RÉSUMÉ
<p><b>OBJECTIVE</b>Exercise induced oscillatory ventilation (EIOB) during cardiopulmonary exercise testing (CPET) is associated with severity and prognosis of disease, but clinical approach for the character of EIOB due to circulatory dysfunction are seldom reported.</p><p><b>METHODS</b>This retrospective analysis of symptom-limited maximum CPET data with an increment of 10-20 W/min in 38 patients with CHF. We calculated the duration, frequency, amplitude and other parameters of EIOB.</p><p><b>RESULTS</b>There were 31 presenting with EIOB (82%) in all patients with CHF. In EIOB group, VE amplitude were (12.4 ± 4.4)L/min (accounting for 81% ± 30% of mean) and duration were (77.0 ± 20.0)s. The number of patients whose EIOB presenting at rest, exercise, recovery stage and the whole eriod were 24, 31, 4 and 4, respectively. Except VE, there were VO2, VCO2, RER and PETO2 presenting EIOB in all 31 patients; VE/VCO2, VO2/VE and breath frequency in 29 patients; PETCO2 in 26 patients; VT and VO2/HR in 25 patients; and HR in 2 patients.</p><p><b>CONCLUSION</b>EIOB may occur in any period of CPET, mostly in severe patient with CHF, and presenting in many variables. Due to it is resulted from the circulatory dysfunction, we should call it circulatory (cardiac) oscillatory breathing abnormality.</p>
Sujet(s)
Humains , Épreuve d'effort , Défaillance cardiaque , Consommation d'oxygène , Phénomènes physiologiques respiratoires , Études rétrospectivesRÉSUMÉ
<p><b>OBJECTIVE</b>This study aimed to investigate the feature of D(L)CO (Diffusion Lung Capacity for Carbon Monoxide) in CHF (left ventricular heart failure) patients, underlying pathophysiological mechanism and clinical significance.</p><p><b>METHODS</b>We retrospectively studied the D(L)CO, pulmonary ventilation function, cardiopulmonary exercise testing and related clinical information in severer HF patients.</p><p><b>RESULTS</b>Peak VO2 severely decreased to 34 ± 7 percentage of predicted(%pred) and anaerobic threshold to 48 ± 11%pred in all patients. D(L)CO moderately decreased to 63 ± 12%pred and there were 25 patients lower than 80%pred. FVC, FEV1, FEV1/FVC and TLC were 75 ± 14%pred, 71 ± 17%pred, 97 ± 11%pred, and 79 ± 13%pred, which indicated borderline or mild restrictive ventilatory dysfunction. The decrease of D(L)CO was more severe than those of TLC, FEV1 and FVC.</p><p><b>CONCLUSION</b>For patients with severe CHF, cardiopulmonary exercise function is extremely limited, D(L)CO generally moderately declines and ventilation function is merely mildly limited. D(L)CO is the parameter for cardiopulmonary coupling, reflecting limitation of the cardiovascular dysfunction while without ventilatory limit.</p>
Sujet(s)
Humains , Gazométrie sanguine , Défaillance cardiaque , Tests de la fonction respiratoire , Études rétrospectives , Dysfonction ventriculaire gaucheRÉSUMÉ
<p><b>OBJECTIVE</b>The aim of this study is to investigate the occurrence and mechanism of Cheyne-Stokes breathing pattern in patients with heart failure.</p><p><b>METHODS</b>Fifty-six patients who performed polusomnography sleep testing at National Center of Cardiovascular Diseases Fuwai Hospital from March to May in 2015. We divided them into chronic heart failure (CHF) group and non-CHF group.</p><p><b>RESULTS</b>The occurrences of sleep apnea in two groups were high. In CHF group (n = 11) , there were 10 patients with apnea hypopnea index (AHI) > 5; and their AHI was 23.93 ±14.63. In non-CHF group (n = 45), there were 33 patients whose AHI > 5; and their AHI was 16.20 ± 18.76. The ratio of center sleep apnea to all gross sleep apnea ratio in CHF group was higher than that in non-CHF group (80.21% ± 30.55% vs 27.16% ± 35.71%, P < 0.01 ).</p><p><b>CONCLUSION</b>Based upon the new theory of holistic integrative physiology and medicine, we explain the mechanism of circulatory dysfunction induce the oscillation breathing in patients with CHF. The sleep apnea and C-S respiration in CHF should be called circulatory sleep apnea, rather than central sleep apnea.</p>
Sujet(s)
Humains , Respiration de Cheyne Stokes , Maladie chronique , Défaillance cardiaque , Polysomnographie , Syndromes d'apnées du sommeil , Apnée centrale du sommeilRÉSUMÉ
