97 research outputs found
Effects of isoproterenol on adrenergic constriction in vascular smooth muscle
No full text A series of isolated segments of carotid arteries from Dutch-belted, adult, male rabbits were studied with respect to their response to a beta receptor agonist. Segments of 3-cm length were mounted in a chamber with constant surrounding temperature and pressure and perfused at constant pressure. Inflow pressure, outflow pressure, and flow rate were measured, and values of resistance (R) were calculated. Subsequent to control R, each vessel was exposed to a vasoconstricting concentration of either norepinephrine (NE: 10(-8), 10(-9), 10(-10) M) or potassium (K+: 100mM, 50 mM) followed by three doses of the beta-adrenergic agonist, isoproterenol (IP: 10(-7), 10(-6), 10(-5)M) administered simultaneously with each constrictor. R was not altered by IP during NE infusion but was significantly increased at all levels of IP during both K+ infusions. When the K+ series was repeated with alpha blockade, IP did not alter R. Thus, beta receptors do not appear to be functionally present in the adult rabbit carotid artery. </jats:p
Sprint training attenuates myocyte hypertrophy and improves Ca<sup>2+</sup>homeostasis in postinfarction myocytes
No full textZhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung. Sprint training attenuates myocyte hypertrophy and improves Ca2+homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544–552, 1998.—Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+exchange currents ( INa/Ca; 3 Na+out:1 Ca2+in) and sarcoplasmic reticulum (SR)-releasable Ca2+contents. These defects in Ca2+regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively; P ≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively; P ≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P ≤ 0.015). Reverse INa/Cawas significantly lower ( P ≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse INa/Ca( P ≤ 0.05) without affecting the amount of Na+/Ca2+exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+content, as estimated by integrating forward INa/Caduring caffeine-induced SR Ca2+release, was also significantly increased ( P ≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.</jats:p
Reciprocal changes in vasoactive hormones in the rat myocardial infarction model of heart failure.
No full textThe purpose of this study was to determine (1) if there is a relationship between the changes in the plasma levels of atrial natriuretic peptide (ANP) and plasma renin activity (PRA) as rats compensated from 3 days to 6 weeks after coronary ligation and (2) if these changes are related to myocardial infarction (MI) size. Arterial blood was drawn twice from 34 conscious rats (control, n = 10; small MI, n = 10; large MI, n = 14). Histologic MI size correlated better with ANP 3 days (r = .72, P < .001) than with ANP 6 weeks after MI (r = .39, P = .021). The reverse was true for an electrocardiographic index of MI size that used the sum of the Q waves minus the sum of the R waves in leads I, aVL, and V5. Atrial natriuretic peptide at 3 days was increased in both MI groups and was highest in the large MI group (control, 25.6; small MI, 41.0; large MI, 58.6 pM). Atrial natriuretic peptide decreased significantly from 3 days to 6 weeks in the large MI group and normalized in the small MI group (control, 25.0; small MI, 26.4; large MI, 44.4 pM). Plasma renin activity was not elevated at either time. However, the change in ANP from 3 days to 6 weeks in the MI rats was negatively related to the change in PRA (r = .48, P = .016). Atrial natriuretic peptide levels early after MI may be a good predictor of infarct size. The pattern of ANP and PRA changing in opposite directions over time suggest a counterregulatory link between these two systems
Toward zero-excess lithium sulfur batteries: a systematic cell parameter study
No full textZero-excess lithium (ZEL) or 'anode-free' batteries aim to minimize negative electrode material and address the challenges associated with handling thin lithium metal foils during fabrication. To date, most studies in the field of ZEL cells have primarily focused on lithium-ion chemistry, with considerably fewer systematic investigations into ZEL-sulfur (ZELiS) cell fabrication and optimization. Here we develop a ZELiS battery, comprising a Li2S-based composite positive electrode on carbon paper paired with a Ni foil current collector (CC) and evaluate the effects of various CC materials, electrolyte volume to Li2S mass ratio and C-rate. The developed cells reproducibly achieve an average Coulombic efficiency of 99% from cycles 2 to 200, and a final capacity of 272 mAh g−1Li2S at a C/10 rate. Furthermore, we employ x-ray computed tomography to elucidate the morphological changes and degradation processes occurring within the positive electrode composite, revealing the irreversible loss of Li2S/S8 during cycling, which is exacerbated at high rates. These results should be useful in the development of commercially viable ZEL energy storage devices
Muscle acidosis during static exercise is associated with calf vasoconstriction
No full text In this study we measured (n = 6) the phosphocreatine-to-inorganic phosphate ratio (PCr/Pi), Pi, and pH with 31P-nuclear magnetic resonance (31P-NMR) in the human forearm during static work at 30% of maximal voluntary contraction (MVC) for 2 min followed immediately by 3 min of circulatory arrest (forearm arterial occlusion). Static exercise, with its central volitional and skeletal muscle metabolic and mechanical afferent components, caused a rise in heart rate (HR, 32%), blood pressure (BP, 29%), and calf vascular resistance (calf R, 30%). During forearm occlusion after static exercise, HR returned to base line, the increase in BP was attenuated by 30%, and calf R remained elevated and unchanged. The percent change in calf R was correlated with forearm cellular pH (R = 0.56, P less than 0.001) but only weakly associated with PCr/Pi (R = 0.33, P less than 0.042). 30% MVC for 1 min followed by arterial occlusion (3 min) reduced PCr/Pi by 65% and pH by 0.16 U (P less than 0.05). Calf R was unchanged. Circulatory arrest alone (20 min) caused no change in either pH or calf R but large changes in PCr/Pi (50% reduction). We conclude that 1) there is an association between forearm cellular acidosis and calf vasconstriction during static forearm exercise and 2) large changes in PCr/Pi without concomitant changes in pH are not associated with changes in calf R. </jats:p
Abnormalities in systemic norepinephrine kinetics in human congestive heart failure
No full text A high venous plasma norepinephrine (NE) level is a predictor of poor prognosis in congestive heart failure (CHF). To evaluate the mechanisms responsible for the high plasma NE in CHF, NE kinetics were studied in 19 patients with CHF and 18 normal subjects during a 90-min steady-state intravenous infusion of tracer [3H]NE of high specific activity. Venous plasma NE between 70 and 90 min of infusion was significantly higher in the CHF patients (CHF, 634, and normal, 247 pg/ml; P less than 0.001). The following equations were used: NE clearance = [3H]NE infusion rate (dpm/min)/plasma [3H]NE (dpm/l), and NE spillover = [3H]NE infusion rate (dpm/min)/[3H]NE specific activity (dpm/nmol). In CHF, a decreased clearance and an increased spillover contributed nearly equally to the high plasma NE (NE clearance: CHF, 0.99; normal, 1.48 l.min-1.m-2; P less than 0.001; NE spillover: CHF, 3.60; normal, 2.08 nmol.min-1.m-2; P less than 0.001). These data document that both NE clearance and NE spillover are abnormal in CHF, and they raise the new possibility that the factors responsible for the reduced NE clearance could be related to the factors linking a high plasma NE with early mortality. </jats:p
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