Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Recovery phases”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources
PubMed1997

Heart-rate variability in chronic traumatic brain injury.

Heart-rate variability (HRV), a measure of fluctuation around the mean heart rate, reflects the sympathetic and parasympathetic balance of the autonomic nervous system, and is an excellent technique to study cardiovascular tone in patients with neurological injuries. The purpose of this study was to determine whether abnormal HRV is present in patients with traumatic brain injury (TBI) during the post-acute recovery phase. Using a prospective, case/control design, we performed 24-h ambulatory ECG monitoring in seven TBI patients and in seven controls (C). There was a significant difference in root mean squared successive difference of RR intervals (C 40.4 +/- 10.3, TBI 23.3 +/- 16.5, p = 0.04) between TBI and C. Four patients with TBI (compared to one control) had abnormal standard deviation of the RR interval. When these four patients were compared to their matched controls, significant differences were found in frequency domain measure (In total power: TBI 4.4 +/- 0.9 ms2, C 7.1 +/- 1.4 ms2, In low frequency: TBI 3.3 +/- 1.1 ms2, C 6.4 +/- 1.4 ms2; In high frequency TBI 2.0 +/- 1.0 ms2, C 4.8 +/- 1.3 ms2, all p < 0.05). Thus, abnormalities in both time and frequency domains of HRV are present in TBI during the post-acute recovery phase.

Adolescent↗
PubMed1997

[Evaluation of changes in hepatic energy metabolism during exercise by ketone body ratio in humans].

Changes in the redox state of liver mitochondria were investigated by measuring the arterial ketone body ratio (acetoacetate/3-hydroxybutyrate: AKBR) in nine healthy volunteers (eight males and one female, mean age 38.4 +/- 5.0 years) during exercise. The correlation between the changes in AKBR and levels of various hormones controlling energy metabolism was also investigated. Subjects participated in symptom-limited exercise test using the ramping bicycle ergometer with expired gas analysis, blood pressure and 12 lead electrocardiogram monitoring. Anaerobic threshold by gas exchange parameters (ATge) was determined from the expired gas data with the v-slope method. AKBR, glucose, non-esterified fatty acid (NEFA) and lactate were measured in arterial plasma samples. Catecholamines (epinephrine, norepinephrine, dopamine), insulin, glucagon, antidiuretic hormone (ADH), growth hormone (GH), thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), human-atrial natriuretic peptide (hANP) and brain natriuretic peptide (BNP) were measured in venous plasma samples. AKBR was gradually decreased by exercise from the resting value of 1.82 +/- 0.20. AKBR reduction was potentiated after ATge to 0.93 +/- 0.18 (p < 0.01 vs rest) at peak exercise. AKBR was further decreased during recovery to the minimum value of 0.70 +/- 0.06 (p < 0.01) at 6 min in the recovery phase. AKBR then began to increase and reached 0.95 +/- 0.07 30 min after peak exercise. Epinephrine increased from 45.9 +/- 11.0 to 210 +/- 75 pg/ml (p < 0.01), norepinephrine increased from 348 +/- 52 to 1,277 +/- 111 pg/ml (p < 0.01), and dopamine increased from 13.0 +/- 1.9 to 25.0 +/- 2.5 pg/ml (p < 0.01) between rest and peak exercise, respectively. Insulin decreased from 22.0 +/- 3.5 to 14.2 +/- 2.1 pg/ml (p < 0.05). No significant change was observed in glucagon, ADH, GH, TSH, T3, T4, hANP or BNP. Glucose decreased from 124 +/- 9 to 84 +/- 8 mg/dl (p < 0.05), whereas NEFA increased from 94 +/- 10 to 190 +/- 66 mg/dl (p < 0.05). A negative correlation was observed between AKBR and lactate (r = -0.41, p < 0.001). These results indicate that hepatic adenosine triphosphate production is promoted as energy demand increases by exercise, and maximizes early in the recovery phase when hepatic energy demand is maximum due to active gluconeogenesis. The levels of catecholamines, insulin and lactate contribute to the control of liver energy metabolism.

