Joke (fun) answer : 1) inhalation 2) exhalation 3) O2 exchange 4) CO2 exchange 5) phonation (voice)
6) buoyancy (while swimming) 7) cushion (for the heart).
Real answer :
1) Gas exchange.
2) Vascular reservoir : between right and left heart.
3) Filter : embolized material gets caught at the level of the capillary radius.
4) Homestasis : heat & fluid transfer.
5) Defense barrier : foreign organisms (bacteria) and particles (dust).
6) Endocrine function : angiotensinogen gets converted to angiotensin.
7) Metabolic function : surfactant synthesis & fibrinolytic systems.
The lung is a top shelf organ that is not given its due respect in the field of medicine.
Tons of research is done on the heart and the brain and the immune system.
However, the lung is simply seen as an oxygenation / ventilation tool and possible considered
as a gateway for foreign objects from entering the inner milieu of the human body.
Great interest should also be given to the fact that the lung is a vascular reservoir.
When this pulmonary vascular reservoir is overwhelmed is when the pulmonary edema starts.
It is incredibly versatile and it should be followed by the research community as to
the result of the demise of the lung.
The evolution of the understanding of the lung / alveolus in the last 30 years.
Old textbooks (circa 1970s) mostly offer hand drawings.
Since then, we have an improving understanding that has gone
from a view at the level of the microscope to the electron microscope
to the scanning electron microscope.
What is missing in the literature is giving the clinicians at bedside a
good understanding of the physics and physiology of the lung and the alveolus.
I’ll give one example :
One of the major functions of the lung is an endocrine function : that of
converting Angiotensinogen to Angiotensin.
The lung is the primary place where ACE (angiotensinogen converting enzyme is
located. The kidney is the secondary place where ACE is found.
What happens to this pulmonary feature of conversion via enzymatic process in the
lung when the lung is significantly atelectatic or the lung is in serious crisis during
a pulmonary edematous event?
Angiotensin is the endogenous hormone that keeps vasculature constricted as the
body deems necessary.
Is it that we as a medical society do not know?
Is it that we do not understand this mechanism of action?
Is it that we have never entertained this notion?