Breathing relies on pulmonary surfactant, a remarkable substance within our lungs. This complex mixture lines the delicate air sacs, ensuring efficient gas exchange with every breath. Without it, the respiratory system would struggle.
What is Lung Surfactant and What is it Made Of?
Pulmonary surfactant is a complex mixture of lipids and proteins that coats the inner surface of the alveoli, the tiny air sacs in the lungs where gas exchange occurs. It consists of approximately 90% lipids and 10% proteins. The lipid portion is primarily composed of phospholipids, with dipalmitoylphosphatidylcholine (DPPC) making up about 80% of these phospholipids. DPPC is considered the strongest surfactant molecule within this mixture due to its unique structure.
Other phospholipids like phosphatidylglycerol, phosphatidylinositol, and phosphatidylethanolamine also contribute, making up about 20% of the total phospholipids. The protein component includes four distinct surfactant proteins (SPs): SP-A, SP-B, SP-C, and SP-D. SP-B and SP-C are hydrophobic proteins that are particularly involved in reducing surface tension, while SP-A and SP-D are hydrophilic proteins that play significant roles in the lung’s immune defense system.
How Lung Surfactant Works to Keep Lungs Open
The physical principle of surface tension describes the cohesive forces that cause liquid molecules at a surface to be more attracted to each other than to the air above them, leading to a tendency to minimize surface area. In the fluid-lined alveoli of the lungs, this natural force would cause the tiny air sacs to collapse, much like a deflating balloon. This collapsing pressure is inversely proportional to the radius of the alveolus, meaning smaller alveoli would be at a greater risk of collapse.
Lung surfactant molecules counteract this by positioning themselves at the air-liquid interface within the alveoli. The hydrophobic tails of the surfactant molecules, particularly those of DPPC, repel the water molecules, disrupting the strong hydrogen bonds between them. This interruption significantly lowers the surface tension, reducing the inward pull that would otherwise lead to alveolar collapse, especially during exhalation when the lung volume decreases. By reducing surface tension, surfactant also helps equalize pressure between larger and smaller alveoli, ensuring that all air sacs inflate uniformly and efficiently, making breathing less strenuous.
Conditions and Consequences of Surfactant Problems
Insufficient or dysfunctional lung surfactant can lead to serious respiratory conditions, particularly affecting newborns and adults.
Respiratory Distress Syndrome (RDS), also known as Hyaline Membrane Disease, is a breathing disorder primarily affecting premature infants. It occurs because their lungs are underdeveloped and do not produce enough surfactant, which begins to be synthesized in the fetus during the third trimester, around 26 to 35 weeks of gestation. Symptoms of RDS in newborns include rapid and shallow breathing, grunting sounds with each breath, flaring of the nostrils, and a bluish tint to the skin and lips due to low oxygen levels. Without sufficient surfactant, the alveoli collapse, making breathing difficult and potentially leading to organ oxygen deprivation. Treatments often involve supplemental oxygen, continuous positive airway pressure (CPAP), and surfactant replacement therapy, where artificial surfactant is directly administered into the baby’s lungs.
Acute Respiratory Distress Syndrome (ARDS) affects adults and is characterized by severe lung injury and inflammation. While some issues with surfactant production or secretion may occur, the primary problem is often the inactivation or damage of existing surfactant by inflammatory mediators and plasma protein leakage. This leads to increased alveolar surface tension, causing instability and collapse of air sacs, which impairs gas exchange. Symptoms of ARDS include severe shortness of breath, rapid and labored breathing, and a fast heart rate, often requiring mechanical ventilation and oxygen therapy. Unlike RDS in infants, surfactant replacement therapy has shown less consistent success in adult ARDS, partly due to the complex and varied nature of the underlying lung injury and the rapid degradation of administered surfactant. Management focuses on supportive care, such as lung-protective ventilation and prone positioning, to improve oxygenation and minimize further lung damage.
The Body’s Surfactant Cycle: Production and Renewal
The continuous supply of lung surfactant is maintained through a dynamic process of production, secretion, and recycling carried out by specialized cells within the alveoli.
Type II pneumocytes are solely responsible for synthesizing and secreting pulmonary surfactant. These cells contain granules, known as lamellar bodies, where surfactant components are stored before release.
After synthesis, surfactant components are packaged into these lamellar bodies, which then move to the cell surface and fuse with the membrane to release surfactant into the alveolar fluid. Once secreted, the surfactant forms a film at the air-liquid interface. A significant portion of this secreted surfactant is then reabsorbed by the Type II pneumocytes through a process called reuptake. The internalized components are processed and can be re-secreted, ensuring a continuous renewal and efficient use of surfactant within the lungs.