Newswise — A team of researchers from the Medical College of Wisconsin, Marquette University and the VA Medical Center-Milwaukee has introduced a promising new technique to study the arteries of the lungs and their role in pulmonary hypertension.
Pulmonary hypertension* is high pressure in the blood vessels of the lungs, the circulation responsible for oxygenating blood as it travels from the right side to the left side of the heart. The mortality rate for severe pulmonary hypertension is virtually 100 percent.
The researchers are using micro-computed tomography, a high-resolution form of CT imaging, to capture and document the intact three-dimensional structure of pulmonary vessels. The group has combined physiology, engineering and mathematics to develop quantitative models of the pulmonary arterial tree architecture to study blood vessel changes occurring in a rat model of pulmonary hypertension.
The study, led by Robert C. Molthen, Ph.D., assistant professor of medicine in the division of pulmonary and critical care at the Medical College, is featured, with commentary in the highlighted topics series on "Lung Growth and Repair" , in the December, 2004 Journal of Applied Physiology.
According to Dr. Molthen, these new imaging tools could provide a basis for developing strategies in the clinical diagnosis, course of treatment, or even screening for patients susceptible to pulmonary artery disease and pulmonary hypertension.
"Our broad focus is on the structure/function relationship in the pulmonary circulation, with a goal of better understanding the causes, progression and hemodynamic impact of the vascular remodeling process," he says. "In rats various stimuli, such as exposure to lower than normal oxygen levels, as experienced when living at higher altitudes or with chronic obstructive pulmonary disorders (COPD), or exposure to certain toxins/drugs or blood-borne metabolic wastes, can lead to progressive pulmonary vascular remodeling, heart failure and ultimately death.
Specifically, the team studied the impact of animals living in a 10% oxygen environment (the normal level is about 21%) on changes in the structure and function of lung arteries, and the role these changes play in pulmonary hypertension. It revealed that after 21 days, there was a reduction in the total length and number of branches detected in the pulmonary arterial tree of the rats who received less oxygen when compared to those measured in control rats receiving a normal amount of oxygen.
Also, the pulmonary arteries in the rats raised in a low oxygen environment were much stiffer than in those receiving normal levels of oxygen, a change that would significantly increase arterial blood pressure in the lungs.
Dr. Molthen is also an adjunct research assistant professor in the department of biomedical engineering at Marquette University, and based at the Zablocki VA Medical Center, a major teaching affiliate of the Medical College. His co-investigators in this study were Kelly L. Karau, Ph.D., who currently works at General Electric Medical Systems, and the late
Christopher A. Dawson, Ph.D., professor of physiology at the Medical College and of biomedical engineering at Marquette.
The study was funded by National Heart, Lung and Blood Institute Grants, the W.M. Keck Foundation, and the Department of Veterans Affairs.
* There are 2 types of pulmonary hypertension, primary and secondary. Primary or idiopathic pulmonary hypertension (PPH) is of unknown origin, it appears to affect predominately women in their thirties and forties, and certain individuals have been shown to have a familial or genetic predisposition. PPH has been linked to using diet drugs or anorectic compounds such as Phen-Fen. In PPH the pulmonary hypertension is itself the underlying health problem.
Although PPH has a low incidence and typically strikes 1 to 2 people per million, the incidence of Secondary pulmonary hypertension (SPH) is much higher. SPH occurs when the pulmonary hypertension is a side effect of another health condition, such as lung disease, chronic obstructive pulmonary disorder (COPD), HIV, severe sleep apnea, emphysema, pulmonary emboli, congenital heart defects, left heart failure or an autoimmune disorder.
Until the last 10 years there were very few treatments available for pulmonary hypertension and the projected survival rate after diagnosis was two to four years. A number of treatments have become available that are able to slow progression of the disease and possibly even reverse some of the damage to lungs and heart. New treatments are continually being investigated in clinical trials. The advent of lung transplantation has provided another alternative, but it is usually implemented as a last resort and still has many complications and a relatively high mortality.
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Journal of Applied Physiology (Dec-2004)