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Post by David Feder on Oct 5, 2006 21:52:49 GMT -5
Michelle: I found and I post the summary of the research. My son use ACE inhibitor and carvedilol to treat cardiac dysfunction and for us it's easy to chance ACE inhibitor to losartan. I can't stimulate self medication but I think that it's important discuss the possibility of this use because the drug can be used in DMD to prevent cardiac dysfunction, in special after 10 years. Your cardiology and/or pediatrician and/or neurologist can indicate losartan. If the drug don't increase muscle force or delay the evolution of disease at least the drug can delay cardiac symptoms.
Another question: TGF beta is one of several causes of muscle degeneration in DMD. I look for a drug to block TGF beta since 2003. I try with tamoxifen but I had some problems with my pathological studies but I want complete this studies. I still believe that tamoxifen can help. I believe that early use of TGF beta inhibitor can help to reduce pathological alterations of dystrophic muscles.
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Post by bingo mum on Oct 6, 2006 0:53:09 GMT -5
what would the side effects of the bloodpressure drug be on a dmd paitent.
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Post by David Feder on Oct 6, 2006 4:56:19 GMT -5
No problem with blood pressure. The dose is ajustable to each patient as ACE inhibitor.
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Post by David Feder on Oct 11, 2006 15:55:51 GMT -5
Hi: This recent article isn't about DMD but can explain why losartan can help in DMD. They studied normal rats and they concluded that angiotensin II increases muscle ROS (reactive oxygen species). These findings may have implications for muscle oxidative stress and sympathetic vasoregulation when the renin–angiotensin system is chronically activated. Dystrophic musles present increase of ROS. Locartan block the action of angiotensin II and can reduce ROS. Reactive Oxygen Species Impair Sympathetic Vasoregulation in Skeletal Muscle in Angiotensin II–Dependent Hypertension Weiying Zhao; Scott A. Swanson; Jianfeng Ye; Xilong Li; John M. Shelton; Weiguo Zhang; Gail D. Thomas -USA Sympathetic vasoconstriction is attenuated in exercising muscle by locally generated vasodilators, including NO. Skeletal muscle also produces reactive oxygen species (ROS), such as superoxide (O2–), which inactivates NO. We, therefore, hypothesized that excessive ROS production would result in enhanced sympathetic vasoconstriction in exercising muscle. To increase O2– by activating NADPH oxidase, rats underwent chronic infusion of angiotensin II (Ang II) or unilateral renal artery stenosis (2K1C) to increase endogenous Ang II. At rest, sympathetic nerve stimulation (range: 1 to 5 Hz) evoked similar graded decreases in femoral vascular conductance (range, –34% to –66%) in rats infused with vehicle, Ang II, or norepinephrine and in 2K1C or sham-operated rats. These sympathetically mediated decreases in femoral vascular conductance were markedly attenuated during hindlimb contraction in the vehicle, norepinephrine, and sham rats (range, –3% to –26%) and to a lesser degree in the Ang II (range, –16% to –47%) and 2K1C (range, –16% to –45%) rats. In muscles from Ang II and 2K1C rats, ROS were elevated and the NADPH oxidase subunit gp91phox was upregulated. The O2– scavenger tempol restored the normal attenuation of sympathetic vasoconstriction in the contracting hindlimbs of the Ang II and 2K1C rats, but this effect was prevented by pretreatment with an NO synthase inhibitor. Taken together, these data indicate that chronically elevated Ang II increases muscle ROS, which disrupts the normal NO-dependent attenuation of sympathetic vasoconstriction. These findings may have implications for muscle oxidative stress and sympathetic vasoregulation when the renin–angiotensin system is chronically activated. hyper.ahajournals.org/cgi/content/abstract/48/4/637?maxtoshow=&HITS=&hits=&RESULTFORMAT=1&andorexacttitle=and&fulltext=muscular+dystrophy&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=date&fdate=10/1/2006&resourcetype=HWCIT |
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