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Left ventricular wall motion abnormalities secondary to stress-induced myocardial ischemia can be detected with difficulty by mentally comparing echocardiographic images sequentially recorded on videotape. Digital stress-echocardiography, a combination of ultrasound imaging and digital archiving technologies, at least partially can overcome this problem: the technique is based on reviewing images at rest and after stress (exercise or pharmacological) side by side in dual- or quad screen digital format, in a synchronized cine-loop, as if obtained simultaneously. This technique however is presently not widely used, due to the high cost of most commercially available systems. We have developed a digital stress echo system, which is easy to use and relatively inexpensive, running on a Macintosh II personal computer with g-bit graphics. The 2-D echocardiographic images recorded on videotape are digitized offline using a video digitizing board. The image can be displayed and analyzed using the public domain NIH image software developed by Wayne Resband, without loss in image quality and resolution, particularly if using Super-VHS videotape. We have made a macro procedure for the montage in a qued-screen format of four digital recorded echocardiographic cardiac cycles of six frames that takes only a little more time than commercially available systems. In conclusion, the use of a personal computer and low-cost software may help to make digital stress-echo techniques more widely feasible in the clinical setting and increase the diagnostic power of the ultrasound technique in the evaluation of patients with known or suspected coronary artery disease. Copyright 1995, 1999 Academic Press

The antioxidant activity of vitamin A against lipid peroxidation induced by doxorubicin in rat tissues in vivowas investigated. A single ip injection of doxorubicin (30 mg/kg body wt) markedly raised the level of peroxidated lipids measured as TBARS and conjugated dienes in heart and brain membrane preparations. Other tissues, such as retina and liver, did not show any increase of lipid peroxides over control values. Pretreatment of rats with two daily subcutaneous injections of retinol palmitate (0.25 g/kg body wt), for 2 days, before injecting doxorubicin, inhibited peroxidation of heart and brain membrane lipids. The antioxidant action of vitamin A does not appear to be mediated by enhancement of antioxidant enzyme activities committed to detoxify oxygen radicals. Superoxide dismutase and catalase, measured in heart and brain cytosol, were not affected by the vitamin A treatment. On the contrary, a slight increase of catalase activity was observed in heart and brain cytosol from rats that had been treated with doxorubicin. Excess vitamin A may be localized in membranes. Appreciable increase of retinyl esters and retinol was measured in membrane preparations from rats that had been treated with vitamin A, with respect to control animals. Brain and heart membrane preparations from rats receiving vitamin A, assayed in vitroin the presence of an Fe3+ascorbate induction system, showed a delay at the beginning of the lipid peroxidation and generated lesser amounts of TBARS, with respect to membranes from control rats. Thus, the increase of vitamin A within cell membranes results in an increased resistance of membrane lipids to peroxidation, both endogenously produced and induced in vitro. These results may be consistent with the hypothesis that vitamin A may act as a physiological antioxidant in cell membranes where it is localized.

The peroxyl radical-scavenging activity of vitamin A has been exploited to obtain protection against peroxidative damages induced in rat heart by administration of an acute dose of doxorubicin (10 mg/kg, in vein). Peroxidative lesions were evaluated by both biochemical and histological assays, 48 hr after the injection of doxorubicin. Heart tissue from rats receiving doxorubicin showed a marked increase of protein carbonyl levels, and of membrane conjugated dienes, as well as a decrease of membrane protein thiols. Abnormal chemistries, including a large increase of the activity of serum lactate dehydrogenase and creatine phosphokinase, an index of the myocardial damage caused by doxorubicin, were also observed. Pretreatment of rats with 25 I.U./kg b.wt. of vitamin A, once a day for 2 days, before injecting doxorubicin, substantially reduced the peroxidative damage to heart lipids and proteins, and markedly lowered the serum values of lactate dehydrogenase and creatine phosphokinase to values close to those of control rats. The significant prevention of doxorubicin-induced cardiomyopathy by vitamin A was evident from the histopathological pattern observed after light microscopy. The dosage of vitamin A useful to obtain the protective effect appears safe and does not injure the liver, as indicated by light microscopy of the tissue. A survival study, carried out by injecting rats with a single injection of 10 mg/kg of doxorubicin, showed that pretreatment with 25 I.U. of vitamin A per kg significantly increased survival rate of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)