<p><b>OBJECTIVE</b>We investigate the magnitudes of waveform changes of arterial blood gas (ABG) in patients with heart failure.</p><p><b>METHODS</b>Five patients with heart failure were selected, continuous collecting radial artery blood and measured PaO2, PaCO2, pHa and Sao2. We selected two typical breaths cycles of waveform changes of ABG from each patient for data analysis. Comparison of the adjacent highest and lowest values to verify the presence of a periodic waveform changes of ABG, and in addition, we used t test to analysis the range of waveform changes of ABG in patients with heart failure and patients with normal cardiac function and compared whether the difference between them.</p><p><b>RESULTS</b>The 5 patients (2 surgical and 3 ICU) with heart failure, were 4 male and 1 female, (69 ± 7)year, (169 ± 10) cm, (75 ± 19)kg, LVEF = (38 ± 3)%. The heart beat numbers for full blood into the blood sampling pipe were 17 ± 2, and all covered more than 2 breath cycles. There were significant changes of PaO2, PaCO2, [H+]a and SaO2 (P < 0.05). The magnitudes of changing PaO2, PaCO2, [H+]a and Sao2 were (7.94 ± 2.02)mmHg, (1.18 ± 0.56)mmHg, (0.54 ± 0.17)nmol/L and (0.21 ± 0.07)%, and they were (6.1 ± 1.5)%, (3.2 ± 1.5)%, (1.5 ± 0.5)% and (0.2 ± 0.1)% from their mean respectively. Even these magnitudes fo all ABG parameters were trendily lower than those of patients with normal cardiac function, but only PaO2 and [H+]a were significant (P < 0.05).</p><p><b>CONCLUSION</b>Using this simple continuous beat-by-beat arterial blood sampling method, we obtained a clear evidence of periodic waveform of ABG parameters following by breath cycle in patients with heart failure, but the magnitude trendily be decreased.</p>
Sujet(s)
Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Gazométrie sanguine , Maladies cardiovasculaires , Défaillance cardiaque , Rythme cardiaque , Monitorage physiologique , MéthodesRÉSUMÉ
<p><b>OBJECTIVE</b>Since 2011 EB-APS conference, we hypotheses that phase switching of inspiration-expiration is dominantly initiated by oscillatory information PaO2, PaCO2 and [H+] via fast peripheral chemical receptors. However, the evidence of the waveform of ABG is lack.</p><p><b>METHODS</b>Six surgery patients with normal heart function and negative Allen test, had been placed the arterial catheterization directly connected to 3 x 1 000 mm pre-heparin plastic pipe for continuous collecting arterial blood. We counted the number of heart beat for the blood collecting time, and separated the blood pipe into the heart beat numbers' short pieces using haemostatic forceps, then put pipe into iced water at once fir analyzing PaO2, PaCO2, pH and SaO2 as soon as possible. We selected two breaths cycles of waveform from each patient for data calculations of magnitudes and time interval.</p><p><b>RESULTS</b>The heart beat numbers for filling blood into pipe were 16 ± 2, and all covered more than 2 breathing cycles. Each breathing cycle is cover 5 ± 0.6 heart beat. There were significant changes of PaO2, PaCO2, [H+] a and SaO2 (i.e. the highest high values compare to the next lowest values, P < 0.05). The time interval of changing PaO2, PaCO2, [H+]a and SaO2 magnitudes were 11.28 ± 1.13 mmHg, 1.77 ± 0.89 mmHg, 1.14 ± 0.35 nmol/L and 0.52% ± 0.44% respectively.</p><p><b>CONCLUSION</b>This simple continuous beat-by-beat arterial blood sampling and ABG analyzing method is new and practicable. We obtain a clear evidence of periodic parameters ABG waveform, which following breathing cycle.</p>
Sujet(s)
Humains , Artères , Physiologie , Gazométrie sanguine , Rythme cardiaque , Monitorage physiologique , Méthodes , RespirationRÉSUMÉ
