If the heart stops beating – a cardiac arrest – brain damage can start after just a few minutes. When medics reach the patient they use defibrillators to shock the heart into restarting. If that fails, they try cardiopulmonary resuscitation (CPR), which involves manually pumping the patient’s heart and inflating the lungs. But CPR delivers only 10 to 15 per cent of normal blood flow to the brain.

The “shock sheet” is designed to be wrapped round a patient and inflated to raise upper body blood pressure within 30 seconds. And it can be put in place while normal CPR is being carried out.

“This device buys you time,” says its inventor, Mark Wilson, an anaesthetist at East Surrey Hospital in Redhill, UK. “It’s a cheap and simple way to save lives.”

Septic shock

So far Wilson has only shown that the shock sheet increases blood pressure in healthy volunteers. The device will have to undergo clinical trials before it can be used routinely in ambulances and hospitals.

Heart disease is a leading cause of death in western countries, and a quarter of the people who suffer a heart attack die before they reach hospital. Experts believe the shock sheet could help save some of them.

Keeping the blood flowing to the brain is more important than supplying the limbs, says Desmond Sheridan, a cardiologist at St Mary’s Hospital in London. The device should help shift blood flow away from the lower body.

Wilson believes the shock sheet might also help doctors treat other conditions that cause blood pressure to fall, such as septic shock (systemic bacterial infection) and anaphylactic shock which is caused by massive allergic reactions.

The receptors are only present on the outer surface of the heart, which may explain why some “silent” heart attacks produce no pain. The new research also identifies a new target for drugs that alleviate chest pain caused by coronary heart disease, scientists say.

Vanilloid receptor 1 (VR1) is a pain sensor that is abundant in the skin and tongue and picks up the searing sensation of chilli peppers. Hui-Lin Pan, at Pennsylvania State University in the US, investigated whether it is also present in the heart.

“What was very striking was that we found the receptors were localised only on the surface of the heart,” he told 91av. The outer surface was densely covered with VR1, but no receptors were detected on the inner surface.

“This is the first time anyone has documented these receptors in the heart,” says Harold Schultz at the University of Nebraska Medical Center in Omaha.

Inner feeling

Pan also found that VR1 was important in triggering the cardiac reflex response, which causes the chest pain associated with most heart attacks.

However, patients with silent ischaemia suffer damage on the inner surface of the heart. The lack of VR1 receptors on the inner surface could explain why no pain is felt.

VR1 could also be a target for drugs that reduce or prevent chest pain, Pan says. Schultz agrees: “If these receptors are involved in pain perception in heart attack, then it could open an avenue for looking for drugs that can block this pain.”

Pungent ingredient

Capsaicin, the pungent ingredient in chilli peppers, activates VR1. Previous studies had shown that, when applied to the heart surfaces of animals, capsaicin causes changes in blood pressure and heart rate similar to those seen in heart attacks. But the receptors involved in producing these changes were not known.

Pan used immunofluorescence labelling to show that VR1 was located on the outer surface of the heart. To determine whether the receptor was involved in the cardiac reflex response, he destroyed the nerves containing VR1 in one group of rats and compared their response with a group with intact VR1 receptors.

In the intact rats, both capsaicin and bradykinin – a chemical released during heart attacks – led to an increase in blood pressure and nerve activity. But in rats with no VR1, no increases were detected at all.

This surprised Pan. “We initially expected a partial response when we tried to trigger a reflex, because we thought other receptors would compensate for the lack of VR1.” The absence of response suggests that VR1 is the most important receptor in chest pain.

Journal reference: Journal of Physiology (vol 551, p 515)

The discovery not only highlights the known dangers of smoking, but shows that tobacco use could be helping to sustain the TB epidemics that are plaguing many parts of the world.

The researchers, led by Vendhan Gajalakshmi of the Epidemiological Research Center in Chennai, India, and Richard Peto, at the University of Oxford, UK, compared the smoking habits of 43,000 Indian men who had died of various diseases with those of 35,000 men who were still alive and from the same area.

The risk of TB among smokers was four times that of non-smokers, says Gajalakshmi. “Almost 200,000 people a year in India die from TB because they smoked,” she says.

Billion carriers

More than a billion people worldwide carry the tuberculosis microbe, Mycobacterium tuberculosis, but only eight million people a year become seriously ill from it.

“Most of the billion people who have TB will just carry it and not die from it – their bodies are keeping that infection under control,” Peto told 91av. “But smoking makes the breakdown of that control more likely.”

The exact mechanism by which smoking increases TB risk is uncertain, but Gajalakshmi adds: “Smoking damages the lung’s defence mechanism against chronic TB infection and the infection becomes uncontrollable.”

The link between smoking and TB suggests that tobacco use may play a role in increasing TB infections in the general population. Another member of the research team, Prabhat Jha at the University of Toronto, Canada, says: “Not only in Asia and Africa, but also throughout America and Europe, smoking will increase the number of people who develop clinical TB themselves and can then infect others, unless they are properly treated and cured.”

The researchers’ next step is to follow up TB sufferers who are currently alive to determine whether smoking is playing a role. “And we need to determine the proportion of TB caused by smoking in lots of different countries – Africa, Asia, America, Russia,” says Peto.

The researchers also want to emphasise the dangers of smoking to people in India. “We have to bring out smoking cessation clinics in India and promote awareness in the community about the harm of smoking,” Gajalakshmi concludes.

Journal reference: The Lancet (vol 362, p 507)

Microbiologists Derek Lovley and Kazem Kashefi, at the University of Massachusetts say the discovery will help scientists determine where and when life might have evolved on Earth, and how deep life might exist below the surface.

The pair first cultured a sample from the black smoker at 100°C, to mimic the hot environment of the hydrothermal vent. When they saw a bug continuing to grow at that temperature, they increased the heat to find its limit. “What surprised us was that we kept ratcheting up the temperature and the organism kept growing,” Lovley told 91av.

The researchers then put the bacterium in an autoclave, an oven used to sterilise medical equipment at 121°C. “Even when we left it there for 10 hours it was still alive,” says Lovley. “That was when we were truly amazed.” The bug was also found to survive two hours at 130°C, but did not replicate until returned to a lower temperature.

Heatproof proteins

How the organism can survive such high temperatures is unknown, and the next step in Lovley’s research. Finding out more about the bacterium’s proteins is crucial, says Don Cowan, at the University of the Western Cape, South Africa.

“The higher the upper limit goes, the more questions are asked about molecular stability and function,” he says. “The biggest excitement from a biochememical point of view is looking at the organism’s proteins to see why they can withstand 121°C when other proteins cannot.”

The previous record holder was a bug called Pyrolobus fumarii. But its discoverer, Karl Stetter at Regensburg University, Germany, says he is not convinced that Strain 121 would grow at 121°C in its natural environment.

He points out that the bacteria grew fastest at about 106°C, taking an hour to double in number. At 121°C, this took 25 hours.

Journal reference: Science (vol 301, p 934)