Influence of arm position change from adduction to abduction on intracavitary electrocardiogram.

PURPOSE: The aim of this study is to evaluate the influence of arm movements from adduction to abduction on intracavitary electrocardiogram and the position of a catheter tip. METHODS: Overall, 192 peripherally inserted central catheter lines were placed under intracavitary electrocardiogram guidance and 188 of them were enrolled in the study. The catheter was first placed at a time point corresponding to the peak P wave with the arm in adduction. The arm was then abducted to 90° without changing catheter insertion length. During the procedure, basal electrocardiogram, intracavitary electrocardiogram, and radiographs with the arm in adduction and abduction were recorded. Amplitude wave changes and catheter movements were measured on electrocardiogram records and radiographs, respectively. RESULTS: In 188 cases, the P wave displayed typical changes, and 97.8% (184/188) catheters were successfully placed correctly. At the peak P wave, the amplitude of the peak P wave was 8.64 times greater than that of the basal P wave, and the P/R ratio was 0.61. When the arm was abducted to 90°, the amplitude of the P wave dropped to 57% of its peak, P/R decreased from 0.61 to 0.34, and the catheter tip moved cephalad 1.00 and 0.77 vertebral body units in male and female patients, respectively. CONCLUSION: Peripherally inserted central catheter moves toward the heart when the arm position changes from abduction to adduction. Peripherally inserted central catheter tip placement at the peak P wave with patient's arm in adduction is accurate and can prevent the catheter from advancing too low. R wave can function as a reference for observing P wave changes during peripherally inserted central catheter placement.

Doxorubicin induces apoptosis in H9c2 cardiomyocytes: role of overexpressed eukaryotic translation initiation factor 5A.

The cardiotoxicity of doxorubicin limits its clinical use in the treatment of a variety of solid tumors and malignant hematologic disease. Although the mechanism by which it causes cardiac injury is not yet known, apoptosis has been regarded as one of mechanisms underlying the cardiotoxic effects of doxorubicin. Eukaryotic translation initiation factor 5A (eIF5A) is a ubiquitously expressed multifunctional protein that interacts with a range of ligands and is implicated in cell signaling. However, there has been no direct evidence for the critical involvement of eIF5A in doxorubicin-induced apoptosis. Overexpression of eIF5A induced by doxorubicin in cardiomyocyte leads to growth perturbation along with initiation of apoptosis. Overexpression of eIF5A results in a gradual increase in reactive oxygen species (ROS) generation. This mitochondrial dysfunction is due to a gradual increase in ROS generation in eIF5A-overexpressing H9c2 cells. Along with ROS generation, increased Ca(2+) influx in mitochondria leads to loss of the mitochondrial transmembrane potential, release of cytochrome-c, and caspase activation. However, small interfering RNA (siRNA)-mediated suppression of eIF5A results in inhibition of apoptosis. Interestingly, upon overexpression of eIF5A induced by doxorubicin, cell apoptosis was shown to be significantly inhibited when cells were treated with SB202190 (p38 mitogen-activated protein kinase inhibitor) and SP600125 (anti-c-Jun N-terminal kinase inhibitor) for 18 h. The reduction in oxidant generation and reduction in the apoptotic cell population were the results of the disruption of eIF5A expression, corroborating the hypothesis that excess ROS generation with overexpression of eIF5A induced by doxorubicin leads to apoptosis due to the accumulation of eIF5A.

Proteomic adaptation to chronic high intensity swimming training in the rat heart.

Cardiac hypertrophy induced by exercise is associated with less cardiac fibrosis and better systolic and diastolic function, suggesting that the adaptive mechanisms may exist in exercise-induced hypertrophy. To identify molecular mechanisms by which exercise training stimulates this favorable phenotype, a proteomic approach was employed to detect rat cardiac proteins that were differentially expressed or modified after exercise training. Sixteen male Sprague-Dawley rats were divided into trained (T) and control(C). T rats underwent eight weeks of swimming training seven days/week, using a high intensity protocol. Hearts were used to generate 2-D electrophoretic proteome maps. Training significantly altered 23 protein spot intensities (P<0.05), including proteins associated with the mitochondria oxidative metabolism, such as prohibitin, malate dehydrogenase, short-chain acyl-CoA dehydrogenase, triosephosphate isomerase, electron transfer flavoprotein subunit beta, ndufa10 protein, ATP synthase subunit alpha and isocitrate dehydrogenase [NAD] subunit. Additionally, Prohibitin was increased in the exercise-induced hearts. Cytoskeletal, signal pathway, stress and oxidative proteins also increased within T groups. These results strongly support the notion that the observed changes in the expression of energy metabolism proteins resulted in a potential increase in the capacity to synthesise ATP, probably via mitochondrial oxidative metabolism. The observed changes in the expression of these metabolic and structural proteins induced by training may beneficially influence heart metabolism, stress response and signalling paths, and therefore improve the overall cardiac function.

Swimming training can affect intrinsic calcium current characteristics in rat myocardium.

Endurance exercise is widely assumed to improve cardiac function in humans, but the mechanisms involved in such changes are not clearly understood. The purpose of this study is to determine whether training elicits adaptations at the level of the L-type Ca(2+) channel. Sprague-Dawley rats performed swimming training at either moderate intensity (MOD) or high intensity (HIGH) during 8 weeks. The trained rats were studied by echocardiography and the whole-cell L-type Ca(2+) currents (I (Ca,L)) characteristics in a single cell were measured by standard whole-cell patch-clamp recording technique. Echocardiography showed that septal and posterior wall thickness in MOD and HIGH increased with the increased LV mass by 43 and 41%, respectively (P < 0.05). Training (P < 0.05) increased mean myocyte capacitance (approximately 38% in MOD and HIGH) and myocyte length (approximately 20% longer in MOD and 26% longer in HIGH), thus providing electrophysiological and morphological evidence that the training elicited LV cardiocyte hypertrophy. Mean peak I (Ca,L) was not different in three groups. However, whole-cell I (Ca,L) density was decreased in MOD and HIGH versus sedentary (P < 0.05), but there was no significant difference between MOD and HIGH. The present study provides the evidence of a training adaptation in intrinsic I (Ca,L) characteristics in ventricular myocardium, which demonstrates a remarkable adaptive plasticity of L-type channel characteristics in training rat heart.

[Assessment of cardiac structure and function by echocardiographic values for male Balb/c mice].

AIM: To assess the parameters of cardiac structure and function of male Balb/c mice by the echocardiography. METHODS: A total of 27 male Balb/c mice (from five to seven week old) were examined with a 13-MHz transthoracic linear-array transducer, hearts were removed from mice anesthetized with Nembutal, and the left ventricular (LV) mass were weighed. RESULTS: Complete 2-dimensional echocardiography for cardiac structure and function were obtained. Hemodynamic parameters were recorded. A correlation existed between LV weight (x) and echocardiographic LV mass (y) with the 2D) guided M-mode method: y = 1.15x + 3.26, (r = 0.80). CONCLUSION: Echocardiography appears to be a promising approach for noninvasively assessing LV mass and function in mice.