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At least 19 recordsLinked to original sources

PubMed2005

Changes in heart rate, heart rate variability, and heart rate turbulence during evolving reperfused myocardial infarction.

Depressed cardiac parasympathetic activity is associated with electrical instability and adverse outcomes after myocardial infarction (MI). Heart rate turbulence (HRT), reflecting reflex vagal activity, and heart rate variability (HRV), reflecting tonic autonomic variations are both reduced in the subacute phase of MI. However, the evolution of these components of cardiac autonomic control between subacute and chronic phase of MI has not been defined. We prospectively studied 100 consecutive patients with a recent first MI with ST-segment elevation, who underwent successful direct percutaneous coronary interventions. Beta-adrenergic blockers and angiotensin-converting enzyme (ACE) inhibitors were administered according to the state-of-the-art medical practice guidelines. HRT and HRV were measured from 24-hour ambulatory electrocardiographic recordings 10 days and 12 months after the index MI. There was no significant difference in mean RR interval between the subacute and chronic phase of MI (875 +/- 145 versus 859 +/- 122 ms). Indices of HRV increased significantly during the observation period (SDNN: from 88.8 +/- 26.8 to 116.0 +/- 35.7 ms, P < 0.001; SDNNi: from 37.9 +/- 15.9 to 46.0 +/- 16.3 ms, P < 0.001; SDANN: from 79.6 +/- 34.7 to 105.6 +/- 35.4 ms, P < 0.001). In contrast, there were no significant changes in indices of HRT (turbulence onset: from -0.008 +/- 0.022 to -0.012 +/- 0.025%; turbulence slope: from 7.78 +/- 5.9 to 8.06 +/- 6.8 ms/beat). In contrast to reflex autonomic activity, there was a significant recovery of tonic autonomic activity within 12 months after MI. These different patterns of recovery of reflex versus tonic cardiac autonomic control after MI need to be considered when risk stratifying post-MI patients.

Aged↗

PubMed2006

Effects of omega-3 fatty acids on resting heart rate, heart rate recovery after exercise, and heart rate variability in men with healed myocardial infarctions and depressed ejection fractions.

We explored possible mechanisms by which recommended intakes of omega-3 fatty acids may decrease the risk for sudden cardiac death in patients with documented coronary heart disease. The cardioprotective effects of omega-3 fatty acids have been documented in epidemiologic and randomized controlled trials. These fatty acids are presumed to decrease susceptibility to fatal arrhythmias, but whether this is mediated by classic risk factors or direct cardiac mechanisms is not known. Eighteen white men with a history of myocardial infarction and ejection fractions <40% were randomized to placebo or omega-3 fatty acids (585 mg of docosahexaenoic acid and 225 mg of eicosapentaenoic acid) for two 4-month periods in a crossover design. At the end of each period, heart rate (HR), HR variability, and rate of HR recovery after exercise were determined, as were effects on arterial compliance, blood pressure, cardiac function, and fasting serum levels of lipids and inflammatory markers. Omega-3 fatty acids decreased HR at rest from 73 +/- 13 to 68 +/- 13 beats/min (p <0.0001) and improved 1-minute HR recovery after exercise (-27 +/- 10 to -32 +/- 12 beats/min, p <0.01). HR variability in the high-frequency band increased (p <0.02), but no change was noted in overall HR variability. There were no significant effects on blood pressure, arterial compliance, lipids, or inflammatory markers. These changes are consistent with an increase in vagal activity and may in part explain the observed decrease in risk for sudden cardiac death seen with omega-3 fatty acid supplementation.

Aged↗

PubMed1995

Effects of age on intrinsic heart rate, heart rate variability, and AV conduction in healthy humans.

