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1.
Tamion F Le Cam-Duchez V Menard JF Girault C Coquerel A Bonmarchand G 《Critical care (London, England)》2004,8(5):R328-R335
Introduction
During sepsis the endocrine, immune and nervous systems elaborate a multitude of biological responses. Little is known regarding the mechanisms responsible for the final circulating erythropoietin (EPO) and renin levels in septic shock. The aim of the present study was to assess the role of EPO and renin as biological markers in patients with septic shock.Methods
A total of 44 critically ill patients with septic shock were evaluated.Results
Nonsurvivors had significantly higher serum EPO levels than did survivors on admission (median [minimum–maximum]; 61 [10–602] versus 20 [5–369]). A negative relationship between serum EPO and blood haemoglobin concentrations was observed in the survivor group (r = -0.61; P < 0.001). In contrast, in the nonsurvivors the serum EPO concentration was independent of the blood haemoglobin concentration. Furthermore, we observed significant relationships between EPO concentration and lactate (r = 0.5; P < 0.001), arterial oxygen tension/fractional inspired oxygen ratio (r = -0.41; P < 0.005), arterial pH (r = -0.58; P < 0.001) and renin concentration (r = 0.42; P < 0.005). With regard to renin concentration, significant correlations with lactate (r = 0.52; P < 0.001) and arterial pH (r = -0.33; P < 0.05) were observed.Conclusion
Our findings show that EPO and renin concentrations increased in patients admitted to the intensive care unit with septic shock. Renin may be a significant mediator of EPO upregulation in patients with septic shock. Further studies regarding the regulation of EPO expression are clearly warranted.2.
3.
Abergel E Chatellier G Hagege AA Oblak A Linhart A Ducardonnet A Menard J 《Journal of the American College of Cardiology》2004,44(1):144-149
OBJECTIVES: The purpose of this research was to study long-term left ventricular (LV) adaptations in very-high-level endurance athletes. BACKGROUND: Knowledge of cardiac changes in athletes, who are at particularly high risk of sudden cardiac death, is mandatory to detect hypertrophic cardiomyopathy (HCM) or dilated (DCM) cardiomyopathy. METHODS: We carried out echocardiographic examinations on 286 cyclists (group A) and 52 matched sedentary volunteers (group C); 148 cyclists participated in the 1995 "Tour de France" race (group A1), 138 in the 1998 race (group A2), and 37 in both (group B). RESULTS: In groups A, A1, A2, and C, respectively, diastolic left ventricular diameter (LVID) was 60.1 +/- 3.9 mm, 59.2 +/- 3.8 mm, 61.0 +/- 3.9 mm, and 49.0 +/- 4.3 mm (A vs. C and A1 vs. A2, p < 0.0001), and maximal wall thickness (WT) was 11.1 +/- 1.3 mm, 11.6 +/- 1.3 mm, 10.6 +/- 1.1 mm, and 8.6 +/- 1.0 mm (A vs. C and A1 vs. A2, p < 0.0001). Among group A, 147 (51.4%) had LVID >60 mm; 17 of them had also a below normal (<52%) left ventricular ejection fraction (LVEF). Wall thickness exceeded 13 mm in 25 athletes (8.7%) (always <15 mm), 23 with LVID >55 mm. In group B, LVID increased (58.3 +/- 4.8 mm to 60.3 +/- 4.2 mm, p < 0.001) and WT decreased (11.8 +/- 1.2 mm to 10.8 +/- 1.2 mm, p < 0.001) with time. CONCLUSIONS: Over one-half of these athletes exhibited unusual LV dilation, along with a reduced LVEF in 11.6% (17 of 147), compatible with the diagnosis of DCM. Increased WT was less common (always <15 mm) and scarce without LV dilation (<1%), eliminating the diagnosis of HCM. Serial examinations showed evidence of further LV dilation along with wall thinning. These results might have important implications for screening in athletes. 相似文献
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7.
