The shared characteristics of different hibernators mean it’s likely that these species have inherited fragments of protective mechanisms against cold, inactivity, starvation and asphyxiation from common ancestors and developed these into a comprehensive low-metabolic syndrome. There are even hints that we humans might, to some extent, retain some of these abilities. For a long time, there was no evidence that primates could hibernate. But in 2004, a species of Madagascan lemur was shown to practice regular bouts of torpor. “If you look at the lemur and look at us, we share about 98% of our genes,” says Henning. “It would be very strange if the tools of hibernation were all packed into that 2% difference.”

As their body temperature drops, hibernators also remove the lymphocytes (white blood cells) from their blood and store them in the lymph nodes. And within 90 minutes of awakening, these reappear. This damping down of the immune system prevents a general inflammation in the body during rewarming – the very thing that would cause humans and other non-hibernators to suffer kidney damage. However, it’s a risky strategy, leaving animals unable to mount an immune defence while hibernating. The fungus responsible for white-nose syndrome, currently wiping out bat colonies in the USA, takes advantage of this vulnerability, infecting the bats while they are dormant. In response, the bats frequently exit hibernation and rewarm to fight off the pathogen – the high-energy cost of these interruptions ultimately killing them.

Funny smell

Knowing how hibernators control these changes in their blood could have immediate and far-reaching benefits for us. As well as improving our ability to survive hypothermia and cold suspended-animation states, stripping the blood of white blood cells could prevent the aseptic sepsis caused by heart–lung machines, in which activation of blood cells as they pass through the life-support equipment triggers a body-wide immunological reaction. Transplant organs, often chilled for transport, would also benefit from better cryoprotection. And we could increase the shelf-life of our blood stocks – we still haven’t figured out how to store donated blood platelets at low temperatures, so blood donations can only be kept a week before they must be used or thrown away due to the risk of bacterial infection.

The UMCG team took a giant leap towards achieving these goals quite by accident after a student left a culture of hamster cells in a fridge at 5C. After a week the hamster cells were still alive, and smelling of rotten eggs. The student poured the medium surrounding the cells over a separate batch of cells from a rat, suspecting the smelly cells might have secreted some kind of protective agent. She placed them in the same fridge and waited. Normally, refrigerating rat cells would quickly kill them, but after two days they were still alive.

The team is investigating several compounds that might be responsible for this cryopreservation. One is an enzyme known as cystathionine beta synthase (CBS), which stimulates the production of hydrogen sulphide, the molecule that gives rotten eggs their characteristic whiff. If hamsters are injected with a chemical to inhibit CBS, they can no longer enter torpor, and those that were forced into hypothermic states suffered the kind of kidney damage one would expect in non-hibernators like us.

Of over a hundred compounds Henning’s team has investigated, many had no effect, but a few did, conferring long-term cold protection to cell samples. The team has already patented one of these compounds, Rokepie, as an additive. This would allow cells that normally need to be kept at 37C, such as those from humans or mice, to be stored in the refrigerator, either for transport or so experiments can be put on hold during weekends and busy periods.

The leading cryopreservation molecules extracted from hibernators are incredibly potent, and it seems they work by eliciting changes in the cells themselves – whether these are from hibernators or not. If so, this offers further evidence that we still possess some tools that could help endure hypothermia and low metabolic states.

For now, applying the lessons they’ve learned from hibernators wholesale onto humans is not within the remit of Henning’s group. The space race is long over, and Nasa is not awarding major grants to develop suspended animation. However, the US Army is.

Golden hour

“If you look anywhere near a trauma bay, things are pretty chaotic,” says Professor Sam Tisherman. “It’s controlled chaos, but the chaos mainly comes from the fact you never know what’s going on with the patient.”

In frenetic hospital emergency wards, it’s often not possible for doctors to identify the problem, fix it and keep the patient alive all at the same time. Patients suffering uncontrolled blood loss, for example, may go into cardiac arrest. When this happens, surgeons must fight the clock to stop the bleeding before they can start resuscitation efforts. “Somebody rolls in and they’re basically dying,” says Tisherman. “We’re quickly trying to resuscitate them, and figure out what’s wrong with them, and repair injuries all at the same time.” This is the fundamental underpinning of trauma medicine: you are always against the clock.

Tisherman wants to buy doctors a little more time. He believes that by inducing hypothermia we can extend the “golden hour” in which surgeons battle to save the lives of critically injured patients. To do this, he’s pushing human endurance of hypothermia far beyond its normal limits.

After graduating from MIT in 1981, Tisherman built a career in critical care medicine. He won a Lifetime Achievement Award in Trauma Resuscitation Science from the American Heart Association in 2009, and is now an Associate Director of the Safar Center for Resuscitation Research in Pittsburgh. It was founded by Peter Safar, the Austrian physician who popularised the “kiss of life”, CPR, and drove the creation of the Resusci Anne doll used in teaching it. At Pittsburgh, Safar created the world’s first intensive care training programme. His lifelong aim was to “save the hearts and brains of those too young to die.”

The procedure that Tisherman is pioneering is called emergency preservation and resuscitation. His work is supported through the US Army’s Telemedicine and Advanced Technology Research Center, which funds research on topics as niche as advanced prosthetics and robots to carry wounded soldiers out of the battlefield.

Some of his surgeons will already be familiar with hypothermic techniques, having routinely chilled patients to the low 30s or high 20s. For procedures that require zero blood flow, cardiac surgeons will even cool patients to around 15C, the point at which their heart stops.