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William Rouslin - One of the best experts on this subject based on the ideXlab platform.
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atpase activity if1 content and proton conductivity of esmp from control and ischemic slow and Fast Heart Rate Hearts
Journal of Bioenergetics and Biomembranes, 1995Co-Authors: William Rouslin, Charles W Broge, F Guerrieri, G CapozzaAbstract:Earlier studies by Rouslin and coworkers showed that, during myocardial ischemia in slow Heart-Rate species which include rabbits and all larger mammals examined including humans, there is an IF1-mediated inhibition of the mitochondrial ATPase due to an increase in the amount of IF1, bound to the ATPase (Rouslin, W., and Pullman, M.E.,J. Mol. Cell. Cardiol.19, 661–668, 1987). Earlier work by Guerrieri and colleagues demonstRated that IF1 binding to bovine Heart ESMP was accompanied by parallel decreases in ATPase activity and in passive proton conduction (Guerrieri, F.,et al., FEBS Lett.213, 67–72, 1987). In the present study rabbit was used as the slow Heart-Rate species and rat as the Fast Heart-Rate species. Rat is a Fast Heart-Rate species that contains too little IF1 to down regulate the ATPase activity present. Mitochondria were prepared from control and ischemic Hearts and ESMP were made from aliquots by sonication at pH 8.0 with 2 mM EDTA. Oligomycin-sensitive ATPase activity and IF1 content were measured in SMP prepared from the control and ischemic mitochondrial samples. After identical incubation procedures, oligomycin-sensitive ATPase activity, oligomycin-sensitive proton conductivity, and IF1 content were also measured in ESMP samples. The study was undertaken to corroboRate further what appear to be fundamental differences in ATPase regulation between slow and Fast Heart-Rate mammalian Hearts evident during total myocardial ischemia. Thus, passive proton conductivity was used as an independent measure of these regulatory differences. The results show that, consistent with the low IF1 content of rat Heart cardiac muscle mitochondria, control rat Heart ESMP exhibit approximately twice as much passive proton conductivity as control rabbit Heart ESMP regardless of the pH of the incubation and assay. Moreover, while total ischemia caused an increase in IF1 binding and a commensuRate decrease in passive proton conductivity in rabbit Heart ESMP regardless of pH, neither IF1 content nor proton conductivity changed significantly in rat Heart ESMP as a result of ischemia.
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content and binding characteristics of the mitochondrial atpase inhibitor if1 in the tissues of several slow and Fast Heart Rate homeothermic species and in two poikilotherms
Journal of Bioenergetics and Biomembranes, 1995Co-Authors: William Rouslin, Gerald D Frank, Charles W BrogeAbstract:We determined the IF1 contents of pig, rabbit, rat, mouse, guinea pig, pigeon, turtle, and frog Heart mitochondria and the effects of varying ionic strength upon the IF1-mediated inhibition of the ATPase activity of IF1-depleted rabbit Heart mitochondrial particles (RHMP) by IF1-containing extracts from these same eight species. The IF1 binding experiments were run at both species-endogenous IF1 levels and at an IF1 level normalized to that present in rabbit Heart mitochondria. When species-endogenous levels of rabbit Heart IF1 or either speciesendogenous or normalized levels of pig Heart IF1 were incubated with RHMP over a range of KCl concentrations, increasing the [KCl] to 150 mM had relatively little effect on IF1-mediated ATPase inhibition. When either species-endogenous or normalized levels of guinea pig, pigeon, turtle, or frog Heart IF1 were incubated with RHMP under the same conditions, increasing [KCl] to 150 mM nearly completely blocked IF1-mediated ATPase inhibition. While species-endogenous levels of rat and mouse Heart IF1 inhibited the ATPase activity of RHMP virtually not at all at any [KCl] examined, normalized levels of rat and mouse IF1 inhibited the ATPase activity of RHMP to the same extents as species-endogenous levels of pig and rabbit Heart IF1, respectively, in the presence of increasing [KCl]. These experiments suggest that, while pig and rabbit Heart mitochondria contain a full complement of higher-affinity IF1, pigeon, guinea pig, turtle, and frog Heart mitochondria cell contain essentially a full complement of a lower-affinity form of IF1. In contrast, rat and mouse Heart mitochondria contain only low levels of IF1 which exhibit binding characteristics similar to those of the pig and rabbit Heart inhibitor. The guinea pig is the only mammal thus far examined that contains a loweraffinity form of IF1. In the present study we also determined the IF1 contents and IF1-to-F1 ATPase activity ratios of cardiac muscle, skeletal muscle, liver, and brain mitochondria of rabbit, pigeon, and rat, species representative of the three homeothermic regulatory classes.