Adult↗
PubMed1989

[Prediction of coronary artery disease using post exercise T wave change].

In the evaluation of the exercise stress test, conventional electrocardiographic criteria using 1 or 2 mm ST segment depression below the isoelectric line yields many false positive results and is not so useful to predict the severity of coronary artery disease. In this study, we have attempted to predict the presence and the severity of coronary artery disease from the post exercise T wave change. Fifty-six patients who had positive treadmill exercise test results by conventional ST segment criteria and underwent selective coronary arteriography were studied. T wave change was defined as inversion or biphasic change in one or more of leads aVF, V4, V5, V6 during the recovery phase, and in the cases who showed T wave changes, T wave configuration were also analysed. Seventeen of 28 patients with and 11 of 28 patients without significant coronary artery disease showed post exercise T wave changes. This difference was not statistically significant. But in the cases who showed T wave changes, the maximum amplitude of the negative component of T wave was significantly greater in the true positive group than in the false positive group. And the development of deeply negative component (more than 1.5 mm) indicated the presence of multivessel coronary artery disease. In the cases who showed the negative component of T wave less than 1 mm, the characteristics of T wave configuration including the amplitude, height of positive component, and the depth from the isoelectric line were different between the 2 groups. These results suggest that careful observation of T wave during the recovery phase is useful to improve the diagnostic accuracy of the exercise electrocardiogram.

Adult↗
PubMed1993

Determinants of 6-month mortality in survivors of myocardial infarction after thrombolysis. Results of the GISSI-2 data base. The Ad hoc Working Group of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-2 Data Base.

BACKGROUND: Current knowledge of risk assessment in survivors of myocardial infarction is largely based on data gathered before the advent of thrombolysis. It must be determined whether and to what extent available information and proposed criteria of prognostication are applicable in the thrombolytic era. METHODS AND RESULTS: We reassessed risk prediction in the 10,219 survivors of myocardial infarction with follow-up data available (ie, 98% of the total) who had been enrolled in the GISSI-2 trial, relying on a set of prespecified variables. The 3.5% 6-month all-cause mortality rate of these patients compared with the higher value of 4.6% found in the corresponding GISSI-1 cohort, originally allocated to streptokinase therapy, indicates a 24% reduction in postdischarge 6-month mortality. On multivariate analysis (Cox model), the following variables were predictors of 6-month all-cause mortality: ineligibility for exercise test for both cardiac (relative risk [RR], 3.30; 95% confidence interval [CI], 2.36-4.62) and noncardiac reasons (RR, 3.28; 95% CI, 2.23-4.72), early left ventricular failure (RR, 2.41; 95% CI, 1.87-3.09), echocardiographic evidence of recovery phase left ventricular dysfunction (RR, 2.30; 95% CI, 1.78-2.98), advanced (more than 70 years) age (RR, 1.81; 95% CI, 1.43-2.30), electrical instability (ie, frequent and/or complex ventricular arrhythmias) (RR, 1.70; 95% CI, 1.32-2.19), late left ventricular failure (RR, 1.54; 95% CI, 1.17-2.03), previous myocardial infarction (RR, 1.47; 95% CI, 1.14-1.89), and a history of treated hypertension (RR, 1.32; 95% CI, 1.05-1.65). Early post-myocardial infarction angina, a positive exercise test, female sex, history of angina, history of insulin-dependent diabetes, and anterior site of myocardial infarction were not risk predictors. On further multivariate analysis, performed on 8315 patients with the echocardiographic indicator of left ventricular dysfunction available, only previous myocardial infarction was not retained as an independent risk predictor. CONCLUSIONS: A decline in 6-month mortality of myocardial infarction survivors, seen within 6 hours of symptom onset, has been observed in recent years. Ineligibility for exercise test, early left ventricular failure, and recovery-phase left ventricular dysfunction are the most powerful (RR, > 2) predictors of 6-month mortality among patients recovering from myocardial infarction after thrombolysis. Qualitative variables reflecting residual myocardial ischemia do not appear to be risk predictors. The lack of an independent adverse influence of early post-myocardial infarction angina on 6-month survival represents a major difference between this study and those of the prethrombolytic era.