Heart rate, heart rate variability, and atrioventricular (AV) conduction were studied in 20 young (30 +/- 5 yr) and 19 older (69 +/- 7 yr) healthy men and women before and after single and double autonomic blockade (randomized order: atropine, 0.04 mg/kg i.v.; propranolol, 0.2 mg/kg i.v.). Basal R-R intervals did not differ, but older age increased P-R intervals (177 +/- 24 vs. 149 +/- 17 ms, P < 0.001) and decreased SD of R-R (43 +/- 17 vs. 70 +/- 18 ms, P = 0.001) and heart rate spectral content (area under the power vs. frequency curve from 0.04 to 0.32 Hz: 3.01 +/- 2.1 vs. 7.82 +/- 4.8 beats/min2, P < 0.009), as well as postural responses (R-R decreases of 107 +/- 80 vs. 250 +/- 72 ms, P < 0.002). Atropine decreased R-R intervals, SD of R-R, and high-frequency (0.24-0.32 Hz) spectral content less in elderly subjects compared with younger subjects. Propranolol increased R-R and P-R intervals equally in old and young and abolished low-frequency (0.04-0.12 Hz) increases with standing (P < 0.0008). After double blockade, R-R, P-R, and paced AV intervals were longer in old subjects. Mean values were as follows: R-R intervals, 859 +/- 176 vs. 677 +/- 106 ms, P < 0.001; P-R intervals, 179 +/- 23 vs. 149 +/- 17 ms, P = 0.0002; paced P-R intervals (500 ms), 251 +/- 39 vs. 215 +/- 47 ms; and AV block cycle length, 413 +/- 51 vs. 385 +/- 69 ms (multivariate analysis of variance, P < 0.03). After double autonomic blockade, heart rate variability was nearly eliminated in young and old (reduced > 98%, P < 0.0001). We conclude that age differences in heart rate variability can be explained by autonomic influences, but heart rate and AV conduction differences exist independently of beta-adrenergic and/or parasympathetic influences.

Adult↗

PubMed1988

The relationship between heart rate, heart rate variability and depression in patients with coronary artery disease.

Seventy-seven patients undergoing elective cardiac catheterization were administered a diagnostic psychiatric interview and their mean heart rates and heart rate variability were determined from the results of a 24 hr ambulatory ECG. The mean heart rate for depressed patients with coronary artery disease (CAD) was significantly higher than for nondepressed CAD patients, independent of the patient's age, smoking status, and beta blocker therapy. Heart rate variability was lower in depressed patients but did not achieve significance. With the exception of smoking, which was more common in depressed patients, there were no significant differences between the depressed and nondepressed patients on any other medical or demographic variable assessed. It is concluded that elevated heart rate may represent increased sympathetic tone in depressed CAD patients, and may help to explain the increased morbidity and mortality reported in these patients.

Arousal↗

PubMed2005

Heart rate, heart rate variability, and heartbeat detection with the method of constant stimuli: slow and steady wins the race.

The literature on heartbeat detection is fraught with disagreement about appropriate methods. Some laboratories advocate the heartbeat counting method, whereas others advocate the method of constant (MCS) stimuli task. Advocates of the MCS task argue that the heartbeat counting task is confounded by expectancies of heart rate, whereas the MCS task has the virtue of assessing individual heartbeat sensations. In this paper, we present preliminary evidence that heart rate information may also influence performance on the MCS task. Heartbeat detection was predicted by decreased heart rate variability and decreased heart rate. The results suggest that the temporal patterning of heartbeats may influence performance on the MCS task.

Adult↗

PubMed1990

Percentages of maximal heart rate, heart rate reserve and VO2max for determining endurance training intensity in male runners.

The use of 60%-95% of maximal heart rate (HR), heart rate reserve (HRR) and VO2max as exercise training intensities was examined in male runners, and these intensities were related to VO2 observed at the lactate threshold (LT) and fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM. Thirty-one subjects (means age = 29.9 +/- 9.1 yrs; means ht = 177.3 +/- 8.2 cm; means wt = 69.2 +/- 9.9 kg) completed a level running treadmill protocol. The mean values at LT, FBLC of 2.0, 2.5, 4.0 mM and max for VO2 were 52.7, 56.4, 58.0, 61.2 and 63.5 ml/kg.min -1, respectively: for velocity they were 237.4, 252.2, 260.6, 274.4 and 286.5 m/min, respectively; and for HR were 165.7, 172.7, 176.5, 182.3 and 187.4 bts/min, respectively. The majority of subjects were not above LT (N = 20), until an intensity of 90% HR max was attained. At 95% HR max the majority of subjects were above 2.0 mM (N = 23) and 2.5 mM (N = 17) but below 4.0 mM (N = 26). For HRR, 85% HRR was necessary for the majority of subjects to be above LT (N = 20), 90% HRR resulted in the majority of subjects being above 2.0 mM (N = 19), while 95% HRR was required for the majority of subjects to be above 2.5 mM (N = 23). At 95% HRR 14 subjects were above 4.0 mM. For % VO2max, the intensities required for the majority of subjects to be above LT, FBLC of 2.0, and 2.5 mM were 90%, 95% and 95% VO2max, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Percentages of maximal heart rate, heart rate reserve, and VO2peak for determining endurance training intensity in sedentary women.

