Carbon monoxide has unexpected benefits, but don't try it at home

April 29, 2001

New York, NY - April 27, 2001 -- A toxic component of industrial emissions, exhaust and cigarette smoke, carbon monoxide starves our cells of oxygen by replacing oxygen molecules in the blood. Exposure to carbon monoxide can have fatal consequences. But surprisingly, according to a new study by Columbia University researchers, carbon monoxide may also have a life-saving effect when blood vessels are blocked, such as during heart attack or stroke. The results "point to potential therapeutic uses for inhaled carbon monoxide," the study's authors say. The paper is published in the May issue of Nature Medicine.

Lead author David J. Pinsky, M.D., associate professor of medicine at the Columbia University College of Physicians & Surgeons, also has signaled a need for caution. "There's more work that needs to be done to identify the conditions under which this is useful and the doses that are safe," he said. "Like many other molecules that are beneficial in the right doses, too much of them can have a lethal effect."

Carbon monoxide (CO) appears to help restore blood flow to organs threatened with a cut off blood supply, according to the authors. It does so by enhancing the body's own clot-dissolving mechanisms and by dilating blood vessels. The researchers demonstrated the results in mice.

At lower than lethal doses, it seems, "CO can paradoxically either imperil or salvage tissue by disparate mechanisms," the authors report.

The body itself produces carbon monoxide when a part of the organism becomes oxygen-starved due to blood vessel blockage, a condition called ischemia. The carbon monoxide is created as part of a natural process in which an enzyme called heme oxygenase type 1 breaks down vital molecules called hemes, when the cells carrying them wear out.

Through as-yet poorly understood mechanisms, heme oxygenase type 1 levels rise during ischemia, stepping up this process and increasing carbon monoxide levels.

Carbon monoxide next activates an enzyme called guanylate cyclase, which aids in blood vessel dilation and eases the way for blood flow, restoring needed oxygen to the tissues. This, in turn, prevents other harmful processes, such as the activation of a gene that leads to increased production of plasminogen activator inhibitor-1. This is a substance that inhibits dissolution of blood clots, and therefore would worsen the condition if allowed to function. In this process, carbon monoxide's activation of guanylate cyclase may be especially critical. This is because during ischemia, there is a steep drop in the levels of the compound that usually does this job, nitric oxide.

Future research will include a more detailed analysis of the molecular processes involved and studies of other situations in which carbon monoxide may have benefits Dr. Pinsky said.
-end-
The research was supported by the U.S. Public Health Service of the National Institutes of Health.

Columbia University Medical Center

Related Heart Attack Articles from Brightsurf:

Top Science Tip Sheet on heart failure, heart muscle cells, heart attack and atrial fibrillation results
Newly discovered pathway may have potential for treating heart failure - New research model helps predict heart muscle cells' impact on heart function after injury - New mass spectrometry approach generates libraries of glycans in human heart tissue - Understanding heart damage after heart attack and treatment may provide clues for prevention - Understanding atrial fibrillation's effects on heart cells may help find treatments - New research may lead to therapy for heart failure caused by ICI cancer medication

Molecular imaging identifies link between heart and kidney inflammation after heart attack
Whole body positron emission tomography (PET) has, for the first time, illustrated the existence of inter-organ communication between the heart and kidneys via the immune system following acute myocardial infarction.

Muscle protein abundant in the heart plays key role in blood clotting during heart attack
A prevalent heart protein known as cardiac myosin, which is released into the body when a person suffers a heart attack, can cause blood to thicken or clot--worsening damage to heart tissue, a new study shows.

New target identified for repairing the heart after heart attack
An immune cell is shown for the first time to be involved in creating the scar that repairs the heart after damage.

Heart cells respond to heart attack and increase the chance of survival
The heart of humans and mice does not completely recover after a heart attack.

A simple method to improve heart-attack repair using stem cell-derived heart muscle cells
The heart cannot regenerate muscle after a heart attack, and this can lead to lethal heart failure.

Mount Sinai discovers placental stem cells that can regenerate heart after heart attack
Study identifies new stem cell type that can significantly improve cardiac function.

Fixing a broken heart: Exploring new ways to heal damage after a heart attack
The days immediately following a heart attack are critical for survivors' longevity and long-term healing of tissue.

Heart patch could limit muscle damage in heart attack aftermath
Guided by computer simulations, an international team of researchers has developed an adhesive patch that can provide support for damaged heart tissue, potentially reducing the stretching of heart muscle that's common after a heart attack.

How the heart sends an SOS signal to bone marrow cells after a heart attack
Exosomes are key to the SOS signal that the heart muscle sends out after a heart attack.

Read More: Heart Attack News and Heart Attack Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.