Regional pulmonary blood flow and volume was measured in ten rabbits
anesthetized with pentobarbital (30 mg/kg). Tracheostomy was performed and
catheters were placed into the jugular vein and carotid artery. The cardiac
⁹⁹mtc output was measured using the indicator-dilution technique using Tc labelled RBC followed by an injection of radiolabelled macroaggregates (MAA) to mark regional blood flow. Measurements were made both before and after either exposure to cigarette smoke (3 cigarettes for ten minutes at 4 puffs/minute) or sham exposure to air. The animals were sacrificed and the lungs were removed with the vessels tied. The lungs were then inflated and rapidly frozen over liquid nitrogen. The lungs were sampled into slices by vertical height, each slice was further sampled and then gamma counted for the injected isotopes. Regional pulmonary blood flow was calculated by setting the total lung MAA counts for each MAA equal to the cardiac output so that the sample flow was calculated as the fraction of sample counts to total counts times the cardiac output. The blood volume was marked by the labelled RBC and RBC transit was calculated as blood volume (ml) divided by blood flow (ml/sec).
In a second series of experiments (N=10) , ⁵¹Cr PMN were injected as a bolus along with ⁹⁹mtc RBC in an indicator-dilution run. Following the injection of the cells, the blood flow was marked with MAAs and then the same sham or smoke treatments were given as in the previous experiments. At the end of ten minutes, the animals were sacrificed and the lungs were processed the same as before. Regional PMN retention was calculated as the [formula omitted]. The data show that smoke exposure increased pulmonary blood volume (p<.01), pulmonary transit time (p<C.05) and the ratio of lung blood volume to central blood volume (p <C-05) without changing central blood volume or cardiac output. Smoke exposure also caused a redistribution of blood flow from upper to lower lung regions (p <C-05). This lengthened the regional RBC transit times in all regions but particularly in the upper zones. These changes in RBC transit had no effect on PMN retention.
We conclude that acute smoke exposure lengthens the RBC transit through the pulmonary circulation by increasing blood volume and redistributing blood flow. This change in red cell behavior was not associated with a consistent change in PMN retention in the lungs. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate
| Identifer | oai:union.ndltd.org:UBC/oai:circle.library.ubc.ca:2429/24840 |
| Date | January 1985 |
| Creators | Lee, Sherman |
| Publisher | University of British Columbia |
| Source Sets | University of British Columbia |
| Language | English |
| Detected Language | English |
| Type | Text, Thesis/Dissertation |
| Rights | For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. |
Page generated in 0.0176 seconds