Biomedical subjects

Ryan P Taylor

Publications and source records attributed to Ryan P Taylor.

6 recordsLinked to original sources

PubMed2006

Improved postischemic function following acute exercise is not mediated by nitric oxide synthase in the rat heart.

The mediators of acute exercise-induced preconditioning against ischemia-reperfusion injury are not understood. This study assesses the role of nitric oxide synthase (NOS), a reported mediator of other forms of preconditioning. Male Fischer 344 rats were divided into five groups (n = 6-7): sedentary (Sed); exercised 2 days on a treadmill at 20 m/min, 6 degrees grade, for 60 min (Run); sedentary, perfused with 100 microM N(omega)-nitro-l-arginine methyl ester hydrochloride (l-NAME) to inhibit NOS (Sed/L-N); exercised, perfused with l-NAME (Run/L-N); and exercised in a 4 degrees C environment, perfused with l-NAME (CRun/L-N). Twenty-four hours following exercise, isolated, perfused working hearts were subjected to 22.5 min of global ischemia plus 30 min of normoxic reperfusion. Left ventricle contents of several putative preconditioning mediators were determined. Postischemic recovery of cardiac output times systolic pressure was better in Run than Sed (78.4 vs. 50.2% of preischemia, P < 0.05). Inhibition of NOS did not abrogate the improved recovery in the exercise groups or alter recovery in Sed. All exercise groups also displayed improved myocardial efficiency (cardiac output times systolic pressure/oxygen consumption) postischemia and less lactate dehydrogenase release (P < 0.05). l-NAME appeared to lower lactate dehydrogenase release independent of exercise. The only change in antioxidant enzyme activity was a decrease in manganese superoxide dismutase in CRun/L-N (P < 0.05). Heat shock protein 72 expression increased only in Run and Run/L-N and endothelial NOS only in CRun/L-N (P < 0.05). Acute exercise-induced preconditioning of the Fischer 344 rat heart is not mediated by NOS and does not require increases in heat shock protein 72 or antioxidant enzymes.

Animals↗

PubMed2005

Small heat shock proteins: a new classification scheme in mammals.

Small MW heat shock proteins (i.e. sHSPs approximately 15-30 kDa) share significant sequence similarity within the "alpha-crystallin domain" but exhibit different patterns of gene expression, transcriptional regulation, sub-cellular localization, and, perhaps, function. The chaperone-like properties of many sHSPs are defined biochemically by their ability to prevent protein aggregation and/or restore biological activity of client substrates in vitro. Furthermore, such functions are widely believed to mitigate protein misfolding and denaturation triggered by noxious environmental stimuli such as hyperthermia stress, decreased pH(i), osmotic stress, heavy metals, hypoxia, and ischemic injury in vivo. At least 10 mammalian sHSPs, several with tissue-restricted expression, have been identified in recent genome surveys of mice, rats, and humans, but their functions have remained poorly understood. Here, we propose a simple classification scheme for sHSPs to reflect emerging evidence that their specialized roles (e.g. apoptosis, protein trafficking, redox control, and cytoskeletal interactions) might be inextricable linked to both coordinate regulation and multimeric protein complexes in a lineage-specific manner. Thus, Class I proteins display ubiquitous expression, whereas the tissue distribution of Class II proteins is primarily restricted to myogenic and testicular lineages. Because the expression patterns and modifications of sHSPs are potentially surrogate biosignatures for underlying pathophysiological events, we propose that this classification should accelerate progress to define the functional diversification for sHSPs especially in selective tissues predisposed to inheritable, degenerative, and other acquired diseases in humans.

Amino Acid Sequence↗

PubMed2005

Myocardial heat shock protein 70 expression in young and old rats after identical exercise programs.

Synthesis of inducible heat shock protein 70 (HSP70) is impaired in aged animals following acute stresses including exercise. In this study we determined whether aging affects expression of this cytoprotective protein following chronic exercise participation. Male Fischer 344 rats, final ages 6 and 24 months, exercised identically for 10 weeks on a treadmill (15 degrees incline, 15 m/min for up to 60 minutes, 5 days/week). In 6-month-old animals, exercise increased HSP70 in heart (44%), liver (216%), and skeletal muscle (126%) (p <.05 vs sedentary). In 24-month-old animals, exercise increased HSP70 in muscle (69%), but not in heart or liver. In heart, antioxidant enzyme activities and HSP70 messenger RNA were measured and found to be unaffected by exercise at both ages. Our results indicate an age-related decrease in HSP70 production in heart and liver following chronic exercise. Furthermore, the aged heart does not increase its antioxidant enzyme defenses to compensate for the HSP70 deficit.