Aged↗
PubMed2000

Phosphorylation by cyclin-dependent protein kinase 5 of the regulatory subunit of retinal cGMP phosphodiesterase. I. Identification of the kinase and its role in the turnoff of phosphodiesterase in vitro.

Cyclic GMP phosphodiesterase (PDE) is an essential component in retinal phototransduction. PDE is regulated by Pgamma, the regulatory subunit of PDE, and GTP/Talpha, the GTP-bound alpha subunit of transducin. In previous studies (Tsuboi, S., Matsumoto, H. , Jackson, K. W., Tsujimoto, K., Williamas, T., and Yamazaki, A. (1994) J. Biol. Chem. 269, 15016-15023; Tsuboi, S., Matsumoto, H., and Yamazaki, A. (1994) J. Biol. Chem. 269, 15024-15029), we showed that Pgamma is phosphorylated by a previously unknown kinase (Pgamma kinase) in a GTP-dependent manner in photoreceptor outer segment membranes. We also showed that phosphorylated Pgamma loses its ability to interact with GTP/Talpha, but gains a 10-15 times higher ability to inhibit GTP/Talpha-activated PDE than that of nonphosphorylated Pgamma. Thus, we propose that the Pgamma phosphorylation is probably involved in the recovery phase of phototransduction through shut off of GTP/Talpha-activated PDE. Here we demonstrate that all known Pgammas preserve a consensus motif for cyclin-dependent protein kinase 5 (Cdk5), a protein kinase believed to be involved in neuronal cell development, and that Pgamma kinase is Cdk5 complexed with p35, a neuronal Cdk5 activator. Mutational analysis of Pgamma indicates that all known Pgammas contain a P-X-T-P-R sequence and that this sequence is required for the Pgamma phosphorylation by Pgamma kinase. In three different column chromatographies of a cytosolic fraction of frog photoreceptor outer segments, the Pgamma kinase activity exactly coelutes with Cdk5 and p35. The Pgamma kinase activity ( approximately 85%) is also immunoprecipitated by a Cdk5-specific antibody, and the immunoprecipitate phosphorylates Pgamma. Finally, recombinant Cdk5/p35, which were expressed using clones from a bovine retina cDNA library, phosphorylates Pgamma in frog outer segment membranes in a GTP-dependent manner. These observations suggest that Cdk5 is probably involved in the recovery phase of phototransduction through phosphorylation of Pgamma complexed with GTP/Talpha in mature vertebrate retinal photoreceptors.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1974

Tension responses to quick length changes of glycerinated skeletal muscle fibres from the frog and tortoise.

1. Twitch fibres isolated from the sartorius muscle of the frog were glycerinated (cf. Heinl, 1972) and thin fibre bundles dissected from the m. ileofibularis of the tortoise were briefly glycerinated as described by Julian (1971).2. The glycerinated fibres (length 0.3-0.5 cm) were fixed to an apparatus which performed length changes within 5 msec and recorded the time course of tension changes in the fibres.3. The fibres were suspended in a relaxing medium, containing ATP and 4 mM-EGTA. Contraction was induced by raising the calcium concentration to 4 mM-CaEGTA.4. The tension time course of activated fibres following quick length changes (0.1-1% L(0)) was studied. The tension records produced by quick releases and stretches could be resolved into four phases similar to the kind shown in Fig. 1 a.5. The phase of quick tension recovery was found to take place more rapidly in frog than in tortoise fibres: it was completed in approximately 30 msec (after stretch) and in approximately 20 msec (after release) in frog fibres (3 degrees C). The corresponding values obtained for tortoise fibres were approximately 300 and approximately 400 msec (3 degrees C).6. In tortoise fibres the size of the elastic and quick recovery phase increased with rising isometric tension (induced by raising the calcium concentration (pCa 8 to 5)), and decreased with increasing sarcomere length (2.5-4.2 mum). In fibres, in which the rigor state was induced by withdrawal of ATP, no quick tension recovery was recorded.7. It is suggested that the rotational movement of the crossbridge head on the actin filament, postulated by Huxley & Simmons (1971 b) is taking place more slowly in the tortoise than in the frog muscle. Furthermore, it is suggested that this rotational movement does not occur in the rigor state, as no quick tension recovery was recorded there.