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mechanisms of atp conservation during ischemia in slow and Fast Heart Rate Hearts
American Journal of Physiology-cell Physiology, 1993Co-Authors: William Rouslin, C W BrogeAbstract:In the present study we compared the quantitatively most important, Pi-activated mechanisms for conserving ATP during ischemia in dog and rat cardiac muscle. Earlier studies by ourselves showed tha...
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atp depletion and mitochondrial functional loss during ischemia in slow and Fast Heart Rate Hearts
American Journal of Physiology-heart and Circulatory Physiology, 1990Co-Authors: William Rouslin, C W Broge, I L GruppAbstract:In the present study, isolated dog and rat Hearts were perfused in the Langendorff mode with Krebs bicarbonate buffer in the absence and presence of 10(-5) M oligomycin. The perfusion protocols emp...
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regulation of the mitochondrial adenosine 5 triphosphatase in situ during ischemia and in vitro in intact and sonicated mitochondria from slow and Fast Heart Rate Hearts
Archives of Biochemistry and Biophysics, 1990Co-Authors: William Rouslin, Charles W BrogeAbstract:Abstract In the present study we examined the regulation of the cardiac muscle mitochondrial ATPase both in situ and in vitro in intact and sonicated mitochondria from rabbit, pigeon, and rat. We chose to study these three species because each is representative of one of the three classes into which all species thus far studied may be placed with respect to the in situ activity of their cardiac muscle mitochondrial ATPase inhibitor and with respect to the amount of ATPase inhibitor present in their cardiac muscle mitochondria (1). Class A species (rabbit) contain a full complement of ATPase inhibitor and show a marked ATPase inhibition during ischemia. Class B species (pigeon) also contain a full complement of inhibitor but exhibit only a low level of ATPase inhibition in situ . Class C species (rat) contain only low levels of inhibitor and, like class B species, don't appear to utilize the inhibitor they possess during ischemia in situ . We found that, while Hearts from all three species developed a marked cytosolic acidosis during ischemia, only rabbit exhibited a marked ATPase inhibition in situ . In in vitro experiments in which matrix pH values close to 6.2 and ΔΨ values close to zero were measured in intact mitochondria from all three species, matrix pH appeared to be an important factor regulating ATPase inhibition in rabbit, but it had little effect upon ATPase-inhibitor interaction in pigeon and rat despite the lack of membrane potential. However, a pH-dependent further release of ATPase inhibitor was observed in sonicated pigeon Heart mitochondria only. This latter observation suggests that, while slow Heart-Rate Heart mitochondria appear to be designed for ATPase down regulation during ischemia by inhibitor binding to the ATPase, Fast Heart-Rate Heart mitochondria appear to be designed primarily for ATPase up regulation by a further release of inhibitor from the enzyme.
Paolo Palatini - One of the best experts on this subject based on the ideXlab platform.
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Importance of Heart Rate in Determining Cardiovascular Risk
Blood Pressure Monitoring in Cardiovascular Medicine and Therapeutics, 2020Co-Authors: Paolo PalatiniAbstract:A body of evidence indicates that subjects with tachycardia are more likely to develop hypertension (1–3) and atherosclerosis in future years (4–6). However, the connection between Heart Rate and the cardiovascular risk has long been neglected, on the grounds that tachycardia is often associated with the traditional risk factors for atherosclerosis, such as hypertension or metabolic abnormalities (7). A high Heart Rate is currently considered only an epiphenomenon of a complex clinical condition rather than an independent risk factor. However, most epidemiogic studies showed that the predictive power of a Fast Heart Rate for cardiovascular disease remains significant even when its relative risk is adjusted for all major risk factors for atherosclerosis and other confounders (4–7). In this chapter, the results of the main studies that dealt with the relation between tachycardia and cardiovascular morbidity and mortality will be summarized, and the pathogenesis of the connection between Fast Heart Rate and cardiovascular disease will be the focus.
