CHRONIC CORONARY OCCLUSION, EXERCISE TRAINING, AND PLASMA LIPIDS IN MINIATURE SWINE

2001 ◽  
Vol 33 (5) ◽  
pp. S214
Author(s):  
K Wooten ◽  
S E. Martin ◽  
J L. Parker ◽  
M Mattox ◽  
J Fogarty ◽  
...  
2000 ◽  
Vol 278 (6) ◽  
pp. H1984-H1992 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Julie A. Rapps ◽  
M. Harold Laughlin ◽  
Janet L. Parker

We previously reported that canine collateral-dependent coronary arteries exhibit impaired relaxation to adenosine but not sodium nitroprusside. In contrast, exercise training enhances adenosine sensitivity of normal porcine coronary arteries. These results stimulated the hypothesis that chronic coronary occlusion and exercise training produce differential effects on cAMP- versus cGMP-mediated relaxation. To test this hypothesis, Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCx) of female Yucatan miniature swine 8 wk before initiating sedentary or exercise training (treadmill run, 16 wk) protocols. Relaxation to the cAMP-dependent vasodilators adenosine (10− 7 to 10− 3 M) and isoproterenol (3 × 10− 8 to 3 × 10− 5 M) were impaired in collateral-dependent LCx versus nonoccluded left anterior descending (LAD) arterial rings isolated from sedentary but not exercise-trained pigs. Furthermore, adenosine-mediated reductions in simultaneous tension and myoplasmic free Ca2+ were impaired in LCx versus LAD arteries isolated from sedentary but not exercise-trained pigs. In contrast, relaxation in response to the cAMP-dependent vasodilator forskolin (10− 9 to 10− 5 M) and the cGMP-dependent vasodilator sodium nitroprusside (10− 9 to 10− 4 M) was not different in LCx versus LAD arteries of sedentary or exercise-trained animals. These data suggest that chronic occlusion impairs receptor-dependent, cAMP-mediated relaxation; receptor-independent cAMP- and cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMP-mediated relaxation of collateral-dependent coronary arteries.


2006 ◽  
Vol 290 (3) ◽  
pp. H1128-H1135 ◽  
Author(s):  
Cristine L. Heaps ◽  
Mildred L. Mattox ◽  
Katherine A. Kelly ◽  
Cynthia J. Meininger ◽  
Janet L. Parker

Endurance exercise training increases basal active tone in coronary arteries and enhances myogenic tone in coronary arterioles of control animals. Paradoxically, exercise training has also been shown to augment nitric oxide production and nitric oxide-mediated relaxation in coronary arterioles. The purpose of the present study was to examine the effect of exercise training on basal active tone of arterioles (∼150 μm ID) isolated from the collateral-dependent region of hearts exposed to chronic coronary occlusion. Ameroid occluders were surgically placed around the proximal left circumflex coronary artery of miniature swine. Arterioles were isolated from both the collateral-dependent and nonoccluded myocardial regions of sedentary (pen confined) and exercise-trained (treadmill run; 14 wk) pigs. Coronary tone was studied in isolated arterioles using microvessel myographs and standard isometric techniques. Exposure to nominally Ca2+-free external solution reduced resting tension in all arterioles; decreases were most profound ( P < 0.05) in arterioles from the collateral-dependent region of exercise-trained animals. Furthermore, nitric oxide synthase (NOS) inhibition ( Nω-nitro-l-arginine methyl ester; 100 μM) unmasked markedly increased nitric oxide-sensitive tone in arterioles from the collateral-dependent region of exercise-trained swine. Blockade of K+ channels revealed significantly enhanced K+ channel contribution to basal tone in collateral-dependent arterioles of exercise-trained pigs. Protein content of endothelial NOS (eNOS) and phosphorylated eNOS (pS1179), determined by immunoblot, was elevated in arterioles from exercise-trained animals with the greatest effect in collateral-dependent vasculature. Taken together, we demonstrate the interaction of opposing exercise training-enhanced arteriolar basal active tone, nitric oxide production, and K+ channel activity in chronic coronary occlusion, potentially enhancing the capacity to regulate blood flow to collateral-dependent myocardium.


1999 ◽  
Vol 87 (5) ◽  
pp. 1948-1956 ◽  
Author(s):  
Kawanza L. Griffin ◽  
M. Harold Laughlin ◽  
Janet L. Parker

The present study evaluated combined effects of chronic coronary occlusion and exercise training on endothelial function. Gradual occlusion was produced by placement of an ameroid constrictor around the proximal left circumflex (LCX) coronary artery of female swine. Two months after placement of the ameroid, animals were restricted to their pens or exercise trained for 16 wk. Epicardial arteries (>500 μm ID) were isolated from the collateral-dependent LCX coronary artery distal to the occlusion and the nonoccluded left anterior descending (LAD) coronary artery. Bradykinin- and ADP-mediated relaxation of LCX and LAD coronary arteries was enhanced after exercise training. Inhibition of nitric oxide synthase with N G-nitro-l-arginine methyl ester decreased bradykinin- and ADP-mediated relaxation in LCX and LAD myocardial regions. Importantly, combined inhibition of effects of endothelium-derived hyperpolarizing factor with increased extracellular K+ (20–30 mM) and nitric oxide synthase completely abolished coronary LAD and LCX relaxation to bradykinin. Our data indicate that exercise training improves endothelium-mediated relaxation of arteries isolated after chronic coronary artery occlusion, likely as a result of enhanced production of nitric oxide and endothelium-derived hyperpolarizing factor.


2018 ◽  
Vol 3 (7) ◽  
pp. 60-63
Author(s):  
E. V. Aksenov ◽  
◽  
V. B. Golovenko ◽  
B. M. Gumenyuk

Author(s):  
J P Després ◽  
S Moorjani ◽  
A Tremblay ◽  
E T Poehlman ◽  
P J Lupien ◽  
...  

1997 ◽  
Vol 82 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Richard M. McAllister ◽  
M. Harold Laughlin

McAllister, Richard M., and M. Harold Laughlin.Short-term exercise training alters responses of porcine femoral and brachial arteries. J. Appl. Physiol. 82(5): 1438–1444, 1997.—The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity ( P < 0.05). Vascular rings ∼3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 ± 0.09 (−log M); Trn, 9.07 ± 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 ± 0.17 (−log M); Trn, 8.97 ± 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.


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