Microvascular and myocardial contractile responses to ischemia: influence of exercise training

Abstract

We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.

Nandrolone decanoate impairs exercise-induced cardioprotection: Role of antioxidant enzymes

“…Myocardial ischemia occurs when the requirement for oxygen exceeds the supply and may arise in a diversity of conditions such as physical exertion, coronary artery disease, reduction in blood pressure and coronary bypass surgery [38,39]. Depending on the intensity and duration of myocardial ischemia, ventricular contractile dysfunction may result [2,4,5,[8][9][10].…”

Hyperhomocysteinemia Evoked by Folate Depletion

“…Third-order branches of this artery were isolated, removed, and mounted on a wire-type myograph using methods we have described. 23,24 After a 30-minute equilibration period, a series of internal circumference-active tension curves was constructed to determine the vessel diameter that evoked the greatest tension development (L MAX ) to 100 mmol/L KCl. 23,24 L MAX was determined for every vessel, and this optimal resting tension was maintained throughout the study.…”

“…Tension data were recorded and processed continuously by a computer through an analog-to-digital interface card (Biopac Systems Inc) that allowed for subsequent off-line quantitative analyses. 23,24 NPSS contained (in mmol/L) NaCl 125, KCl 4.7, KH 2 PO 4 1.2, MgSO 4 1.2, CaCl 2 2.5, NaHCO 3 18, Na 2 EDTA 0.026, and glucose 11.2. Acetylcholine, sodium nitroprusside, L-NMMA (Sigma Chemical), and serotonin (Peninsula Laboratories) were purchased commercially and prepared daily from stock solutions with distilled deionized water.…”

“…In this regard, EDHF has been shown to contribute to acetylcholine-evoked relaxation in canine coronary microvessels 43 and rat mesenteric arteries. 44 We tried several alternate endothelium-dependent vasorelaxing substances and precontracting agents in preliminary studies 23,24 but there was a lack of reproducibility and unstable tension development, respectively, rendering them unacceptable. In any case, we refer to our assessment of endothelial function as acetylcholine-evoked vasorelaxation and believe that nitric oxide release evoked by muscarinic receptor stimulation is largely responsible for the observed vasorelaxation.…”

Exercise training improves functional post-ischemic recovery in senescent heart

“…This result has particular relevance because endothelium dysfunction appears to be an important early and integral manifestation of coronary artery disease and is responsible, at least in part, for many of the cardiovascular complications associated with aging (Valgimigli et al, 2003). However, the beneficial effects of endurance training on coronary flow could also result from a decrease in responsiveness to vasoconstrictive stimuli such as endothelin (Besse et al, 2001;Symons et al, 2000) and/or a coronary vascular remodeling such as angiogenesis (Brown, 2003;Linke et al, 2006;Iemitsu et al, 2006;Marini et al, 2008;Leosco et al, 2008). Moreover, increased eNOS myocardial content by endurance training could also improves the postischemic contractile function by cardiomyocyte-specific mechanisms (Jugdutt, 2002;Razavi et al, 2005 ;Elrod et al, 2006).…”