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Arterial Distensibility, Physical Activity, and the Metabolic Syndrome.
Current Hypertension Reports, 2018Co-Authors: Francesca Saladini, Paolo PalatiniAbstract:Purpose of Review Metabolic syndrome (MetS), a cluster of risk factors including central obesity, metabolic abnormalities, and arterial hypertension, is a well-known determinant of arterial wall remodeling and stiffening. The mechanisms whereby MetS promotes arterial stiffening include increased sympathetic activity with the associated Fast Heart Rate, enhanced activity of the renin-angiotensin-aldosterone system, increased production of inflammatory cytokines and reactive oxygen species, and reduction of nitric oxide availability. These adverse effects can explain why aerobic physical activity can retard the age-related decline in arterial elasticity in subjects with MetS.
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Impact of Increased Heart Rate on Clinical Outcomes in Hypertension
Drugs, 2006Co-Authors: Paolo Palatini, Athanase Benetos, Stevo JuliusAbstract:Thirty-eight studies have been published to date on the association between elevated Heart Rate and mortality. After adjustment for other risk factors, only two studies for all-cause mortality and four studies for cardiovascular mortality reported an absence of association between Heart Rate and mortality in male populations. This relationship has been found to be generally weaker among females. Most of these studies investigated samples of general populations. The four studies performed in hypertensive men found a positive association between Heart Rate and all-cause mortality (hazard ratios ranging from 1.9 to 2.0) or cardiovascular mortality (hazard ratios ranging from 1.3 to 1.7). In spite of this evidence, elevated Heart Rate remains a neglected cardiovascular risk factor in both genders. The pathogenetic mechanisms connecting high Heart Rate, hypertension, atherosclerosis and cardiovascular events have also been explicated in many studies. Elevated Heart Rate is due to an increased sympathetic and decreased parasympathetic tone. This altered balance of the autonomic nervous system tone could explain the increase in events with the increased Heart Rate. However, it has also been proved that blood flow changes associated with high Heart Rate favour both the formation of the atherosclerotic lesion and the occurrence of the cardiovascular event. Reduction of Heart Rate in hypertensive patients with increased Heart Rate could be an additional goal of antihypertensive therapy. Several trials retrospectively showed the beneficial effect of cardiac-slowing drugs, such as β-adrenoceptor antagonists (β-blockers) and non-dihydropyridine calcium channel antagonists, on mortality, notably in patients with coronary Heart disease, but no published data are available in patients with hypertension free of coronary Heart disease. Other antihypertensive drugs that have been shown to reduce the Heart Rate are centrally acting drugs and angiotensin II receptor antagonists, but their bradycardic effect is rather weak. The f-channel antagonist ivabradine is a selective Heart Rate-lowering agent with no effect on blood pressure. Although it has not been proven in existing trials, it would seem reasonable to recommend antihypertensive agents that decrease the Heart Rate in hypertensive patients with a Heart Rate higher than 80–85 beats per minute. Since the Fast Heart Rate per se causes cardiovascular damage, all drugs that lower the Heart Rate have the potential of further reducing cardiovascular events in patients with elevated Heart Rate. Unfortunately, lowering of the Heart Rate is not a clinically recognised goal. Prospective trials investigating whether treatment of high Heart Rate can prevent cardiovascular events, notably in hypertensive patients, are warranted.
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Elevated Heart Rate: a major risk factor for cardiovascular disease.
