused rat lungs.

The fate of [4-14C]-cortisol and [16,16 alpha-3H]-beclomethasone dipropionate following intratracheal application of the substrates into isolated perfused rat lungs was studied. Both substrates were transferred to the perfusion medium, cortisol at a much higher rate than beclomethasone dipropionate. The proportion of different metabolites of the total radioactivity was larger with beclomethasone dipropionate in both the perfusion medium and the lung tissue. The lungs are considered to have a catabolic role in cortisol metabolism.

Absorption↗