Robert Henning, a pharmacologist from the University of Groningen, The Netherlands, is fascinated by how our bodies react to low temperatures. He and his colleagues explain that human lungs are particularly susceptible to damage: even running in cold air can cause injury. However, hibernating animals routinely experience low body temperatures, in a process called torpor, that would prove fatal to humans. They repeatedly allow their bodies to cool to temperatures barely above ambient, before rewarming briefly and then recooling. Henning and his colleagues decided to find out how hibernating Syrian hamster lungs respond to these low body temperatures ().
Creating the perfect hibernation conditions for the hamsters, Henning's colleagues, Ate Boerema and Arjen Strijkstra, collected lung tissue from the animals when they had low body temperatures (were in torpor) and as they raised their body temperatures. Then Henning teamed up with Fatemeh Talaei, Hjalmar Bouma, Martina Schmidt and Machteld Hylkema to begin looking for changes in the animals' lungs.
Henning explains that lungs are made up of smooth muscle around the airways – which allows them to expand and constrict – and collagen, the connective tissue between lung cells that collapses the lungs during exhalation. Monitoring the levels of one of the smooth muscle components – actin – in the hamsters' lungs, the team found that the actin levels began to rise slowly after the animals had dropped their body temperature and continued rising steadily, peaking just before the animals raised their body temperature at the end of torpor. However, within 2 h of rewarming, the animals had completely reversed the actin change and the actin levels had returned to normal.
The team also analysed the hamsters' lung collagen levels, and found that they increased dramatically in the first 24 h of cooling, but then gradually decreased, returning to prehibernation levels when the animals' body temperature rose. The hibernating hamsters had modified their lung structure in response to the low temperatures and the levels of key molecules that regulate tissue changes had altered too.
Henning admits that he was surprised that the response was rapid and continued while the hamsters were in torpor. ‘Most people think that once you are cold all the molecular process come to a standstill and nothing happens until you rewarm, yet we show that there is on-going change in the collagen and the smooth muscle actin,’ says Henning.
Even more remarkably, the team realised that the changes in the hibernating hamsters' lungs looked similar to some of the changes seen in asthma patients. However, instead of being permanent, the hamsters' lungs recovered rapidly when their body temperature returned to normal.
Henning explains that the airways (lumen) of asthma patients constrict during an asthma attack so that sufferers have problems exhaling and their lungs overinflate. The team suspects that the hamsters alter their lung structure so that they overinflate slightly to prevent them from collapsing during torpor when their breathing rate falls to 2–3 breaths min–1.
However, more importantly, hibernators may be able to show us how to reverse the changes that asthma patients endure. ‘Hamsters do not prevent lung remodelling, but they are good at reversing it,’ says Henning, who is optimistic that we may be able to develop new therapies that reverse some of the structural changes found in the lungs of asthma patients in the same way that hibernating hamsters return their lungs to normal when they warm up.