Clinical and Experimental Hypertension, 2004Co-Authors: Paolo Palatini, Stevo JuliusAbstract:Mounting evidence shows that elevated Heart Rate is associated with a greater risk of developing hypertension and atherosclerosis and that it is a potent predictor of cardiovascular morbidity and mortality. These relationships have been shown not only in general populations but also among hypertensive individuals, with important implications for the treatment of hypertension. In spite of this evidence Heart Rate has been overlooked as a risk factor, but the fact that in most studies the risk related to Fast Heart Rate remained highly significant after controlling for major risk factors for atherosclerosis suggests that it plays a direct role in the induction of the risk. The clustering of several risk factors for coronary artery disease in subjects with Fast Heart Rate suggests that sympathetic overactivity accounts for the increased cardiovascular morbidity in subjects with tachycardia. In fact, experimental studies have shown that a heightened sympathetic tone can cause obesity, hyperinsulinemia, and insulin resistance which in the long run can promote the development of atherosclerosis. Moreover, experimental studies in the animal suggest that the heamodynamic disturbances related to high Heart Rate have a direct impact on the arterial wall promoting the development of atherosclerotic plaques. Preliminary results in the experimental animal and pooled data from intervention studies in patients with myocardial infarction or congestive Heart failure suggest that drug-induced reduction of Heart Rate may be beneficial in several clinical conditions.
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Heart Rate as a Risk Factor for Atherosclerosis and Cardiovascular Mortality
Drugs, 1999Co-Authors: Paolo PalatiniAbstract:The aim of this review is to highlight the importance of Heart Rate (HR) as a risk factor for cardiovascular disease, and to discuss the classes of drugs which can be potentially useful in clinical conditions in which an elevated HR may be present. Numerous studies have shown that high resting HR is prospectively related to the development of atherosclerosis and of cardiovascular events. This relationship was independent of other major risk factors for atherosclerosis and was observed in the general population, in elderly people, in hypertensive cohorts and in patients with myocardial infarction or Heart failure. The clustering of several risk factors in individuals with Fast Heart Rate may explain why cardiovascular morbidity is higher in individuals with tachycardia. Sympathetic overactivity seems to be responsible for both the increase in HR, blood pressure and the metabolic abnormalities. Experimental studies in monkeys have shown that HR can also exert a direct atherogenetic action on the arteries through increased wall stress. Moreover, tachycardia can favour the occurrence of ventricular arrhythmias and sudden death. Reduction of HR appears as an additional goal of antihypertensive therapy. If Fast HR in hypertension is a marker of increased sympathetic tone, agents which decrease HR through a decline of sympathetic outflow should be particularly efficacious. β-Blockers retard the development of coronary atherosclerosis in cholesterol-fed monkeys and have proven to be beneficial in patients with myocardial infarction or with Heart failure, but their efficacy appear limited in hypertension, probably on account of their unfavourable metabolic profile. Phenylalkylamines are devoid of this untoward effect, and seem to act also through inhibition of sympathetic discharge from the CNS. Mibefradil, a more recent calcium antagonist that selectively blocks voltage-dependent T-type calcium channels decreases HR without affecting left ventricular contractility. New drugs with agonistic properties at the I_1-imidazoline receptors of the rostral ventrolateral medulla are effective in reducing blood pressure and HR by inhibiting the sympathetic outflow and improved metabolic parameters in obese or fructose-fed rats. The goal of antihypertensive therapy in the future will be to prevent or reverse those functional abnormalities which accompany the hypertensive condition. In patients with tachycardia the reduction of HR appears a desirable additional goal of therapy.
Charles W Broge - One of the best experts on this subject based on the ideXlab platform.
