PubMed Health⌕ Search

Biomedical subjects

David W Rodenbaugh

Publications and source records attributed to David W Rodenbaugh.

9 recordsLinked to original sources
PubMed2006

Spinal cord injury alters cardiac electrophysiology and increases the susceptibility to ventricular arrhythmias.

The autonomic nervous system modulates cardiac electrophysiology and abnormalities of autonomic function are known to increase the risk of ventricular arrhythmias. The abnormal and unstable autonomic control of the cardiovascular system following spinal cord injury also is well known. For example, individuals with mid-thoracic spinal cord injury have elevated resting heart rates, increased blood pressure variability, episodic bouts of life-threatening hypertension as part of a condition termed autonomic dysreflexia, and elevated sympathetic activity above the level of the lesion. Furthermore, cardiovascular morbidity and mortality are high in individuals with spinal cord injuries due to a relatively sedentary lifestyle and higher prevalence of other cardiovascular risk factors, including obesity and diabetes. Therefore, spinal cord injury may alter cardiac electrophysiology and increase the risk for ventricular arrhythmias. In this chapter, we discuss how the autonomic changes associated with cord injury can influence cardiac electrophysiology and the susceptibility to ventricular arrhythmias.

Animals↗
PubMed2003

Paraplegia differentially increases arterial blood pressure related cardiovascular disease risk factors in normotensive and hypertensive rats.

Older individuals (>50 years of age) are increasingly sustaining spinal cord injuries (SCI) and often have pre-existing medical conditions, including hypertension. Furthermore, the life expectancy of individuals with paraplegia has increased to near that of able-bodied individuals. Thus, chronic diseases associated with aging (e.g. hypertension) are increasing in this population. We tested the hypothesis that paraplegia differentially increases blood pressure related cardiovascular disease (BP-CVD) risk factors in normotensive (Wistar Kyoto rat, WKY) and spontaneously hypertensive rats (SHR). To test this hypothesis, intact and paraplegic SHR and WKY rats were chronically instrumented for recording BP-CVD risk factors over 7 weeks. Paraplegia in both the SHR and WKY rats increased heart rates (27 and 22% in SHR and WKY, respectively), heart rate loads (425 and 323% in SHR and WKY, respectively), the standard deviation of systolic (15 and 23% in SHR and WKY, respectively) and diastolic blood pressure (15 and 13% in SHR and WKY, respectively) and reduced activity (-70 and -57% in SHR and WKY, respectively). Paraplegia in the WKY rats reduced systolic (-4%) and diastolic (-5%) blood pressures while systolic and diastolic loads were not significantly different. In sharp contrast, paraplegia in the SHR increased systolic (6%) and diastolic (5%) blood pressures as well as systolic (41%) and diastolic loads (9%). These data demonstrate that paraplegia increased BP-CVD risk factors in normotensive and hypertensive rats. Importantly, the impact of paraplegia on BP-CVD risk factors was greater in the SHR.

Animals↗
PubMed2003

Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact (n = 10) and paraplegic (n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact (n = 8) and paraplegic (n = 8) rats. Paraplegia significantly (P < 0.05) reduced AV interval (-25%), sinus cycle length (-24%), SNRT (-28%), cSNRT (-53%), WCL (-19%), and the electrical stimulation threshold to induce ventricular arrhythmia (-48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (-28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.

Animals↗
PubMed2003

Student retention of course content is improved by collaborative-group testing.

We recently reported that collaborative testing (i.e., group test taking) increased student performance on quizzes. It is unknown, however, whether collaborative testing improves student retention of course content. Therefore, this study was designed to test the hypotheses that collaborative-group testing improves student retention of course content. To test this hypothesis, our undergraduate exercise physiology class of 38 students was randomly divided into two groups: group A (n = 19) and group B (n = 19). During exam 1, students from both groups answered questions in the traditional format as individuals. Immediately after completing the exam as individuals, students from group A answered a randomly selected subset of questions from exam 1 in groups of two (1 group had 3 students) to test the effectiveness of collaborative-group testing on test performance and level of student retention. On the next exam (exam 2, 4 wk later), students from both groups answered questions in the traditional format as individuals and responded to the same subset of questions from exam 1. The subset of questions was analyzed to determine the level of retention of the original test material. In addition, immediately after completing the exam as individuals, students from group B answered a randomly selected subset of questions from exam 2 in groups of two (1 group had 3 students). Finally, on the next exam (exam 3, 4 wk later), students from both groups answered questions in the traditional format as individuals and responded to the same subset of questions from exam 2. This protocol followed a randomized crossover design to control for time and order effects. Student retention of course content was reduced when students completed the original examinations individually. In sharp contrast, student retention was improved (P < 0.05) when students completed the original examinations in groups. Results suggest that collaborative testing is an effective strategy to enhance learning and increase student retention of course content.

Cooperative Behavior↗
PubMed2002

Daily exercise normalizes the number of diaphorase (NOS) positive neurons in the hypothalamus of hypertensive rats.

It is well known that nitric oxide (NO), within the paraventricular nucleus (PVN) of the hypothalamus, mediates sympatho-inhibition via an inhibitory GABA-ergic mechanism. Furthermore, the inhibitory GABA-ergic mechanism is impaired in the spontaneously hypertensive rat (SHR). These data suggest that the NO system, within the PVN, may also be impaired in the SHR. In addition, previous studies have documented that daily exercise attenuates the development of tachycardia, hypertension and blood pressure related cardiovascular disease risk factors in SHR. These data suggest that daily exercise enhances the inhibitory GABA-ergic and/or NO systems. Therefore, this study was designed to test the hypothesis that hypertension, in the SHR, is associated with a lower number of NADPH-diaphorase (a commonly used marker for neuronal NOS activity) positive neurons within the PVN and that daily exercise increases the number of NOS positive neurons. Using a standard histochemical protocol, NOS positive neurons were measured in the PVN, supraoptic nucleus, median preoptic area, lateral hypothalamus, nucleus of the tractus solitarius and rostral ventrolateral medulla. Results document that SHR have significantly fewer NOS-positive neurons in the PVN than their genetic control, the Wistar-Kyoto (WKY) rats (110+/-11 versus 139+/-17). Furthermore, daily exercise increased the number of NOS positive neurons in the SHR to levels seen in the WKY rats. These data demonstrate that hypertension, in the SHR, is associated with a lower number of NOS positive neurons within the PVN and that daily exercise increases the number of NOS positive neurons within the PVN.

Animals↗