profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the ␤-adrenergic and renin-angiotensin systems. Am J Physiol Heart Circ Physiol 296: H669 -H677, 2009. First published December 26, 2008 doi:10.1152/ajpheart.01046.2008.-Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV), which results in dilation, eccentric hypertrophy, and eventually loss of function. Little is known about the impact of AR on LV gene expression. We, therefore, conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically upregulated and 29 that were downregulated out of 21,910 genes after 2 wk. Of the upregulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after 2 wk persisted in the chronic phase (after 6 and 12 mo) and found that it did persist. Knowing that the adrenergic and renin-angiotensin systems are overactivated in our animal model, we were interested to see if blocking those systems using metoprolol (25 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) and captopril (100 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) would alter the expression of some upregulated LV genes in AR rats after 6 mo. By qRT-PCR, we observed that upregulations of LV mRNA levels encoding for procollagens type I and III, fibronectin, atrial natriuretic peptide, transforming growth factor-␤2, and connective tissue growth factor were totally or partially reversed by this treatment. These observations provide a molecular rationale for a medical strategy aiming these systems in the medical treatment of AR and expand the paradigm in the study of this form of LV volume overload. heart hypertrophy; gene expression; renin-angiotensin system; adrenergic system SEVERE AORTIC VALVE REGURGITATION (AR) is associated with a long asymptomatic period during which the left ventricle (LV) progressively dilates and hypertrophies in response to a chronic volume overload. This process is accompanied by a decrease in LV function, occurrence of symptoms, and eventually heart failure (4, 7). No drug has yet been clearly shown in humans to be effective to slow LV dilation, hypertrophy, and loss of systolic function or to have any impact on morbidity or mortality in chronic AR (5, 15).At the microscopic level, AR is associated with cardiomyocyte elongation and excessive but mostly noncollagen myocardial fibrosis (fibronectin) (6, 23). Although gene expression profiling in LV eccentric hypertrophy resulting from volume overload has been studied recently in an aortocaval fistula rat model (25), very little is known about the mechanisms of LV hypertrophy and extracellular matrix (ECM) remodeling associated with a more clinically common form of LV volume overload, namely AR. Aortocaval fistula models relate to a clinically rather rare complication of aortic aneurysm or secondary to abdominal trauma in humans (21). Moreover, aortocaval ...

BACKGROUND: Protective ventilation implementation requires the calculation of predicted body weight (PBW), determined by a formula based on gender and height. Consequently, height inaccuracy may be a limiting factor to correctly set tidal volumes. The objective of this study was to evaluate the accuracy of different methods in measuring heights in mechanically ventilated patients. METHODS: Before cardiac surgery, actual height was measured with a height gauge while subjects were standing upright (reference method); the height was also estimated by alternative methods based on lower leg and forearm measurements. After cardiac surgery, upon ICU admission, a subject's height was visually estimated by a clinician and then measured with a tape measure while the subject was supine and undergoing mechanical ventilation. RESULTS: One hundred subjects (75 men, 25 women) were prospectively included. Mean PBW was 61.0 ؎ 9.7 kg, and mean actual weight was 30.3% higher. In comparison with the reference method, estimating the height visually and using the tape measure were less accurate than both lower leg and forearm measurements. Errors above 10% in calculating the PBW were present in 25 and 40 subjects when the tape measure or visual estimation of height was used in the formula, respectively. With lower leg and forearm measurements, 15 subjects had errors above 10% (P < .001). CONCLUSIONS: Our results demonstrate that significant variability exists between the different methods used to measure height in bedridden patients on mechanical ventilation. Alternative methods based on lower leg and forearm measurements are potentially interesting solutions to facilitate the accurate application of protective ventilation.

Protective ventilation with low tidal volume has been shown to reduce morbidity and mortality in patients suffering from acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Low tidal volume ventilation is associated with particular clinical challenges and is therefore often underutilized as a therapeutic option in clinical practice. Despite some potential difficulties, data have been published examining the application of protective ventilation in patients without lung injury. We will briefly review the physiologic rationale for low tidal volume ventilation and explore the current evidence for protective ventilation in patients without lung injury. In addition, we will explore some of the potential reasons for its underuse and provide strategies to overcome some of the associated clinical challenges.

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