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atpase activity if1 content and proton conductivity of esmp from control and ischemic slow and Fast Heart Rate Hearts
Journal of Bioenergetics and Biomembranes, 1995Co-Authors: William Rouslin, Charles W Broge, F Guerrieri, G CapozzaAbstract:Earlier studies by Rouslin and coworkers showed that, during myocardial ischemia in slow Heart-Rate species which include rabbits and all larger mammals examined including humans, there is an IF1-mediated inhibition of the mitochondrial ATPase due to an increase in the amount of IF1, bound to the ATPase (Rouslin, W., and Pullman, M.E.,J. Mol. Cell. Cardiol.19, 661–668, 1987). Earlier work by Guerrieri and colleagues demonstRated that IF1 binding to bovine Heart ESMP was accompanied by parallel decreases in ATPase activity and in passive proton conduction (Guerrieri, F.,et al., FEBS Lett.213, 67–72, 1987). In the present study rabbit was used as the slow Heart-Rate species and rat as the Fast Heart-Rate species. Rat is a Fast Heart-Rate species that contains too little IF1 to down regulate the ATPase activity present. Mitochondria were prepared from control and ischemic Hearts and ESMP were made from aliquots by sonication at pH 8.0 with 2 mM EDTA. Oligomycin-sensitive ATPase activity and IF1 content were measured in SMP prepared from the control and ischemic mitochondrial samples. After identical incubation procedures, oligomycin-sensitive ATPase activity, oligomycin-sensitive proton conductivity, and IF1 content were also measured in ESMP samples. The study was undertaken to corroboRate further what appear to be fundamental differences in ATPase regulation between slow and Fast Heart-Rate mammalian Hearts evident during total myocardial ischemia. Thus, passive proton conductivity was used as an independent measure of these regulatory differences. The results show that, consistent with the low IF1 content of rat Heart cardiac muscle mitochondria, control rat Heart ESMP exhibit approximately twice as much passive proton conductivity as control rabbit Heart ESMP regardless of the pH of the incubation and assay. Moreover, while total ischemia caused an increase in IF1 binding and a commensuRate decrease in passive proton conductivity in rabbit Heart ESMP regardless of pH, neither IF1 content nor proton conductivity changed significantly in rat Heart ESMP as a result of ischemia.
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content and binding characteristics of the mitochondrial atpase inhibitor if1 in the tissues of several slow and Fast Heart Rate homeothermic species and in two poikilotherms
Journal of Bioenergetics and Biomembranes, 1995Co-Authors: William Rouslin, Gerald D Frank, Charles W BrogeAbstract:We determined the IF1 contents of pig, rabbit, rat, mouse, guinea pig, pigeon, turtle, and frog Heart mitochondria and the effects of varying ionic strength upon the IF1-mediated inhibition of the ATPase activity of IF1-depleted rabbit Heart mitochondrial particles (RHMP) by IF1-containing extracts from these same eight species. The IF1 binding experiments were run at both species-endogenous IF1 levels and at an IF1 level normalized to that present in rabbit Heart mitochondria. When species-endogenous levels of rabbit Heart IF1 or either speciesendogenous or normalized levels of pig Heart IF1 were incubated with RHMP over a range of KCl concentrations, increasing the [KCl] to 150 mM had relatively little effect on IF1-mediated ATPase inhibition. When either species-endogenous or normalized levels of guinea pig, pigeon, turtle, or frog Heart IF1 were incubated with RHMP under the same conditions, increasing [KCl] to 150 mM nearly completely blocked IF1-mediated ATPase inhibition. While species-endogenous levels of rat and mouse Heart IF1 inhibited the ATPase activity of RHMP virtually not at all at any [KCl] examined, normalized levels of rat and mouse IF1 inhibited the ATPase activity of RHMP to the same extents as species-endogenous levels of pig and rabbit Heart IF1, respectively, in the presence of increasing [KCl]. These experiments suggest that, while pig and rabbit Heart mitochondria contain a full complement of higher-affinity IF1, pigeon, guinea pig, turtle, and frog Heart mitochondria cell contain essentially a full complement of a lower-affinity form of IF1. In contrast, rat and mouse Heart mitochondria contain only low levels of IF1 which exhibit binding characteristics similar to those of the pig and rabbit Heart inhibitor. The guinea pig is the only mammal thus far examined that contains a loweraffinity form of IF1. In the present study we also determined the IF1 contents and IF1-to-F1 ATPase activity ratios of cardiac muscle, skeletal muscle, liver, and brain mitochondria of rabbit, pigeon, and rat, species representative of the three homeothermic regulatory classes.