Adenosine Triphosphate↗
PubMed2005

Short-term predictive changes in the dynamics of disparity vergence eye movements.

Repetitive stimulation of the disparity vergence system to large convergent step stimuli has been shown to increase the dynamics of subsequent responses to smaller step stimuli. Here we show that decreases in the dynamics of both disparity convergence and divergence eye movements can be induced using a frequently occurring small amplitude conditioning stimulus to modify responses to a larger, occasionally presented test stimulus. In one experiment, a simple conditioning stimulus consisting of repetitive 1 degrees step stimuli was used to modify the dynamic vergence response to an occasional 4 degrees step test stimulus. An experimental trial consisted of three phases: baseline, conditioning, and recovery. The baseline and recovery phases used only the 4 degrees test stimuli. The dynamic characteristics of the responses to test stimuli were quantified by measuring the magnitude of the peak velocity. A statistically significant change was observed between the dynamics of conditioned responses compared to baseline and recovery responses indicting modification by the conditioning stimuli. During recovery, the response dynamics returned to levels near baseline levels showing that the decrease in response dynamics was caused by the conditioning stimulus, not fatigue. Another experiment showed that the response dynamics to large stimuli could be decreased whereas the dynamics of small stimuli could be increased by the same intermediate conditioning stimulus. Other experiments suggest that the modifications are due to a predictive mechanism. The results indicate that the dynamics of disparity vergence eye movements are malleable and depend to some extent on the amplitude of preceding stimuli.

Adult↗
PubMed1988

Role of compensatory gain in Eimeria acervulina-induced liver copper accumulation in chicks.

An investigation was conducted to determine whether the Eimeria acervulina-induced increase in liver Cu accumulation in chicks is the result of compensatory gain that accompanies the recovery phase of infection. In experiment 1, chicks inoculated one time with 1 X 10(6) sporulated E. acervulina oocysts had a faster rate of compensatory gain than chicks inoculated serially on three occasions with 4 X 10(5) oocysts. However, liver Cu accumulation was nearly identical for the two infection regimes. In experiment 2, rate of compensatory gain and liver Cu accumulation was compared in 1) ad libitum-fed chicks; 2) restricted-fed chicks fed 40% of ad libitum intake followed by ad libitum intake; 3) coccidiosis-infected chicks, 1 X 10(6) oocysts on d 2 of the experiment; and 4)-6) the same as 1)-3), respectively, but fed 500 mg Cu/kg diet. Restricted-fed chicks had a higher rate of compensatory gain than coccidiosis-infected chicks. Liver Cu accumulation was sixfold higher in coccidiosis-infected chicks than in restricted-fed chicks, however. In addition, liver Cu accumulation of the control (uninfected) chicks and the 40% restricted-fed chicks was identical. Thus compensatory gain during the recovery phase of coccidiosis is not responsible for the coccidiosis-induced increase in liver Cu accumulation.

Animals↗
PubMed2006

Analysis of muscle hardness in patients with masticatory myofascial pain.