The use of 60%-95% of maximal heart rate (HR max), heart rate reserve (HRR), and VO2peak as exercise training intensities was examined in sedentary women, and these intensities were related to HR and VO2 observed at the lactate threshold (LT) and fixed blood lactate concentrations of 2.0, 2.5, and 4.0 mM. Thirty-three subjects (means age = 32.5 +/- 3.9 yrs; means ht = 164.2 +2- 5.0 cm; means wt = 67.6 +/- 13.9 kg) completed a VO2/LT treadmill test using a level running protocol. The values at LT, 2.0, 2.5, 4.0 mM, and peak for VO2 were 22.3, 29.0, 31.0, 36.2, and 39.1 ml/kg.min-1, respectively; for velocity were 107.0, 128.9, 135.8, 152.8, and 164.4 m/min, respectively; and for HR were 142.1, 162.9, 169.4, 183.2, and 189.7 bts/min, respectively. The minimum intensity necessary for the majority of subjects to be above LT (n = 17) was 75% HR max while 90% HR max was required for the majority of subjects to be above 2.0 mM (n = 23) and 2.5 mM (n = 19). At 95% HR max 12 subjects were above 4.0 mM. For the majority of subjects to be above LT (n = 18), 55% HRR was necessary; 75%, 85%, and 95% HRR was required for the majority of subjects to be above 2.0 mM (n = 18), 2.5 mM (n = 19), and 4.0 mM (n = 20), respectively. For percent VO2peak, the intensities required for the majority of subjects to be above LT, 2.0 mM, 2.5 mM, and 4.0 mM were 55%, 75%, 80%, and 95% VO2peak, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Relative heart rate, heart rate reserve, and VO2 during submaximal exercise in the elderly.

BACKGROUND: The purpose of this study was to examine the relationships among relative maximal heart rate (%HRmax), maximal heart rate reserve (%HRmax reserve), and maximal oxygen uptake (%VO2max) during submaximal exercise by elderly subjects. METHODS: VO2max and HRmax were determined on 36 women and 19 men, 60 to 80 yrs of age, by a maximal treadmill test to volitional exhaustion. On a separate day, subjects underwent a submaximal treadmill protocol consisting of three 6-min exercise stages at treadmill speeds and grades estimated to elicit 40%, 60%, and 80% of HRmax reserve. Cardiorespiratory responses were determined during mins 4-5 and 5-6 of each stage. RESULTS: Measured exercise intensities expressed by the three methods were: %HRmax reserve = 36, 55, and 79%; %HRmax = 65, 75, and 88%; %VO2max = 53, 69, and 88%. %HRmax was greater (p < .05) than %VO2max at 53 and 69% of VO2max. %HRmax reserve was less (p < .05) than %VO2max for all three intensities. Slopes and intercepts for the linear regression equations relating %VO2max with %HRmax and with %HRmax reserve differed between men and women (p < .05). The regression equation relating %VO2max and %HRmax was y = -22.8 + 1.2 (%HRmax) -13.0 (Gender) + 0.2 (%HRmax x Gender): standard error of the estimate (SEE) = 9.7% and R2 = .71. The regression equation relating %VO2max and %HRmax reserve was y = 32.4 + 0.7 (%HRmax reserve) -10.9 (Gender) + 0.2 (%HRmax reserve x Gender): SEE = 9.8% and R2 = .70 (Gender: F = 0; M = 1). CONCLUSIONS: The data indicate that there is considerable variability among methods of expressing exercise intensity and that %HRmax more closely represents %VO2max than does %HRmax reserve (p < .05) in older adults. These results are in contrast to what has been shown with younger subjects and with American College of Sports Medicine guidelines for exercise prescription.

Aged↗

PubMed1997

Heart rate, heart rate variability, and blood pressure during perioperative stressor events in abdominal surgery.