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regulation of the mitochondrial adenosine 5 triphosphatase in situ during ischemia and in vitro in intact and sonicated mitochondria from slow and Fast Heart Rate Hearts
Archives of Biochemistry and Biophysics, 1990Co-Authors: William Rouslin, Charles W BrogeAbstract:Abstract In the present study we examined the regulation of the cardiac muscle mitochondrial ATPase both in situ and in vitro in intact and sonicated mitochondria from rabbit, pigeon, and rat. We chose to study these three species because each is representative of one of the three classes into which all species thus far studied may be placed with respect to the in situ activity of their cardiac muscle mitochondrial ATPase inhibitor and with respect to the amount of ATPase inhibitor present in their cardiac muscle mitochondria (1). Class A species (rabbit) contain a full complement of ATPase inhibitor and show a marked ATPase inhibition during ischemia. Class B species (pigeon) also contain a full complement of inhibitor but exhibit only a low level of ATPase inhibition in situ . Class C species (rat) contain only low levels of inhibitor and, like class B species, don't appear to utilize the inhibitor they possess during ischemia in situ . We found that, while Hearts from all three species developed a marked cytosolic acidosis during ischemia, only rabbit exhibited a marked ATPase inhibition in situ . In in vitro experiments in which matrix pH values close to 6.2 and ΔΨ values close to zero were measured in intact mitochondria from all three species, matrix pH appeared to be an important factor regulating ATPase inhibition in rabbit, but it had little effect upon ATPase-inhibitor interaction in pigeon and rat despite the lack of membrane potential. However, a pH-dependent further release of ATPase inhibitor was observed in sonicated pigeon Heart mitochondria only. This latter observation suggests that, while slow Heart-Rate Heart mitochondria appear to be designed for ATPase down regulation during ischemia by inhibitor binding to the ATPase, Fast Heart-Rate Heart mitochondria appear to be designed primarily for ATPase up regulation by a further release of inhibitor from the enzyme.
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Regulation of the mitochondrial adenosine 5′-triphosphatase in situ during ischemia and in vitro in intact and sonicated mitochondria from slow and Fast Heart-Rate Hearts
Archives of Biochemistry and Biophysics, 1990Co-Authors: William Rouslin, Charles W BrogeAbstract:Abstract In the present study we examined the regulation of the cardiac muscle mitochondrial ATPase both in situ and in vitro in intact and sonicated mitochondria from rabbit, pigeon, and rat. We chose to study these three species because each is representative of one of the three classes into which all species thus far studied may be placed with respect to the in situ activity of their cardiac muscle mitochondrial ATPase inhibitor and with respect to the amount of ATPase inhibitor present in their cardiac muscle mitochondria (1). Class A species (rabbit) contain a full complement of ATPase inhibitor and show a marked ATPase inhibition during ischemia. Class B species (pigeon) also contain a full complement of inhibitor but exhibit only a low level of ATPase inhibition in situ . Class C species (rat) contain only low levels of inhibitor and, like class B species, don't appear to utilize the inhibitor they possess during ischemia in situ . We found that, while Hearts from all three species developed a marked cytosolic acidosis during ischemia, only rabbit exhibited a marked ATPase inhibition in situ . In in vitro experiments in which matrix pH values close to 6.2 and ΔΨ values close to zero were measured in intact mitochondria from all three species, matrix pH appeared to be an important factor regulating ATPase inhibition in rabbit, but it had little effect upon ATPase-inhibitor interaction in pigeon and rat despite the lack of membrane potential. However, a pH-dependent further release of ATPase inhibitor was observed in sonicated pigeon Heart mitochondria only. This latter observation suggests that, while slow Heart-Rate Heart mitochondria appear to be designed for ATPase down regulation during ischemia by inhibitor binding to the ATPase, Fast Heart-Rate Heart mitochondria appear to be designed primarily for ATPase up regulation by a further release of inhibitor from the enzyme.
C W Broge - One of the best experts on this subject based on the ideXlab platform.
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Mechanisms of ATP conservation during ischemia in slow and Fast Heart Rate Hearts.
