Search PubMed⌕ Search

Biomedical subjects

Heidi L Collins

Publications and source records attributed to Heidi L Collins.

15 recordsLinked to original sources
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↗
PubMed2002

Insulin suppression of VLDL apo B secretion is not mediated by the LDL receptor.

Insulin inhibits hepatic very low density lipoprotein (VLDL) apo B secretion in rats. Current studies test whether the insulin effect is LDL receptor-mediated by examining the effect of insulin on VLDL apo B secretion in hepatocytes derived from Ldlr-/- and control mice. Primary hepatocytes were incubated overnight with media containing 14C-leucine and either 0.1nM (basal) or 200nM insulin. Afterwards, secreted VLDL B100 and B48 were quantitated. Insulin reduced 14C-labeled B100 and B48 comparably in control and Ldlr-/- hepatocytes with a 62+/-12% vs. 59+/-12% decrease in B100, and a 56+/-11% vs. 61+/-9% decrease in B48. Results indicate: (1) mouse hepatocytes respond to insulin by reducing VLDL apo B output; (2) both VLDL B100 and B48 secretion are suppressed; and (3) insulin inhibition of VLDL apo B secretion is retained in Ldlr-/- hepatocytes.

Animals↗
PubMed2002

"Survivor" torches "Who Wants to Be a Physician?" in the educational games ratings war.

We recently developed an educational game for reviewing respiratory physiology in a large classroom. The "Who Wants to be a Physician?" game encouraged medical students to be active participants in the learning process. An evaluation of the game documented that students enjoyed the active format, and the students reported that the game enhanced their ability to understand and retain information. However, the evaluation also revealed that the game had limitations. Specifically, the students recommended the use of multiple-choice questions to match the Medical Board Examination format and to speed up the game (i.e., cover more topics). The students also wanted to increase their level of participation and interaction. Finally, we wanted to emphasize the benefits of peer instruction as a collaborative learning tool. To address these limitations, we designed a new game, "Survivor." Survivor incorporated multiple-choice questions and emphasized peer instruction and a capacity to gather information and solve novel problems. In addition, participation was increased by including the student audience in the game. Finally, an evaluation instrument was utilized to assess the effectiveness of this instructional tool in an academic setting. As a result of these improvements, the evaluation documents that the newly developed tool is a more effective educational game that couples fun and creative excitement with proven and effective educational concepts.

Computer-Assisted Instruction↗
PubMed2002

Collaborative testing enhances student learning.

Examinations and quizzes should be used as learning as well as assessment tools. To achieve this goal, an assessment procedure was developed to enhance as well as assess student learning. Students were tested on four different topics of cardiovascular physiology. Each topic was tested by a different type of quiz (fill in the blanks, single best response multiple choice, short essay, or true/false). The students first completed a quiz individually. Once the quiz was completed individually, the students completed the same quiz in groups. Eighty percent of the score on the quiz was based on the individual results, and 20% of the score on the quiz was based on the group results. The performance on the quizzes was significantly higher (P < 0.001) when students completed the quizzes in groups than when they completed the quizzes individually. Results document that completing the quizzes in groups enhances the understanding of the material. In addition, students rated this format superior to the traditional method.

Cardiovascular Physiological Phenomena↗
PubMed2002

Muscle metaboreflex control of coronary blood flow.

We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF) and vascular conductance (CVC) in conscious, chronically instrumented dogs during treadmill exercise ranging from mild to severe workloads. Metaboreflex responses were also observed during mild exercise with constant heart rate (HR) of 225 beats/min and beta(1)-adrenergic receptor blockade to attenuate the substantial reflex increases in cardiac work. The muscle metaboreflex was activated via graded partial occlusion of hindlimb blood flow. During mild exercise, with muscle metaboreflex activation, hindlimb ischemia elicited significant reflex increases in mean arterial pressure (MAP), HR, and cardiac output (CO) (+39.0 +/- 5.2 mmHg, +29.9 +/- 7.7 beats/min, and +2.0 +/- 0.4 l/min, respectively; all changes, P < 0.05). CBF increased from 51.9 +/- 4.3 to 88.5 +/- 6.6 ml/min, (P < 0.05), whereas no significant change in CVC occurred (0.56 +/- 0.06 vs. 0.59 +/- 0.05 ml. min(-1). mmHg(-1); P > 0.05). Similar responses were observed during moderate exercise. In contrast, with metaboreflex activation during severe exercise, no further increases in CO or HR occurred, the increases in MAP and CBF were attenuated, and a significant reduction in CVC was observed (1.00 +/- 0.12 vs. 0.90 +/- 0.13 ml. min(-1). mmHg(-1); P < 0.05). Similarly, when the metaboreflex was activated during mild exercise with the rise in cardiac work lessened (via constant HR and beta(1)-blockade), no increase in CO occurred, the MAP and CBF responses were attenuated (+15.6 +/- 4.5 mmHg, +8.3 +/- 2 ml/min), and CVC significantly decreased from 0.63 +/- 0.11 to 0.53 +/- 0.10 ml. min(-1). mmHg(-1). We conclude that the muscle metaboreflex induced increases in sympathetic nerve activity to the heart functionally vasoconstricts the coronary vasculature.

