UMCG is a half-kilometre complex of buildings so tightly huddled together that it’s possible to walk from the grand foyer at one end to the bicycle racks at the other without stepping outside. One of these buildings is the animal laboratory.

In a tiny room set away from the main corridor, Henning’s doctoral student Edwin de Vrij and his colleague are tending to a rat laid prone on a bed of ice. A tangle of fine tubes and wires surrounds the animal, delivering life-preserving fluids and carrying away precious data. A spool of paper inching from one machine shows that from a frenetic 300 beats per minute, the rat’s heart rate has slowed to just 60. The red numbers glowing on another show that the rat’s internal temperature has dropped more than 20 degrees to 15°C. Clicking like a metronome, a ventilator delivers steady breaths to the anaesthetised rodent. As a non-hibernator like us, the rat cannot survive deep hypothermia without medical assistance. “If you cool them down, nerve impulses will be slower, and muscles have a harder time in the cold, so it’s quite physiological that they have a harder time breathing,” explains de Vrij. This isn’t the case for true hibernators – or some other non-hibernating mammals, for that matter. “Somehow hamsters can maintain adequate breathing,” he says. “We don’t have to ventilate them.”

As well as inducing hibernation in hamsters (a process that takes weeks of gradual adjustment in climate-controlled rooms to mimic the onset of winter), the UMCG team also induce forced hypothermia states like that of our rat, chilling the animals rapidly until they fall into a state of metabolic suspension.

Today, de Vrij is searching for platelets, which are essential for blood clotting to prevent bleeding. Hibernating animals avoid getting blood clots despite their lack of activity, an ability that comes down partly to a curious change in the hypothermic body: as they cool, platelets disappear from the blood. Nobody yet knows where they go, but their prompt reappearance on rewarming has de Vrij convinced that they are preserved somewhere in the body, rather than being absorbed and later resynthesised. Surprisingly, this change also happens even in non-hibernators, including rats and – occasionally – human victims of hypothermia.

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 practise regular bouts of torpor. “If you look at the lemur and look at us, we share about 98 per cent of our genes,” says Henning. “It would be very strange if the tools of hibernation were all packed into that 2 per cent 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.

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 5°C. 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 37°C, 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.