The American journal of physiology, 1993Co-Authors: W Rouslin, C W BrogeAbstract:In the present study we compared the quantitatively most important, Pi-activated mechanisms for conserving ATP during ischemia in dog and rat cardiac muscle. Earlier studies by ourselves showed that dog Heart, like all slow Heart Rate mammalian Hearts examined, possesses the ability to inhibit its mitochondrial ATPase by binding IF1, the ATPase inhibitor protein, during ischemia. Rat Heart, like other Fast Heart Rate mammalian Hearts studied, does not. The present study demonstRated that this IF1-mediated ATPase inhibition in ischemic dog Heart, as in other slow Heart Rate Hearts, appears to depend on matrix space acidification mediated largely by Pi-H+ symport via the mitochondrial Pi carrier. The present study further confirmed that maximal glycolytic flux Rates are five- to sixfold greater in ischemic rat than in ischemic dog Heart. Both of these systems are activated by increasing Pi concentration ([Pi]) during ischemia, and both appear to be regulated somewhat differently in dog than in rat Heart. Thus intact dog Heart mitochondria exhibited a [Pi]-dependent ATPase inhibition at low external pH, whereas rat Heart mitochondria did not. The [Pi] required for maximal ATPase inhibition in dog Heart mitochondria was approximately 6 mM. Although both dog and rat Heart phosphofructokinase were stimulated by Pi, the enzyme in dog Heart was maximally activated by approximately 6 mM Pi, whereas the rat Heart enzyme required only approximately 3 mM Pi for its maximal stimulation under otherwise identical conditions. The most active nonmitochondrial ATPase in ischemic dog and rat cardiac muscle, the Ca(2+)-activated actomyosin ATPase, accounted for approximately one-half of the total nonmitochondrial ATPase activity in each species.(ABSTRACT TRUNCATED AT 250 WORDS)
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factors affecting the species homologous and species heterologous binding of mitochondrial atpase inhibitor if1 to the mitochondrial atpase of slow and Fast Heart Rate Hearts
Archives of Biochemistry and Biophysics, 1993Co-Authors: W Rouslin, C W BrogeAbstract:Abstract We examined the effects of a variety of conditions upon the IF 1 -mediated inhibition of the ATPase in both intact and sonicated mitochondria and in IF 1 -depleted submitochondrial particles (SMP) in species-homologous and species-heterologous combinations of IF 1 and ATPase. IF 1 -mediated ATPase inhibition occurred in intact rabbit Heart mitochondria at low matrix pH and low membrane potential, but not in intact pigeon and rat Heart mitochondria under the same conditions. IF 1 -mediated ATPase inhibition was, however, demonstrable in both the rabbit and pigeon Heart systems in sonicated mitochondria incubated at low ionic strength. The rat Heart system failed to exhibit significant IF 1 -mediated ATPase inhibition in either intact or sonicated mitochondria due to the low amount of IF 1 present. When rabbit Heart IF 1 -containing extracts were incubated with IF 1 -depleted rabbit Heart SMP over a range of KCl concentrations, increasing the [KCl] to 100 mM had little effect on IF 1 -mediated ATPase inhibition. When pigeon Heart IF 1 -containing extracts were incubated with IF 1 -depleted pigeon Heart SMP under the same conditions, increasing [KCl] to 100 mM nearly completely blocked IF 1 -mediated ATPase inhibition. While the species-endogenous level of rat Heart IF 1 (i.e., 1× IF 1 ) inhibited IF 1 -depleted rat Heart SMP virtually not at all at any [KCl] examined, the 8× rat Heart IF 1 was nearly as inhibitory as the 1× rabbit Heart IF 1 at varying ionic strengths. When rabbit, pigeon, or rat Heart IF 1 was bound to rabbit versus pigeon IF 1 -depleted SMP, the effect of varying ionic strength on IF 1 -mediated ATPase inhibition was related to the species source of the IF 1 , not to the species source of the enzyme; 1× bovine Heart IF 1 purified to homogeneity behaved much like 1× crude rabbit Heart IF 1 when binding to either the rabbit or the pigeon Heart enzyme. This suggests that an IF 1 -ATPase complex stabilizing factor such as has been isolated from baker′s yeast cells is neither lacking in the pigeon Heart system nor required for the more ionic-strength-resistant binding of IF 1 observed in slow Heart-Rate mammalian Heart mitochondria.
