| dc.contributor.author | Arora, Rakesh Christopher. | en_US |
| dc.date.accessioned | 2014-10-21T12:37:14Z | |
| dc.date.available | 2002 | |
| dc.date.issued | 2002 | en_US |
| dc.identifier.other | AAINQ75692 | en_US |
| dc.identifier.uri | http://hdl.handle.net/10222/55842 | |
| dc.description | The intrinsic cardiac nervous system (ICNS) serves an important role in beat-to-beat regulation of cardiac function. It is unknown if the ICNS undergoes "remodelling" when exposed to ischemic injury or therapeutic modalities utilized to treat myocardial ischemia. Chemical stimuli (adenosine and adenosine antagonists) were utilized to study the role intrinsic cardiac neuron P1 purinergic receptors play in myocardial ischemia and reperfusion. Further investigations examined the influence of spinal cord stimulation (SCS) and transmyocardial laser revascularization (TMLR) on cardiac neuronal control. Lastly, an examination of the human ICNS in patients with ischemic heart disease was performed. | en_US |
| dc.description | Locally administered adenosine reduced neuronal responses during reperfusion following transient myocardial ischemia in the porcine model. However, adenosine did not affect the ICNS during the ischemic phase. This short-lived effect was mediated via adenosine A1 receptors. SCS suppressed canine ICNS activity. However, this effect occurred during both ischemic and the reperfusion phase. Additionally, SCS remodelled the ICNS for prolonged periods after its termination. Chronic TMLR (4 weeks) elicited a long-term remodelling of the canine ICNS, resulting in blunting of neuronal responses to potent chemical stimuli. This was associated with hemodynamic instability; ventricular fibrillation occurred in 1 animal. Human intrinsic cardiac neurons generated spontaneous activity and responded to cardiac sensory inputs. Exogenously administered therapeutic agents modified their behaviour in the perioperative period, implying that human intrinsic cardiac neurons could possibly be manipulated to therapeutic advantage. Collectively, these data provided insight into neurocardiologic mechanisms underlying cardiac dysfunction in disease states and the potential for developing novel therapies used in the treatment of ischemic heart disease. | en_US |
| dc.description | Thesis (Ph.D.)--Dalhousie University (Canada), 2002. | en_US |
| dc.language | eng | en_US |
| dc.publisher | Dalhousie University | en_US |
| dc.publisher | | en_US |
| dc.subject | Biology, Anatomy. | en_US |
| dc.subject | Biology, Neuroscience. | en_US |
| dc.title | The intrinsic cardiac nervous system in ischemic heart disease. | en_US |
| dc.type | text | en_US |
| dc.contributor.degree | Ph.D. | en_US |