Aging↗

PubMed2005

Habitual low-intensity exercise does not protect against myocardial dysfunction after ischemia in rats.

BACKGROUND: It is well established that participation in a chronic exercise program can reduce coronary heart disease (CHD) risk factors and improve myocardial tolerance to ischemia-reperfusion (I-R) injury. Low-intensity exercise programs are known to be effective in reducing CHD risk factors in humans and rats, but whether similar programs are of sufficient intensity to improve intrinsic tolerance to I-R injury has not been established. Thus, the purpose of this study is to determine whether low-intensity exercise provides self-protection to the heart against I-R injury. METHODS: Male, Sprague-Dawley rats were exercised on a treadmill at an intensity of 55-60% VO2max, 40 min/day, 5 days/week for 16 weeks. Reperfusion injury following 20 min of global ischemia was evaluated using the isolated perfused working heart model. Left ventricular content of the cytoprotective protein heat shock protein 70 (HSP70) was determined by Western blotting. RESULTS: The exercise program elevated HSP70 2.7-fold, but did not provide enhanced protection following 20 min of ischemia. Final post-ischemic recovery of cardiac external work was 63+/-9% of pre-ischemic value in the sedentary group (n=9) and 51+/-11% in the exercising group (n=9) (P>0.05). Post-ischemic lactate dehydrogenase release was also similar between groups and the magnitude of release was low, consistent with stunning. CONCLUSIONS: Regular exercise at 55-60% VO2max is below the threshold intensity necessary to induce intrinsic cardioprotection against I-R injury. Furthermore, elevated myocardial HSP70 is not necessarily a marker of improved protection against dysfunction associated with stunning.

Animals↗

PubMed2003

Effect of exercise training on the ability of the rat heart to tolerate hydrogen peroxide.

OBJECTIVE: The purpose of this study was to determine whether exercise training could precondition the myocardium against hydrogen peroxide (H(2)O(2))-induced damage. METHODS: Male Fischer 344 rats ran on a treadmill for 9 weeks (60 min/day, 22 m/min, 6 degrees grade, 5 days/week). Isolated perfused working hearts from exercise trained (ET, n=8) and sedentary (SED, n=10) animals were perfused with 150 microM H(2)O(2). RESULTS: Pre-H(2)O(2) baseline values for cardiac external work (COxSP), coronary flow (CF), and lactate dehydrogenase (LDH) release were similar between groups. At 5 min of H(2)O(2), COxSP was unchanged from baseline but CF was increased 30% in SED and 46% in ET (P<0.05 vs. SED). COxSP began to decline similarly thereafter in both groups, dropping to 20% of baseline at 20 min. CF in ET remained higher than SED throughout (P<0.05). LDH leakage remained near baseline during the first 15 min of H(2)O(2) exposure, but was elevated (P<0.05) 72% in SED and 40% in ET after 20 min, and was 2.2-fold greater in SED than ET (P<0.05) after 25 min. Heat shock protein 70 was 2.1-fold greater in ET than SED (P<0.05), but ET did not change catalase and glutathione peroxidase. CONCLUSIONS: The results of this study indicate that chronic moderate exercise will enhance coronary flow and attenuate the development of myocardial injury when exposed to H(2)O(2), but will not affect H(2)O(2)-induced decrease in pump function.

Animals↗

PubMed2003

Exercise improves postischemic function in aging hearts.

Exercise improves cardioprotection against ischemia-reperfusion in young animals but has not been investigated in older animals, which represent the population most likely to suffer an ischemic event. Therefore, we sought to determine the effects of aging on exercise-induced cardioprotection. Young, middle-aged, and old (4, 12, and 21 mo old) male Fischer 344 rats ran 60 min at 70-75% of maximum oxygen consumption. Twenty-four hours postexercise, isolated perfused working hearts underwent 22.5 min of global ischemia and then 30 min of recovery (reperfusion). Compared with sedentary rats (n = 8-9 rats/group), recovery of function (cardiac output x systolic pressure) improved after exercise (n = 9 rats/group) by 40% at 4 mo, 78% at 12 mo, and 59% at 21 mo. Exercise increased inducible heat shock protein 70 expression 105% at 4 mo but only 27% at 12 mo and 24% at 21 mo. Catalase activity progressively increased with age (P < 0.05) and was increased by exercise at 4 mo (26%) and 21 mo (19%). Manganese superoxide dismutase activity was increased by exercise only at 21 mo (45%). No exercise-related change in any antioxidant enzyme was observed at 12 mo. We conclude that exercise can enhance cardioprotection regardless of age, but the cardioprotective protein phenotype changes with age.

Aging↗