STUDY OBJECTIVE: To define the behavior of power spectral heart rate variability (PSHR) during potentially stressful events in the perioperative period, and relate it to changes in blood pressure (BP) and heart rate (HR). DESIGN: Longitudinal clinical study. SETTING: Operating room and recovery suites of a large tertiary care referral center. PATIENTS: 26 ASA physical status I, II, and III patients undergoing elective abdominal surgery. INTERVENTIONS: Anesthesia was induced with thiopental sodium and fentanyl, and maintained with isoflurane/nitrous oxide (N2O)/relaxant or enflurane/N2O/relaxant. The trachea was intubated and intraabdominal surgery was performed. MEASUREMENTS AND MAIN RESULTS: Observations consisted of HR, noninvasive blood pressure, and PSHR. They were made before and after induction of anesthesia, tracheal intubation, and surgical incision, and during maximal surgical stimulation and skin closure. HR and mean arterial pressure (MAP) maxima were also recorded for one hour before and after emergence from anesthesia. PSHR was obtained using a special algorithm and data acquisition system for real time spectral analysis of the instantaneous HRversus time function. The HR power spectrum parameters analyzed were low-frequency (LFA; powerband = 0.04 to 0.10 Hz), respiratory-induced frequency (RFA; powerband = respiratory frequency +/- 0.06 Hz), and the ratio of LFA to RFA. With induction of anesthesia, only RFA power decreased significantly. LFA power reduction became significant only after intubation and continued so until after incision. Immediately after induction, the decline in RFA power (vs. preinduction) was more pronounced when compared with the decline in LFA power (76% vs. 34%; p = 0.01). Hence, the ratio LFA/RFA increased significantly after induction of anesthesia. It was significantly higher than at postintubation, preincision, or skin closure. A significant elevation in LFA, LFA/RFA ratio, and BP occurred with maximal abdominal surgical stimulation. Only preinduction LFA, RFA, and LFA/ RFA ratio were predictive of MAP changes with induction of anesthesia (p = 0.006). In 8 of the 15 patients who had MAP changes of at least 10 mmHg with induction, PSHR indices correctly predicted a change of this magnitude. Late intraoperative HR maxima were positively correlated with the change in HR and incision (r2 = 0.58; p < 0.01). The change in BP with incision was positively correlated with early postoperative HR maxima (r2 = 0.60; p < 0.01). CONCLUSIONS: On anesthetic induction, preoperative, but not intraoperative, spectral indices were predictive of BP changes. Power spectral analysis of HR may provide information about the autonomic state that is not evident from BP or HR. The HR power spectrum, in particular, indicated a striking autonomic imbalance immediately after the induction of anesthesia despite stable HR and BP. LFA and LFA/RFA ratio appeared to track sympathetic autonomic activation during abdominal surgical stimulation, but not during other perioperative stressor events.

Abdomen↗

PubMed1989

Regulation of mitochondrial matrix pH and adenosine 5'-triphosphatase activity during ischemia in slow heart-rate hearts. Role of Pi/H+ symport.

During ischemia in so-called slow heart-rate hearts, there is a marked inhibition of the mitochondrial ATPase mediated by inhibitor protein binding to the enzyme (Rouslin, W., and Pullman, M. E. (1987) J. Mol. Cell. Cardiol. 19, 661-668). This ischemia-induced ATPase inhibition is triggered by a drop in mitochondrial matrix pH (Rouslin, W. (1987) J. Biol. Chem. 262, 3472-3476) which occurs as a result of the cell acidification which develops rapidly during the ischemic process. One effect of the ATPase inhibition is a marked slowing of the net rate of tissue ATP hydrolysis and, thus, a prolongation of cell viability during ischemia. In the present study, we demonstrate that matrix acidification in intact mitochondria from slow heart-rate hearts appears to be mediated by the Pi transporter. Pi/H+ symport appears to be the primary process which mediates matrix acidification and thus ATPase inhibition in intact slow heart-rate heart mitochondria made acidotic in vitro and, presumably, also in mitochondria in situ during the ischemic process. In contrast, intact mitochondria from a so-called fast heart-rate species, which exhibited only a low level of ischemia-induced ATPase inhibition in situ (Rouslin, W. (1987) Am. J. Physiol. 252, H622-H627), failed to exhibit a Pi- and pH-dependent mitochondrial ATPase inhibition mechanism in vitro. The Pi-dependent mitochondrial ATPase inhibition mechanism reported here for slow heart-rate hearts is consistent with a role for Pi as a coordinating signal promoting the conservation of cell ATP during myocardial ischemia.