Adrenergic beta-Antagonists↗
PubMed2002

TENS attenuates response to colon distension in paraplegic and quadriplegic rats.

Individuals with spinal cord injuries above thoracic level 6 experience episodic bouts of life-threatening hypertension as part of a condition termed autonomic dysreflexia (AD). The hypertension can be caused by stimulation of the skin, distension of the urinary bladder or colon, and/or muscle spasms. Transcutaneous electrical nerve stimulation (TENS) may reduce the severity of AD because TENS has been used to inhibit second-order neurons in the dorsal horn. Therefore, we tested the hypothesis that TENS attenuates the hemodynamic responses to colon distension. Eleven Wistar rats underwent spinal cord transection between thoracic vertebrae 4 and 5 (paraplegic, n = 6) or between cervical vertebra 7 and thoracic vertebra 1 (quadriplegic, n = 5). After recovery, all rats were instrumented with a radiotelemetry device for recording arterial pressure. Subsequently, the hemodynamic responses to graded colon distension were determined before and during TENS. During TENS the hemodynamic responses to colon distension were significantly attenuated. Thus TENS may be a preventive approach to reduce the severity of AD in paraplegic and quadriplegic individuals.

Animals↗
PubMed2002

Acute exercise reduces the response to colon distension in T(5) spinal rats.

Individuals with spinal cord injuries above thoracic level 6 (T(6)) experience life-threatening bouts of hypertension, termed autonomic dysreflexia (AD). AD is mediated by peripheral alpha-adrenergic receptor supersensitivity as well as a reorganization of spinal pathways controlling sympathetic preganglionic neurons. A single bout of dynamic exercise may be a safe therapeutic approach to reduce the severity of AD because mild-to-moderate dynamic exercise reduces postexercise alpha-adrenergic receptor responsiveness, lowers postexercise sympathetic nerve activity, and reduces the postexercise response to stress. Therefore, this study was designed to test the hypothesis that mild-to-moderate dynamic exercise attenuates the postexercise response to colon distension (mechanism to elicit AD). To test this hypothesis, six male Wistar rats (406 +/- 23 g), 5 wk post-T(5) spinal cord transection, were instrumented with an arterial catheter. After recovery, the response to graded colon distension (10, 30, 50, and 80 mmHg, in random order) was determined before and after a single bout of mild-to-moderate dynamic exercise (9-12 m/min, 0% grade for 40 min). After exercise, the pressor response to graded colon distension was significantly attenuated (preexercise change: 2 +/- 1, 9 +/- 1, 14 +/- 1, and 24 +/- 2 vs. postexercise change: 2 +/- 1, 2 +/- 1, 9 +/- 1, and 12 +/- 3 mmHg). Thus acute exercise is a safe, therapeutic approach to reduce the severity of AD in paraplegic subjects.

Animals↗
PubMed2002

Postexercise alpha-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide.

We tested the hypothesis that a single bout of dynamic exercise produces a postexercise hypotension (PEH) and alpha(1)-adrenergic receptor hyporesponsiveness in spontaneously hypertensive rats (SHR). The postexercise alpha(1)-adrenergic receptor hyporesponsiveness is due to an enhanced buffering of vasoconstriction by nitric oxide. Male (n = 8) and female (n = 5) SHR were instrumented with a Doppler ultrasonic flow probe around the femoral artery. Distal to the flow probe, a microrenathane catheter was inserted into a branch of the femoral artery for the infusion of the alpha(1)-adrenergic receptor agonist phenylephrine (PE). A microrenathane catheter was inserted into the descending aorta via the left common carotid artery for measurements of arterial pressure (AP) and heart rate. Dose-response curves to PE (3.8 x 10(-3) - 1.98 x 10(-2)microg/kHz) were generated before and after a single bout of dynamic exercise. Postexercise AP was reduced in male (13 +/- 3 mmHg) and female SHR (18 +/- 7 mmHg). Postexercise vasoconstrictor responses to PE were reduced in males due to an enhanced influence of nitric oxide. However, in females, postexercise vasoconstrictor responses to PE were not altered. Results suggest that nitric oxide- mediated alpha(1)-adrenergic receptor hyporesponsiveness contributes to PEH in male but not female SHR.

Adrenergic alpha-Agonists↗