Alan Y. Deng Julie-Émilie Huot-Marchard Denis deBlois Eric Thorin Cristina Chauvet Annie Menard 《The Canadian journal of cardiology》2019,35(5):661-670
Background
Multiple quantitative trait loci for blood pressure (BP) have been localized throughout human and rodent genomes. Few of them have been functionally identified especially in humans, and little is known about their pathogenic directionality when identified. We focused on Chrm3 encoding the muscarinic cholinergic receptor 3 (M3R) as the causal gene for C17QTL1 in the Dahl salt-sensitive rat model.Methods and Results
Congenic knock-ins, gene-specific knockout, and ex vivo and in vivo function studies were applied in the Dahl salt-sensitive rat model of polygenic hypertension. A Chrm3 missense T1667C mutation in the last intracellular domain functionally correlated with a rise in BP increased the M3R signalling and resensitization, and adrenal epinephrogenesis. Gene targeting that abolished the M3R function without affecting any of noncoding Chrm3 variants caused a decrease in BP, indicating that the M3R-mediated signalling promotes hypertension. In contrast, removing 8 amino acids from the M3R first extracellular loop had no effect on BP.Conclusions
The M3R-specialized signalling constitutes a new pathway of hypertension pathogenesis within the context of a polygenic and quantitative trait. Increased epinephrine in the circulation and secreted from the adrenal glands are suggestive of a molecular mechanism partially mediating M3R to promote hypertension. The structure-function relationships for various M3R domains in their effects on BP pave the way for identifying missense mutations that impact functions on BP as potential diagnostic targets. 相似文献8.
9.
M R Menard A M Penn J W Lee L A Dusik L D Hall 《Archives of physical medicine and rehabilitation》1991,72(12):976-983
To determine the relative metabolic efficiency (metabolic energy used per unit of mechanical energy output) of negative to positive muscular power, we used 31P magnetic resonance spectroscopy to monitor the cellular energy metabolism of limb muscles in eight healthy subjects during a nonfatiguing, mixed concentric-eccentric activity and during its concentric and eccentric components. We also studied isometric contractions. We found that in terms of the flow of metabolic energy through the muscle cells, the cost of concentric exercise at this intensity was proportional to the mechanical power generated, but the cost of eccentric and isometric exercise did not increase significantly as the apparent intensity of the exercise increased over the range studied. Although the pattern was similar in all subjects, the quantitative relationship between metabolic cost and mechanical output was different in subjects with different muscular strength. The qualitative results can be explained in the context of the known biochemistry and biophysics of the cellular contractile apparatus (sliding filament theory, with independent force generators). 相似文献
10.
Effect of antihypertensive treatment on the left ventricular isomyosin profile in one-clip, two kidney hypertensive rats 总被引:1,自引:0,他引:1
J C Dussaule J B Michel C Auzan K Schwartz P Corvol J Menard 《The Journal of pharmacology and experimental therapeutics》1986,236(2):512-518
In order to investigate the cardiac effects of antihypertensive therapies in one-clip two-kidney hypertension in rats, we compared the consequences on myosin isoenzyme profile and on left ventricular hypertrophy of two treatments: one was a new converting enzyme inhibitor (S9490), the second a more standard tripletherapy associating clonidine, dihydralazine and furosemide. The two treatments were initiated 4 weeks after clipping and administered during 5 weeks. During the treatment period average systolic blood pressure was 215 +/- 32 mmHg in the hypertensive untreated group (HC2, n = 12) and 144 +/- 13 mm Hg in the CEI group (HT1, n = 13), which is not significantly different from the value found in the sham-operated group (139 +/- 4 mm Hg, C2, n = 13). Blood pressure was lowered only to 173 +/- 18 mm Hg in the group treated with tripletherapy (HT2, n = 12). The left ventricular weight decreased significantly in the CEI-treated group toward values similar to those of the sham-operated animals (2.2 +/- 0.13 mg/g vs. 1.9 +/- 10 mg/g, respectively NS), whereas it did not change in the tripletherapy group when compared to the untreated hypertensive animals despite the fall in blood pressure. In the hypertensive untreated rats the percentage of V1 isoenzyme of cardiac myosin was lower than in the sham-operated group (42.8 +/- 9.0% vs. 57.5 +/- 7.6% P less than .001). In parallel the V3 form of cardiac myosin increased (24.1 +/- 7.4% vs. 15.7 +/- 4.3%, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献