<p><b>OBJECTIVE</b>To examine the expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1, VEGFR2) in transdifferentiated human proximal tubular epithelial (HK-2) cell induced by transforming growth factor beta1 (TGFbeta1).</p><p><b>METHODS</b>The transdifferentiation of HK-2 cells was detected by evaluation of expression of alpha-SMA by cytoimmunochemistry and RT-PCR. The VEGF mRNA was evaluated with RT-PCR. The secreted VEGF in the culture media was measured with ELISA. The cellular VEGF, VEGFR1, and VEGFR2 were measured with Western blot.</p><p><b>RESULTS</b>The immunostain of alpha-SMA were positive in HK-2 cell induced by TGFbeta1 at the concentration of 5 and 8 ng/ml for 72 h. The expression of alpha-SMA mRNA was induced by TGFbeta1 in concentration- and time-dependent manners. The expressions of mRNA and protein of VEGF were upregulated by TGFbeta1 at the concentration of 0.1 and 1 ng/ml for 72 h and at the concentration of 8 ng/ml for 12 h and 24 h when compared with the control. But expressions of mRNA and protein of VEGF were downregulated by TGFbeta1 at the concentration of 3, 5, and 8 ng/ml for 72 h and at the concentration of 8 ng/ml for 36, 48, and 72 h, respectively. Meanwhile, Protein levels of VEGFR1 and VEGFR2 were upregulated by TGFbeta1 in concentration- and time- dependent manners.</p><p><b>CONCLUSIONS</b>Increased expression of VEGFR1 and VEGFR2 and two-phase change in VEGF expression occurred in the process of tubular epithelial transdifferentiation induced by TGFbeta1. Reduced expression of VEGF may contribute to tubular epithelial transdifferentiation in a vicious circle.</p>
Sujet(s)
Humains , Différenciation cellulaire , Cellules épithéliales , Biologie cellulaire , Tubules contournés proximaux , Biologie cellulaire , ARN messager , Métabolisme , Récepteurs aux facteurs de croissance endothéliale vasculaire , Métabolisme , Facteur de croissance transformant bêta , Pharmacologie , Facteur de croissance transformant bêta-1 , Facteur de croissance endothéliale vasculaire de type A , Métabolisme , Récepteur-1 au facteur croissance endothéliale vasculaire , Métabolisme , Récepteur-2 au facteur croissance endothéliale vasculaire , MétabolismeRÉSUMÉ
<p><b>OBJECTIVE</b>To observe the effect of bone morphogenetic protein-7 (BMP-7) on the transdifferentiation of cultured human tubular epithelial cell (HKC) induced by TGF-beta1 and to elucidate its possible mechanism.</p><p><b>METHODS</b>The cultured HKC cells were divided into 5 groups: serum-free group (negative control); single TGF-beta1 treated group (positive control); single BMP-7 treated group; combined TGF-beta1 and BMP-7 treated group; and BMP-7 pre-treated group. Expression of keratin of HKC cells was assessed by indirect enzyme immunohistochemistry (IEI), expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin by immunohistological method, percentage of alpha-SMA positive HKC cells by flow cytometry, and mRNA expression of alpha-SMA, TGF-beta1, and TGF-beta type II receptor by reverse transcription PCR.</p><p><b>RESULTS</b>The expression of alpha-SMA and the percentage of alpha-SMA positive HKC cells markedly increased after having been treated by TGF-beta1 while the expression of E-cadherin and keratin decreased. In the group pre-treated with BMP-7 (50 ng/ml) and then added with TGF-beta1 (8 ng/ml), expression of alpha-SMA was significantly lower than in the positive control group, while expression of E-cadherin and keratin significantly higher than in the positive control group. Measurement of the percentage of alpha-SMA positive HKC found significant deference between the combined TGF-beta1 and BMP-7 treated group and the positive control group (9.7% vs 19.8%; 5.8% vs 19.8%; P < 0.05). Significant difference existed between the BMP-7 (50 ng/ml) pre-treated group and the positive control group (8.7% vs 19.8%, P < 0.05). mRNA expression of alpha-SMA was measured by RT-PCR and the results showed that it significantly decreased in the group treated or pre-treated with BMP-7 (50 ng/ml) (15% and 12% of the results in the positive control group, respectively). The mRNA expression levels of both TGF-beta1 and its type II receptor significantly decreased (28% and 19%; 47% and 36%, compared with the positive control group, respectively).</p><p><b>CONCLUSION</b>Transdifferentiation of cultured renal epithelial cell induced by TGF-beta1 can be inhibittd by certain levels of BMP-7, cultured together with TGF-beta1 or pretreated. BMP-7 can prevent and inhibit the mRNA expression of TGF-beta1 and its type II receptor, which may be an important mechanism by which BMP-7 inhibit the transdifferentiation of renal tubular epithelial cell.</p>