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mechanisms of atp conservation during ischemia in slow and Fast Heart Rate Hearts
American Journal of Physiology-cell Physiology, 1993Co-Authors: William Rouslin, C W BrogeAbstract:In the present study we compared the quantitatively most important, Pi-activated mechanisms for conserving ATP during ischemia in dog and rat cardiac muscle. Earlier studies by ourselves showed tha...
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atp depletion and mitochondrial functional loss during ischemia in slow and Fast Heart Rate Hearts
American Journal of Physiology-heart and Circulatory Physiology, 1990Co-Authors: William Rouslin, C W Broge, I L GruppAbstract:In the present study, isolated dog and rat Hearts were perfused in the Langendorff mode with Krebs bicarbonate buffer in the absence and presence of 10(-5) M oligomycin. The perfusion protocols emp...
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ATP depletion and mitochondrial functional loss during ischemia in slow and Fast Heart-Rate Hearts.
The American journal of physiology, 1990Co-Authors: W Rouslin, C W Broge, I L GruppAbstract:In the present study, isolated dog and rat Hearts were perfused in the Langendorff mode with Krebs bicarbonate buffer in the absence and presence of 10(-5) M oligomycin. The perfusion protocols employed allowed tissue pH to drop during subsequent ischemic incubations essentially as it would in blood-perfused Hearts. Tissue pH, ATP, lactate, and mitochondrial respiratory function were measured during the course of subsequent zero-flow ischemic incubations. The adenosinetriphosphatase (ATPase) activities attributable to both mitochondrial and nonmitochondrial ATPases in sonicated Heart homogenates and the actomyosin ATPase in isolated cardiac myofibrils were measured in both species. Consistent with earlier results with a different model in which tissue pH was buffered during the ischemic incubations [W. Rouslin, J. L. Erickson, and R. J. Solaro. Am. J. Physiol. 250 (Heart Circ. Physiol. 19): H503-H508, 1986], the inhibition of the mitochondrial ATPase in situ by oligomycin markedly slowed both tissue ATP depletion and the loss of mitochondrial function during ischemia in the dog. However, oligomycin had only a very small and transient effect on ATP depletion and mitochondrial function in the rat. This was apparently so because of the fivefold higher Rate of glycolytic ATP production as well as the nearly threefold higher total nonmitochondrial ATPase activity of ischemic rat compared with ischemic dog Heart. These results suggest that although the inhibition of the mitochondrial ATPase makes a major contribution to ATP conservation in ischemic dog Heart, it makes only a very small contribution in rat.
Meiyu Li - One of the best experts on this subject based on the ideXlab platform.
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Wavelet-Transform-Based Data-Length-Variation Technique for Fast Heart Rate Detection Using 5.8-GHz CW Doppler Radar
IEEE Transactions on Microwave Theory and Techniques, 2018Co-Authors: Meiyu LiAbstract:The Fast detection of Heart Rate (HR) is challenging when using the noncontact continuous-wave (CW) Doppler radar. Applying the Fourier transform (FT) to the baseband signal analysis, the accuracy is degraded due to the insufficient frequency resolution if using less than 5-s time window to realize Fast detection. Moreover, respiratory harmonic peak might be incorrectly picked as the Heartbeat signal if its magnitude is larger than the Heartbeat peak in frequency spectrum. In this paper, a wavelet-transform-based data-length-variation technique is proposed to realize the Fast detection of HR. With this technique, HR can be extracted with 3-5-s data length, and the respiratory harmonics can be distinguished from Heartbeat signals, because the frequency of wavelet harmonic is not as tolerant of the change of the data length as Heartbeat in the wavelet frequency spectrum. The algorithm is verified by simulation using numerical computing tool and demonstRated by human tests utilizing a 5.8-GHz CW Doppler radar platform. Compared to the traditional frequency domain method using FT, the proposed technique reduces the average error of HR from 26.7% to 3.5% using 3-5-s length of data varied in the range of ±0.5 s.