Adenosine Triphosphatases↗

PubMed2004

The association between heart rate, heart rate variability, endocrine and behavioural pain measures in horses suffering from laminitis.

The objective of this study was to compare the stress response of horses suffering from laminitis after short- and long-term treatment with the intent to evaluate power spectral analysis of heart rate variability (HRV) for pain monitoring. Data were collected from 19 horses with acute or chronic exacerbating laminitis without known primary disease before and after treatment with non-steroidal anti-inflammatory drugs (NSAID). Recordings were carried out the day after admission to the equine hospital. Measurements were repeated on day 7 of the treatment. The recorded parameters included a clinical orthopaedic index (OLPI: Obel-grade plus hoof tester score), frequency of weight-shifting between contralateral limbs, mean beat-to-beat interval (R-R) duration, standard deviation of continuous R-R intervals, low- (LF) and high-frequency (HF) components of HRV, sympatho-vagal balance (LF/HF), and plasma concentration of cortisol, adrenalin and noradrenalin. The LF represents mainly sympathetic influences on the heart whereas HF is mediated by the parasympathetic tone. Weight-shifting and OLPI decreased significantly with treatment. The LF normalized units (n.u.) decreased after NSAID from 60.41 +/- 21.42 to 51.12 +/- 19.81 and was 49.33 +/- 22.64 on day 7, whereas HF n.u. increased from 35.07 +/- 20.02 to 43.14 +/- 18.30 and was 45.98 +/- 23.00 on day 7. Hormone levels showed no tendency to change with treatment. The OLPI was only correlated with LF/HF, LF and HF (R = 0.57, 0.55 and -0.54 respectively). Significant negative correlations existed between HFn.u. and weight-shifting frequency (R = -0.37), HFn.u. and adrenalin (R = -0.47), and HFn.u. and noradrenalin (R = 0.33). The LFn.u. only correlated positively with adrenalin. Cortisol levels were poorly associated with the other parameters. Determination of the sympatho-vagal influences on cardiac function may offer complementary information for reliable assessment of pain and may represent a valuable alternative method to catecholamine measurements.

Animals↗

PubMed1990

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.

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 delta psi 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.

Adenosine Triphosphatases↗

PubMed1993

Mechanisms of ATP conservation during ischemia in slow and fast heart rate hearts.

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)

Adenosine Triphosphatases↗

PubMed1989

Metabolic rate, heart rate, and tailbeat frequency during sustained swimming in the leopard shark Triakis semifasciata.

Heart rate, metabolic rate, and tailbeat frequency were simultaneously recorded from seven leopard sharks (Triakis semifasciata) during steady swimming at controlled speeds to evaluate the usefulness of heart rate as a measure of field metabolic rate. Heart rate was monitored by acoustic telemetry using a frequency modulated ECG transmitter. Metabolic rate was measured as oxygen consumption in a swimming tunnel respirometer. For instrumented sharks, mean resting oxygen consumption rate and heart rate were 105.3 +/- 35.6 (SE) mg O2.kg-1.h-1 and 36.6 +/- 1.8 (SE) beats.min-1, respectively. While swimming at the maximum sustained speed (0.84 +/- 0.03 lengths.s-1) for 30-60 min, these rates were 229.3 +/- 13.2 mg O2.kg-1.h-1 and 46.9 +/- 0.9 beats.min-1. Although a significant linear regression was obtained between metabolic rate and heart rate, a low overall correlation coefficient may result from the existence of separate individual regressions and confounding changes in stroke volume and/or arteriovenous oxygen difference. Heart rate was approximately as closely correlated with oxygen consumption rate as swimming speed was. A significant linear relationship was obtained between tailbeat frequency and swimming speed to speeds of 0.75 lengths.s-1.

Animals↗

PubMed1986

Respiration rate, heart rate, and body temperature values in cynomolgus monkeys (Macaca fascicularis) during barbiturate anesthesia.

