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At least 1,081 records · Page 60Linked to original sources
PubMed1988

Vascular pressures and passage of gas emboli through the pulmonary circulation.

Anesthetized dogs received venous air infusions at 0.35 ml.kg-1.min-1. In 60% of a group of 15 dogs, venous bubbles spilled over into the arterial circulation and were detected with the ultrasound Doppler technique. The pulmonary vascular pressure gradient (pulmonary artery pressure-pulmonary venous pressure or left atrial pressure) measured at the instant that spillover occurred was 34.7 +/- 4.7 mmHg. In a 2nd group of dogs we raised the pulmonary vascular pressure gradient before the venous air infusions to achieve spillover of bubbles 100% of the time. The resultant pressure gradient at the time of spillover of venous bubbles was 52.0 +/- 2.0 mmHg (P less than 0.05). It is concluded that venous bubbles can cross the lungs of anesthetized dogs when the driving pressures are sufficient to overcome the normal filtering function.

Animals↗
PubMed1975

[Dopamine effects on the pulmonary circulation of innervated and autotransplanted lungs (author's transl)].

The effects of dopamine on the pulmonary vascular resistance were investigated in 7 normal and 9 autotransplanted canine lungs during perfusion in situ. Dopamine (up to 13,5 gamma/kg BW, rapid injection) acts as a vasoconstrictor by alpha-receptor stimulation. Vasodilative effects could not be registered neither by very small amounts of dopamine nor during alpha-blockade with phentolamine. No difference could be detected between the vascular reactions of normal and autotransplanted lungs.

Animals↗
PubMed1977

The effects of halothane and ether on the pulmonary circulation in the innervated perfused cat lung.

The effects of halothane and diethyl ether on pulmonary vascular resistance and the pulmonary vasoconstrictor response to alveolar hypoxia were studied in the innervated perfused cat lung. A left and right heart bypass technique was used to allow perfusion of the lungs at constant flow. Neither anaesthetic agent caused a significant change in pulmonary vascular resistance but both agents caused a depression of the pulmonary vasoconstrictor response to hypoxia.

Animals↗
PubMed1997

Biotinylation of membrane proteins accessible via the pulmonary circulation in normal and hyperoxic rats.

It is well established that the phenotype of the pulmonary vascular surface can be affected by injurious stimuli, but the few proteins for which the expression and/or activity have been studied make up only a small fraction of the entire spectrum of luminal cell membrane proteins. To expand the capability for studying such proteins, we developed a method for biotinylating cell membrane proteins accessible via the vascular lumen in the isolated-perfused rat lung and examined the impact of hyperoxia on the spectrum of the biotinylated proteins. Labeling was carried out either by single-pass bolus injection of the cell impermeant biotinylation reagent sulfosuccinimidyl 6-biotin-amido hexanoate (NHS-LC-biotin) into the pulmonary artery cannula or by the addition of NHS-LC-biotin to a lung homogenate. Lung membrane fractions were prepared, and the proteins were separated by SDS-polyacrylamide gel electrophoresis and transferred to nitrocellulose by electroblotting. The biotinylated proteins were visualized using a chemiluminescent substrate for streptavidin-linked horseradish peroxidase. The spectrum of proteins biotinylated via the vasculature was distinct from that of the biotinylated lung homogenate. Lectin affinity purification of biotinylated proteins from the lung membrane fractions of normal lungs biotinylated via the vasculature revealed characteristic spectra that were reproducibly different from those from rats exposed to hyperoxia for 48-60 h. These results demonstrate that biotinylation of membrane proteins accessible to an extracellular reagent during a single transit through the pulmonary vascular bed is feasible and that the spectrum of these labeled proteins reveals the effects of hyperoxic lung injury. The affinity of biotin for streptavidin makes this procedure potentially useful as a means of separating the labeled membrane proteins from the much larger population of membrane proteins that are not accessible via the vasculature, e.g., intracellular membrane proteins and plasma membrane proteins of cell types in luminally inaccessible regions of the intact lung. The consistent changes in the spectrum of labeled proteins seen with hyperoxia suggest that in itself the spectrum may be a useful encryption of certain aspects of vascular pathophysiology.

Animals↗