PURPOSE: The aim of the present study was to access any changes in the muscle hardness of the masseter muscle between normal subjects and patients with myofascial pain during brief sustained isometric contractions at various bite force levels, and to compare muscle hardness, especially in terms of the recovery phase, after a clenching task. MATERIALS AND METHODS: Ten patients with masticatory myofascial pain and 10 age- and weight-matched normal healthy controls participated in this study. First, the hardness of the right masseter muscle was measured at the bite force of 0, 3, 6, and 9 kgf with a hand-held hardness meter. Then, the subjects were requested to exert a 9 kgf-clenching task for 30 seconds. The muscle hardness was again measured at 5, 30, and 120 seconds after the task, and the data obtained were compared with the muscle hardness before the clenching task. RESULTS: The results showed that there was no significant difference between the patients and the normal controls, while the muscle hardness increased with contraction in all subjects. The present findings also showed that the patients had a delayed return to baseline after the clenching task compared with the normal subjects, although an immediate increase after the clenching task was seen in all subjects. CONCLUSION: The results indicated that patients with masticatory myofascial pain have different muscle properties in the recovery phase after contraction, probably because of a slower intramuscular reperfusion.

Adult↗
PubMed1999

[Significance of exercise induced ST elevation in patient without a history of previous myocardial infarct].

UNLABELLED: Between 1980 and 1995, we observed twenty-five patients (22 males, 3 females) at the mean age of 50.6 +/- 13 years, without previous myocardial infarction who presented exercise induced ST elevation on a bicycle stress test. METHODS: Significant ST elevation was defined as a > or = 1 mm change present in > or = 1 lead measured 0.08 sec after the J point and in 3 consecutive beats. All patients have undergone coronary angiography in the days following the exercise test. RESULTS: Most of patients (56%) presented a history of typical angina that was either purely exertional (8 pts) or also occurred at rest (6 pts). Others (36%) had non typical angina or no angina (8%); 78% of pts were smokers. Sixteen patients (group I) had ST elevation during exercise (exercise duration: 7.6 +/- 4 min; peak heart rate: 135.5 +/- 29 batt/min; ST = 3.5 +/- 1.5 mm) and nine (group II) during the recovery phase (exercise duration 16.3 +/- 1.6 min; p < 0.05; peak heart rate 168 +/- 22 batt/min; p < 0.05; ST: 5.8 +/- 3 mm; p < 0.05). In group I, 1 patient had no vessel disease, 12 had one vessel disease, 3 had multivessel disease with 6 cases of hypersevere coronary stenose (> 90%). In group II, 4 patients had normal coronary arteries, there was one vessel coronary artery disease in 4 patients and multivessel in one subject, without hypersevere coronary stenosis. Correlation between anatomic location of stenosis and electrocardiographic ST elevation was excellent, particularly in case of single vessel disease (100%). All patients underwent one or more new exercise tests after therapeutic intervention (surgery n = 3; angioplasty n = 7; medical treatment n = 15), only 2 patients had persistent exercise induced ST elevation. During follow-up (5 +/- 3 years), 3 patients died (2 cardiac deaths) and 3 had recurrent angina controlled by new treatment. CONCLUSION: Exercise-induced ST elevation is a rare phenomenon in patients without prior myocardial infarction. When occurring purely during exercise, coronary lesions are frequent and often servere, in the other hand ST elevation of the recovery phase is frequently associate with normal arteries or less severe lesions. In most cases, revascularisation or medical therapy can abolish clinical and electrocardiographic abnormalities.

Adult↗
PubMed1994

[Serum granulocyte-colony stimulating factor (G-CSF) levels in elderly patients with infections].

To clarify the clinical role of granulocyte-colony stimulating factor (G-CSF), we examined the levels of serum G-CSF in elderly patients with infection (n = 48) and elderly normal volunteers (n = 32). G-CSF levels were significantly higher in patients in acute infectious status (571.9 +/- 782.9 pg/ml, mean +/- SD) than in normal volunteers (25.3 +/- 19.7 pg/ml). There was no significant relationship between serum G-CSF levels and age or granulocyte count in normal volunteers. In acute infectious status, there was no relationship between serum G-CSF levels and granulocyte count or c-reactive protein (CRP). We compared the response of G-CSF to infection between patients with frequently repeated infection (repeaters) and others (non-repeaters). Repeaters showed relative lower elevation of G-CSF levels in acute infectious status compared with non-repeaters (197.6 +/- 370.0 pg/ml vs. 1014.1 +/- 927.4 pg/ml p < 0.001). In other clinical data, serum albumin was significantly lower in repeaters than in non-repeaters. There was no significant difference in age, serum total protein, white blood cell count, granulocyte count and CRP. In non-repeaters, G-CSF levels was significantly higher in acute phase of infection than in recovery phase (550 +/- 703 pg/ml vs. 37.5 +/- 39.2 pg/ml p < 0.01 n = 15). We determined the status which showed incomplete recovery of infectious symptoms as chronic phase. In twenty-two of repeaters, we examined serum G-CSF levels and clinical data in acute and chronic phase of infection. There was no significant difference in G-CSF levels between in acute and chronic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Quantitative assessment of the effects of 'inodilators' on the myocardium in patients without primary cardiac insufficiency after coronary surgery: Part I--Amrinone.

