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At least 991 records · Page 55Linked to original sources
PubMed1979

Response of pulmonary (circulating) megakaryocytes to experimentally induced consumption coagulopathy in rabbits.

The effects of slow temporary infusion of a tissue thromboplastin solution into the superior vena cava on pulmonary as well as circulating megakaryocytes were studied in 40 rabbits (2-48 hours after infusion) and related to 6 noninfused and 7 infused with normal saline. This is a simple and specific method of inducing a fall in blood platelet levels and thereby an activation of thrombocytopoiesis and megakaryocytopoiesis. The induced intravascular coagulation is probably counterbalanced by an activated fibrinolysis allowing the animals to survive the infusion and thereby offering the possibility of studying the long-term effects. An increase to about 300% of the normal values in circulating as well as pulmonary megakaryocytes was found 20 and 24 hours after the onset of the infusions respectively. The number of circulating and pulmonary megakaryocytes, showing great individual variations, however, dropped to normal levels within 28 hours after onset of the infusions, which means that megakaryocytes remain detectable for less than eight hours in the lungs. No increase was found in pulmonary megakaryocytes in the control (saline infused) group. In our opinion the entrance of megakaryocytes from the bone marrow into the blood circulation in an incidental event, the number in the circulation reflecting the activity of megakarycocytopoiesis. This experiment supports our suggestion that intravascular coagulation is one of the major pathophysiological mechanisms leading to an increase in pulmonary megakaryocytes.

Animals↗
PubMed1992

Opiate action in the pulmonary circulation.

To gain insight into the mechanisms underlying the association between acute pulmonary edema and narcotic abuse, the direct action of morphine was examined in isolated, perfused left lower lobe (LLL) preparations in dogs and cats. Morphine sulphate injected (0.6 mg/kg) into the pulmonary artery of the LLL increased the pulmonary vascular resistance (PVR) by about 100% in both species. The increase in PVR was primarily due to constriction of the veins, as determined with the arterial and venous occlusion technique. The increase in PVR with morphine injection was unaffected by alpha-adrenergic antagonists, but was reversed by chlorpheniramine, a histamine H1-receptor antagonist. Pretreatment, but not post-treatment with the opiate antagonist, naloxone, blocked the effect of morphine on PVR. Thus, the rapid administration of morphine produces pulmonary venoconstriction via histamine release from the lung, and the latter may account for the well-documented association between acute pulmonary edema and narcotic abuse.

Animals↗
PubMed1976

[Filtration-absorption function of the lungs during hemodynamic stress in the pulmonary circulation].

The transcapillary fluid exchange in the lung during elevation of the pulmonary venous pressure (PVP) was studied in cats. The weighing technique in vivo for a lung lobe, the comparison of the hematocrit of pulmonary arterial and venous blood, and the measurement of the outflow from the lung lobe at constant volume perfusion were used for the estimation of the filtration rate. The latter was not linearly related to PVP. Capillary filtration coefficient was about 0.040-0.055 ml/min/100 g tissue/mm Hg during the PVP rise by 5-10 mm Hg, and about 0.068-0.087 at PVP raised by 20-25 mm Hg. Under conditions of the open chest, the fluid accumulation was observed in the extravascular compartment of the lung even after relatively small and short PVP elevations.

Absorption↗