Emphysema creates an increase in alveolar compliance, a measurement of how the volume changes in response to a change in pressure, V/P. In other words, lung tissue begins to lose its integrity and become a lot more stretchy with less elastic rebound. This sounds like a good thing (since it seems that it would be easier inhale with lungs which have less resistance); however, emphysema’s real problem is in exhalation. Patients who seem to be gasping for air are actually having trouble clearing their lungs (since there’s less rebound).

In the case of α1-antitrypsin deficiency, the immunological protection provided by macrophages in the respiratory tract (ie, the protease trypsin) is unable to be “neutralized” by other substances (like antitrypsin). Consequently, the active protease ultimately begins to self digest the delicate respiratory tissues leading to emphysema.

Now researchers are targeting these macrophages for gene therapy. Gene therapy involves taking a “good” gene, using a vector (usually a virus) to carry it into a host cell, and then have that cell successfully express the protein coded for by the gene. For example, the scientists at Boston University’s School of Medicine used a lentivirus to introduce a functional version of the antitrypsin gene into mice with the deficiency.

Lung tissue is particularly easy to transfect since viral vectors can easily access the entire tracheobronchial tree through inhalation, and this is exactly what researchers took advantage of. The problem was ensuring that the gene expression lasted as long as possible, so transfecting the stem cell line was a potential possibility. Read more about it by clicking on the link above!

So this is just another application of gene therapy. One day, humans will probably have synthetic plasmids containing the insulin gene (for type I diabetes patients), antitrypsin (for α1-antitrypsin), the CFTR gene (for cystic fibrosis patients), etc. Pretty exciting years coming up for medicine!

After removing the lungs from the chest cavity, it became clear that there are many ways to distinguish the left lung from the right. Since much of the heart is situated below the left lung, it tends to be smaller and has imprints due to the heart’s presence. For example, you can see an imprint of the aortic arch (emerging from the superior portion of the heart) on the inside of the left lung. The right lung doesn’t have these markings; however, with three lobes, it’s a little larger than the two lobed left lung.

Lung tissue is awfully squishy, but I suppose that’s what you would expect from something which provides about 80 square meters of surface area for oxygen exchange. The surface anatomy is pretty simple compared to the heart, but I’m sure studying the branching schemes of the bronchioles will be far more complicated. Oh well, still really interesting to see how the cardiovascular system works from an anatomical perspective.