The positive inotropic and peripheral vasodilating effect of amrinone has been measured in 20 patients without manifest cardiac insufficiency during the early (8-18 h postoperative) and late (18-48 h postoperative) recovery phase after coronary surgery. On conclusion of the surgical intervention first the aortocoronary bypass flow was compared during dobutamine and amrinone administration. It increased by 88% with amrinone and by 19% with dobutamine. Then a needle force probe was implanted in the myocardium. Directly measured local myocardial force increased not significantly by 3.5% after the first and by 5.1% after the second bolus injection of 2 mg/kg amrinone. The rate of myocardial contraction increased by 18.7% and 12%. The rate of relaxation decreased by 5.3% after the first and increased by 15% after the second injection. Mean pulmonary arterial pressure fell from 18.5 to 15.5 mmHg and from 19.7 to 17 mmHg. Cardiac output increased by 23% after the first and by 20% after the second injection. Heart rate rose from 88 to 99 bpm and from 86 to 94 bpm. Total peripheral resistance fell from 1,035 to 706 dyn*s*cm-5 and from 1,036 to 819 dyn*s*cm-5. The systolic arterial pressure fell from 132 to 116 mmHg after the first injection and did not change after the second injection. Amrinone was found to be a powerful peripheral vasodilator with a mild positive inotropic action. The variations in the effects between the early and late recovery phases mainly reflect a progressive haemodynamic stabilization with a decreasing tendency toward hypotensive disregulation. Careful consideration has to be paid to a properly balanced filling of the vascular system before administering amrinone.

Adult↗
PubMed1998

Myocardial metabolism studied during warm blood antero-retrograde reperfusion in ischaemic human hearts.

We propose modified warm blood antegrade-retrograde reperfusion (WBARR) of arrested hearts as a metabolic model with which to study substrate exchange and energy metabolism during the recovery phase after 90 min of ischaemia in man. Eleven anaesthetized patients undergoing aorto-coronary bypass were studied during WBARR. The protocol was designed as follows: period 1, a warm blood reperfusion with potassium (3 min); period 2, a warm blood reperfusion without potassium (2 min). The perfusion flow rate averaged 250+/-2 ml/min at the beginning of period 1 and 218+/-19 ml/min at the beginning and at the end of period 2; the perfusion was performed antegradely and retrogradely in the arrested hearts. Samples were simultaneously taken from the coronary venous sinus (CVS) and from the aortic root needle (AR). At the beginning of WBARR lactate release was 85+/-44 micromol/min and at the end it had significantly decreased to 21+/-99 micromol/min (P<0.03). Simultaneously, non-esterified fatty acids (NEFA) and beta-hydroxy-butyrate were initially released (71+/-61 and 22+/-66 micromol/min, respectively), while at the end of the WBARR there was an uptake of both NEFA (20+/-22 micromol/min; P<0.01) and beta-hydroxy-butyrate (12+/-35 micromol/min; P=0.290). Alanine, glycerol and branched chain amino acid balance across the heart did not significantly change. In summary after 90 min of ischaemia the heart energy metabolism is mainly anaerobic and based on glucose consumption, with lactate, NEFA and amino acids, which are mainly released. After 5 min of WBARR (recovery from ischaemia), lactate release is significantly reduced and NEFA becomes the energy supply of the heart. In conclusion, (1) WBARR is a valuable method with which to study myocardial metabolism in anaesthetized humans and may be combined with the use of tracers; (2) the study of myocardial metabolism in arrested hearts eliminates the imprecisions arising from the noncontinuous coronary blood flow; (3) NEFA become an important source of energy utilized by human hearts in the recovery phase from ischaemia.