Respiration rate, heart rate, and body temperature values were obtained from 14 cynomolgus monkeys (Macaca fascicularis) during neurosurgery under barbiturate anesthesia. Vital sign values markedly declined below baseline during the early stages of surgery, steadily increased as surgery progressed and neared completion, and finally returned to baseline by the end of the postsurgical recovery period. There was considerable variability among the 14 monkeys, but the ranking of each monkey relative to the others remained constant across the period of observation. The findings suggested that the cynomolgus monkey may be more sensitive to barbiturates than the rhesus monkey, and cynomolgus monkeys may exhibit considerable individual differences in their sensitivity to barbiturates.

Anesthesia, General↗

PubMed1995

ATPase activity, IF1 content, and proton conductivity of ESMP from control and ischemic slow and fast heart-rate hearts.

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.

Adenosine Triphosphate↗

PubMed1987

The mitochondrial adenosine 5'-triphosphatase in slow and fast heart rate hearts.

A survey of 12 species has revealed that reversible ischemia-induced protonic inhibition of the cardiac muscle mitochondrial adenosine 5'-triphosphatase (ATPase) described by this author earlier (Rouslin, W. J. Biol. Chem. 258: 9657-9661, 1983) occurs only in animals with heart rates lower than approximately 200 beats/min. It was thus fully demonstrable in rabbit, dog, sheep, human, pig, and beef heart mitochondria. In contrast, the in situ ATPase inhibition was completely absent in six smaller species capable of heart rates of approximately 300 or more beats/min. These were chicken, pigeon, guinea pig, rat, hamster, and mouse. Analyses of the cardiac muscle mitochondria of 9 of the 12 species studied showed them to contain normal levels of mitochondrial ATPase inhibitor; the three smallest species, rat, hamster, and mouse contained only very low levels of inhibitor. Thus, although chicken, pigeon, and guinea pig heart mitochondria contained normal levels of ATPase inhibitor, they (like the rat, hamster, and mouse) showed no in situ ischemia-induced ATPase inhibition. This and other observations suggest that the lack of in situ ATPase inhibition in hearts capable of 300 or more beats/min may be due to the presence of either an in situ nonfunctional ATPase inhibitor protein or to an in situ uninhibitable form of the mitochondrial ATPase in the faster-paced hearts. Alternatively, the mitochondria of the fast-paced hearts may be insulated somehow against the cytosolic acidosis which develops during ischemia and which triggers the ATPase inhibition in the slow heart-rate hearts. In the faster paced hearts, ATP hydrolysis does not appear to be regulated by inhibitor binding to the ATPase under nonenergizing conditions.

Adenosine Triphosphatases↗

PubMed2003

Relation between heart rate, heart rhythm, and reverse left ventricular remodelling in response to carvedilol in patients with chronic heart failure: a single centre, observational study.

OBJECTIVE: To determine whether the process of reverse left ventricular remodelling in response to carvedilol is dependent on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR) in response to carvedilol. DESIGN: Retrospective analysis of serial echocardiograms in 257 patients with chronic systolic heart failure at baseline and at 12-18 months after starting carvedilol. Reverse left ventricular remodelling was determined by changes in left ventricular end diastolic dimension (LVEDD), end systolic dimension (LVESD), and fractional shortening (LVFS). SETTING: Heart failure clinic within a university teaching hospital. MAIN OUTCOME MEASURES: Changes in LVEDD, LVESD, and LVFS. RESULTS: LVEDD and LVESD decreased by 2.6 (0.4) mm and 4.9 (0.5) mm, respectively (mean (SEM)), and LVFS increased by 4.3 (0.5)% (all p < 0.0001 v baseline). Simple regression revealed no significant relation between BHR or HRR and the changes in LVEDD, LVESD, or LVFS. Stratification of patients into high and low BHR groups (above and below the mean) or according to the baseline heart rhythm (sinus rhythm v atrial fibrillation) showed no differences between groups in the extent of reverse left ventricular remodelling. Improvements in left ventricular function and dimensions were associated with significant improvements in New York Heart Association functional class. CONCLUSIONS: The benefits of carvedilol in terms of reverse left ventricular remodelling and symptomatic improvement in patients with chronic heart failure are independent of BHR, heart rhythm, and the HRR that occurs in response to carvedilol.

Adrenergic beta-Antagonists↗