Newswise — Millions of people are exposed to hand-transmitted vibration at work by powered-tool usage every day for extended periods of time. Past studies have shown that years of working with hand held powered-tools could cause hand-arm vibration syndrome (HAVS), known as secondary Raynaud's disease of occupational origin. HAVS is characterized by excessively reduced blood flow, limiting blood supply to the nerves, muscles, and tendons, and blanching of the fingers. The symptoms include pain, tingling and numbness of the hand, which progresses to loss of dexterity. All patients complain of excessive finger blanching when exposed to cold.
Now, researchers at the Medical College of Wisconsin have developed a new rat-tail vibration model for studying the early stages of vibration injury. By studying the structure of the blood vessels, the researchers led by Danny Riley, Ph.D., professor of cellular biology, neurobiology and anatomy, demonstrated that four hours of vibration causes blood vessel constriction and produces damage to arterial smooth muscle and the endothelial cells which line the vessels. The researchers also showed that blocking vasoconstriction by premedicating the animal with nifedipine, a calcium blocker, to prevent smooth muscle contraction during vibration, prevented arterial damage.
Sandya Govindaraju, a graduate student in the laboratory of Dr. Riley, presented the study today at Experimental Biology 2004 as part of the scientific program of the American Association of Anatomists.
"These novel findings indicate that vibration and vasoconstriction act synergistically to damage arteries. The types of early morphological damage observed are likely to lead to vibration syndrome in the long term. Thus, our data suggest that medications and other countermeasures that prevent vibration-induced vasoconstriction may reduce the chances of hand-arm vibration syndrome," says Dr. Riley.
The management of HAVS is non-specific and symptomatic with little therapeutic advancement in the past few decades. While HAVS is well described in its last stages, when it is not reversible, there is very little information about the cellular events involved in the early development of the disease.
The rat-tail, whose anatomy is comparable to that of the human hand, was an ideal model to study. Both contain blood vessels of similar size, have motor and sensory peripheral nerves and have muscles and tendons of intrinsic and extrinsic origin. This similarity permits extrapolation of what happens to cells during tail vibration to that expected in the arteries in the human hand. The rats were not anesthetized and handled the vibration exposure well. They slept through most of the experiment.
Physiological measurement studies have shown that blood flow is reduced by vibration. The Medical College study was designed to provide structural evidence for vibration-induced vasoconstriction during vibration and to identify possible mechanisms of damage. The researchers compared arteries vibrated for five minutes, one hour and four hours to those treated with a known pharmacological vasoconstrictor, epinephrine. All the arteries were constricted. Arterial diameter was decreased, and vacuoles, or cavities, appeared in vascular smooth muscle cells. The cavities were similar to those induced by epinephrine-induced vasoconstriction.
Nifedipine, a calcium channel blocker that blocks vascular smooth muscle contraction, was used to test if the pre-treatment protects against vibration-induced damage. This proved successful, and the pretreated arteries were dilated after four hours of vibration, with lesser number of vacuoles in the smooth muscle cells. Govindaraju hastens to add that while vasoconstriction is clearly a mechanism of damage following exposure to extended vibration, it may not be the only one. Repeated mechanical displacement also may contribute to vascular injury. When something is vibrating at a frequency of 60 Hz, it creates a sinusoidal wave pattern 60 times a second and literally moves the tissue up and down a small distance (0.98 mm) 60 times a second. For example, a motorized toothbrush has a much lower frequency but this movement can be felt.
The frequency of the vibration also may play a role, since the amplitude -- or transfer of energy from the source of the vibration to the tissue - is higher for lower frequencies at constant acceleration than for higher frequencies. Dr. Riley's laboratory is studying the interaction of vasoconstriction and mechanical damage in vibration injury in peripheral arteries and nerves.
"These findings provide evidence that vibration indeed causes vasoconstriction, which is calcium dependent. Preventing vasoconstriction by pharmaceutical agents limits vibration-induced vascular damage. The potential for harm by vibrating tools is under appreciated by the public and not well known. Knowing what happens early on, would not only aid awareness but also help formulate preventive strategies, better screening procedures and specific treatment of HAVS before it becomes irreversible," explains Dr. Riley.
In addition to Govindaraju and Dr. Riley, other authors of the study were Brian D. Curry, Ph.D., former graduate student of Dr. Riley's whose work Govindaraju is continuing, and Jim L. W. Bain, lab manager.