Adult↗
PubMed2006

The relationship between heart rate recovery and heart rate variability in coronary artery disease.

BACKGROUND: Reduced heart rate recovery (HRR) in coronary artery disease (CAD) is predictive of increased cardiovascular mortality and is related to reduced parasympathetic tonus. OBJECTIVE: To investigate HRR and heart rate variability (HRV) measured at steady state condition and the relationship between these two parameters in CAD. MATERIALS AND METHODS: In our study, we enrolled 33 (28 males, mean age 52.4 +/- 9.6 years) patients with CAD who did not have heart failure, atrial fibrillation, pacemaker, and any disease state that could affect the autonomic functions and 38 age-matched healthy subjects (21 males, mean age 48.3 +/- 7.8 years). All the patients underwent submaximal treadmill exercise testing (Bruce protocol). HRR was calculated by subtracting the heart rate values at the 1st, 2nd, and 3rd minutes of the recovery phase from the peak heart rate (HRR(1), HRR(2), HRR(3)). Before exercise testing, short-term steady state HRV analyses of all subjects were obtained with the time- and frequency-domain methods and were correlated to HRR. For frequency-domain analysis, low-frequency HRV (LF, 0.004-0.15 Hz), high-frequency HRV (HF, 0.15-0.5 Hz), and LF/HF ratio were measured for 5 minutes in the morning. For time-domain analysis, standard deviation of the normal-to-normal NN intervals (SDNN), square root of the mean squared differences of successive N-N intervals (RMSSD), and proportion derived by dividing the number of interval differences of successive N-N intervals greater than 50 ms by the total number of N-N intervals (pNN50) were obtained. Only HRR(3) was used for the correlation analysis. RESULTS: In CAD groups, the HF, an indicator of parasympathetic activation, was significantly reduced, whereas the LF and LF/HF values, which are indicators of sympathetic activity, were increased (P = 0.0001 for each parameter). The time-domain parameters SDNN, RMSSD, and pNN50 were significantly reduced in the patient group (P = 0.0001, P = 0.009, and P = 0.0001, respectively). Similar to the HRV parameters, the HRR(1), HRR(2), and HRR(3) values were significantly reduced in the patient group (P = 0.0001 for each parameter). We observed a significant negative correlation between HRR(3) and LF (r =-0.67, P = 0.0001) and between HRR(3) and LF/HF (r =-0.62, P < 0.0001), while there was a significant positive correlation between HRR(3) and HF, SDNN, RMSSD, and pNN50 (r = 0.69, P = 0.0001; r = 0.41, P = 0.0001; r = 0.31, P = 0.008; and r = 0.44, P = 0.0001). CONCLUSIONS: HRR and HRV are significantly reduced in CAD. The reduction in HRR is parallel to the changes in HRV parameters. HRR, which can be measured easily in the recovery phase of exercise testing, can be used to detect the depression of parasympathetic tonus and to evaluate the basal autonomic balance in this patient group.

Case-Control Studies↗
PubMed2000

The intensive care unit as a trauma unit.

The ICU plays a pivotal role in the care of the critically injured patient. From the resuscitative phase of care through the life-support phases and finally the recovery phase, advances in ICU care have been made in recent years. As a result, an improved outcome for traumatically injured patients often is seen, and the third peak in the trimodal distribution of trauma deaths has been affected significantly.

Critical Care↗
PubMed2005

Recovery of phase inconsistencies in continuously moving table extended field of view magnetic resonance imaging acquisitions.

