Abstract:Rocha AM, Salemi VMC, Neto PAL, Matsumoto AY, Pereira VFA, Fernandes F, Nastari L, Mady C. Endothelial and non-endothelial coronary blood flow reserve and left ventricular dysfunction in systemic hypertension. Clinics. 2009;64(4):327-35 OBJECTIVES: We evaluated the impairment of endothelium-dependent and endothelium-independent coronary blood flow reserve after administration of intracoronary acetylcholine and adenosine, and its association with hypertensive cardiac disease. INTRODUCTION: Coronary blood fl… Show more
“…At the same time, cardiac function was significantly suppressed during 2.5% isoflurane inhalation compared with during 1% isoflurane inhalation or adenosine infusion in those mice, especially in the AR mice. We also found that CFR was closely related to cardiac function, which was in accord with previous studies in humans (20) and mice (10). All of the evidence suggests that high-concentration isoflurane-induced cardiac dysfunction may lead to underestimation of CFR.…”
Section: Discussionsupporting
confidence: 91%
“…Nevertheless, CFR is closely related with cardiac function (10,20). Given that isoflurane can depress cardiac function through myofilament desensitization (5), the findings in mice without significant cardiac overloading could not be simply extrapolated to mice with loading changes (e.g., pressure or volume overload) or cardiac remodeling (concentric or eccentric hypertrophy).…”
Adenosine and high-concentration isoflurane are commonly used to induce hyperemia for assessment of coronary flow reserve (CFR) in mice, but high-concentration isoflurane may exacerbate cardiac dysfunction, leading to impaired CFR. However, there is no study be found comparing the effects of adenosine and isoflurane on CFR and corresponding cardiac function. High-resolution echocardiography and invasive hemodynamic assessment were performed in 20 mice 2 wk after transverse aortic constriction (TAC), aortic regurgitation (AR), and corresponding sham operation. CFR was calculated as the ratio of hyperemic to basal peak diastolic velocity (CFRpdv) or diastolic velocity-time integral (CFRdvti). In the sham-operated mice, no differences were observed between the effects of adenosine and isoflurane on CFR, left ventricular systolic function (left ventricular ejection fraction and fractional shortening), left ventricular end-systolic pressure, maximal contraction and relaxation velocity (+dp/dt and -dp/dt), alteration of left ventricular pressure (ΔLVP), or ±dp/dt (Δdp/dt). But adenosine-derived results were significantly higher than isoflurane-derived ones in both the TAC and the AR groups. Moreover, CFRpdv or CFRdvti was positively correlated with both LVEF and LVFS. Compared with adenosine-derived CFR, isoflurane-derived CFR may be underestimated in the TAC and the AR mice, which is probably associated with suppressed cardiac function.
“…At the same time, cardiac function was significantly suppressed during 2.5% isoflurane inhalation compared with during 1% isoflurane inhalation or adenosine infusion in those mice, especially in the AR mice. We also found that CFR was closely related to cardiac function, which was in accord with previous studies in humans (20) and mice (10). All of the evidence suggests that high-concentration isoflurane-induced cardiac dysfunction may lead to underestimation of CFR.…”
Section: Discussionsupporting
confidence: 91%
“…Nevertheless, CFR is closely related with cardiac function (10,20). Given that isoflurane can depress cardiac function through myofilament desensitization (5), the findings in mice without significant cardiac overloading could not be simply extrapolated to mice with loading changes (e.g., pressure or volume overload) or cardiac remodeling (concentric or eccentric hypertrophy).…”
Adenosine and high-concentration isoflurane are commonly used to induce hyperemia for assessment of coronary flow reserve (CFR) in mice, but high-concentration isoflurane may exacerbate cardiac dysfunction, leading to impaired CFR. However, there is no study be found comparing the effects of adenosine and isoflurane on CFR and corresponding cardiac function. High-resolution echocardiography and invasive hemodynamic assessment were performed in 20 mice 2 wk after transverse aortic constriction (TAC), aortic regurgitation (AR), and corresponding sham operation. CFR was calculated as the ratio of hyperemic to basal peak diastolic velocity (CFRpdv) or diastolic velocity-time integral (CFRdvti). In the sham-operated mice, no differences were observed between the effects of adenosine and isoflurane on CFR, left ventricular systolic function (left ventricular ejection fraction and fractional shortening), left ventricular end-systolic pressure, maximal contraction and relaxation velocity (+dp/dt and -dp/dt), alteration of left ventricular pressure (ΔLVP), or ±dp/dt (Δdp/dt). But adenosine-derived results were significantly higher than isoflurane-derived ones in both the TAC and the AR groups. Moreover, CFRpdv or CFRdvti was positively correlated with both LVEF and LVFS. Compared with adenosine-derived CFR, isoflurane-derived CFR may be underestimated in the TAC and the AR mice, which is probably associated with suppressed cardiac function.
“…Hemodynamic overload promotes myocyte stretch, the release of intracellular calcium, the activation of calcineurin and the induction of gene expression reprogramming 1. In athletes, left ventricular hypertrophy (LVH) is regarded as a physiological response that results from a hemodynamic overload; this physiological response does not result in the harmful effects of hypertension development or other heart diseases 10–12. The literature explains physiological LVH as the result of a volume and pressure overload that results from intense physical training (the hemodynamic stimulus), which is not necessarily accompanied by neural and humoral changes 13…”
OBJECTIVES:There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature.METHODS:The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy.RESULTS:The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective β1 receptor antagonist) with respect to LVH regression.CONCLUSION:The anti-hypertensive drugs induced various degrees of hypertrophic regression.
“…1 Endothelial dysfunction is an important, early and reversible feature of atherogenesis. 6 Noninvasive transthoracic ultrasound imaging of coronary blood flow is increasingly being used to identify derangements of coronary microcirculation at the level of coronary flow in the absence of epicardial coronary stenosis. 4,5 Impairment of endothelium-dependent coronary vasodilatation capacity is one of the mechanisms responsible for inadequate myocardial flow early in hypertensive patients before the development of morphological alterations.…”
Offspring of hypertensive parents have coronary endothelial dysfunction that appears in response to physiological stimuli (CPT). The coronary endothelial dysfunction is associated with latent LV diastolic dysfunction.
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