MR images formed using extended FOV continuously moving table data acquisition can have signal falloff and loss of lateral spatial resolution at localized, periodic positions along the direction of table motion. In this work we identify the origin of these artifacts and provide a means for correction. The artifacts are due to a mismatch of the phase of signals acquired from contiguous sampling fields of view and are most pronounced when the central k-space views are being sampled. Correction can be performed using the phase information from a periodically sampled central view to adjust the phase of all other views of that view cycle, making the net phase uniform across each axial plane. Results from experimental phantom and contrast-enhanced peripheral MRA studies show that the correction technique substantially eliminates the artifact for a variety of phase encode orders.

Artifacts↗
PubMedDate not supplied

Effects of fatiguing exercise on high-energy phosphates, force, and EMG: evidence for three phases of recovery.

Experiments were designed to evaluate the relative contribution of impulse propagation failure, high-energy phosphate depletion, lowered pH, and impaired excitation-contraction coupling to human muscle fatigue and recovery. 31P nuclear magnetic resonance spectroscopy measurements were made on adductor pollicis muscle, together with simultaneous measurements of M-wave, force, and rectified integrated EMG (RIEMG). During fatigue, maximum voluntary contraction force (MVC) fell by 90%, pH fell from 7.1 to 6.4, and phosphocreatine was almost totally depleted. Neuromuscular efficiency (NME = force/RIEMG) was reduced to 40% of control at the end of the fatiguing contraction, and the M wave was reduced in amplitude and prolonged in duration. Following exercise, the M wave returned to normal within 4 minutes. pH, high-energy phosphates, and MVC recovered within 20 minutes. By contrast, neuromuscular efficiency did not recover within 60 minutes. These findings indicate three different components of fatigue. The first is reflected by the altered M wave and indicates impaired muscle membrane excitation and impulse propagation. The second, associated with reduced MVC, correlates with the metabolic state of the muscle (PCr and pH). The third, indicated by reduced NME, is independent of changes in high-energy phosphates and pH and is probably due to impaired excitation-contraction coupling.

Adolescent↗
PubMed1998

Interleukin-10 reduces morbidity and mortality in murine multiple organ dysfunction syndrome (MODS).

HYPOTHESIS: IL-10 will reduce morbidity and mortality in murine MODS. Introduction. Intraperitoneal (ip) zymosan causes a triphasic inflammatory process leading to MODS. Phase I is an acute systemic inflammatory response to sterile peritonitis. Phase II is the recovery phase. Phase III is characterized by recurrent illness, progressive organ dysfunction, and elevated proinflammatory cytokines. METHODS: Male ICR mice were randomized (on Experiment Day 0, time = 0 h) into four initial groups (A-D): Control Group A received no zymosan and no IL-10. Group B received zymosan (1 mg/g mouse BW, t = 0) and no IL-10. Group C received no zymosan and IL-10 at t = 2 h. Group D received zymosan and IL-10 at t = 2 h. On Experiment Day 4, mice in Groups B-D were randomized into six further treatment groups (B1 and B2, C1 and C2, D1 and D2). Group B1 received no treatment. Group B2 received IL-10 when clinical signs of recurrent illness developed (Phase III, 12-18 days after zymosan treatment). Mice were sacrificed when they were preterminal (clinical signs of shaking, shivering, or paralysis) or on Experiment Day 28 (survivors). Plasma total bilirubin and creatinine levels were measures of organ function. Terminal pulmonary compliance was measured in situ through a physiologic range of tidal volumes. RESULTS: Mice entering Phase III consistently progressed to MODS characterized by elevated bilirubin and hemorrhagic lungs which, if left untreated, was lethal. Mice treated with IL-10 (Group B2) when they entered Phase III had lower mortality (28.6% vs 100%, P < 0.02), longer survival (25 vs 18 days, P < 0.05), and improved lung pulmonary compliance (slope beta1 = 0.082 ml/mm Hg vs 0.059 ml/mm Hg, P < 0.001) compared to untreated (Group B1) mice in Phase III. CONCLUSIONS: IL-10 improves survival even when given after clinical signs of illness are present.

Animals↗