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181
between ΔSBP and ΔPU (hSymp) on this side represents the resistance of the vessels. In
the other words, the changes in pressure applying to the resistance will cause a change in
current or perfusion. This resistance can be altered when smooth muscles on the wall of
large capillaries or arterioles constrict, in response to changes of the firing rate of the
peripheral sympathetic neurons. This relationship is also assumed to be present on the
ipsi-lateral side. In addition, on this side, the effect of the change in peripheral resistance
due to the NO effect is modeled as another additive input to ΔPU. We use ΔSBP as the
driving force for this part, and the impulse response which relates ΔSBP to ΔPU is
denoted as hEndo. The stochastic and other influences on ΔSBP are denoted as ωPUcontra
and ωPUcontra for contra-lateral ΔPU and ipsi-lateral ΔPU, respectively.
To obtain both impulse responses, we will first use the measurement from the
contra lateral side to quantify hSymp(t):
ΔPUcontra t hSymp iΔSBPt i TSymp
M1
i0
ωPUcontra t
Equation 6.1
Substitute hSymp(t) into Equation 6.2 for the ipsi-lateral side, we can obtain the impulse
response for the endothelial effect, hEndo(t).
ΔPUipsi t hSymp iΔSBPt i TSymp
M1
i0
Σ hEndo iΔSBPt i TEndo M1
i0 ωPUipsi t
Equation 6.2
Object Description
| Title | Modeling of cardiovascular autonomic control in sickle cell disease |
| Author | Sangkatumvong, Suvimol "Ming" |
| Author email | sangkatu@usc.edu; mingsuvimol@hotmail.com |
| Degree | Doctor of Philosophy |
| Document type | Dissertation |
| Degree program | Biomedical Engineering |
| School | Viterbi School of Engineering |
| Date defended/completed | 2011-03-03 |
| Date submitted | 2011 |
| Restricted until | Unrestricted |
| Date published | 2011-04-26 |
| Advisor (committee chair) |
Khoo, Michael C.K. Coates, Thomas |
| Advisor (committee member) |
Wood, John C. Meiselman, Herbert J. |
| Abstract | Sickle cell disease (SCD) is a genetic disorder that is characterized by recurrent episodes of vaso-occlusive crisis (VOC) from the sickling behavior of red blood cells. Currently, no technique can distinguish the cause or predict the occurrence of a crisis accurately and reliably. One area which has rarely been studied in SCD patients is their autonomic nervous system (ANS). Since the ANS is responsible for the moment-to-moment control of the vascular tone, we hypothesized that the ANS plays an important role in the initiation of their VOC. Computational techniques, including spectral analysis of HRV and a model which characterizes the dynamics of baroreflex and respiratory-cardiac coupling, were used to assess cardiovascular autonomic control in SCD patients and normal control (CTL) subjects. These analysis techniques were applied to responses elicited from the subjects during the application of non-invasive and easily reproducible physiological interventions, such as transient-controlled hypoxia and the cold face test.; Our results demonstrate impairment in the ANS in SCD patients. In particular, hypoxic responses in SCD subjects showed a significantly stronger parasympathetic withdrawal compared to the CTLs. Furthermore, the autonomic responses to the cold face stimulus in SCD subjects showed an absence of the shift to parasympathetic dominance, as evidenced in the CTLs. In addition to the HRV analysis, model-based assessment also revealed the absence of both arterial baroreflex and respiratory-cardiac coupling augmentations in SCD patients during the cold face stimulus, while in CTL subjects both mechanisms showed tendencies to increase during the test.; During the data analysis period, we noticed that spontaneous sighs triggered marked periodic drops in peripheral microvascular perfusion. While the sigh frequency was the same in both groups, the probability of a sigh inducing a perfusion drop was significantly higher in SCD subjects in comparison to the CTLs. Evidence for sigh-induced sympathetic nervous system dominance was seen in SCD subjects, but was not significant in CTL. HRV analysis suggested that the cardiac ANS responses to sighs are not different between the two groups, after adjusting for the effect of post-sigh respiration. However, the peripheral sympathetic response in SCD subjects appeared to be enhanced in this group relative to the CTLs; and, furthermore, sighs may play a role in initiation of vaso-occlusive events in this group of patients.; In brief, all assessments we performed in this study suggested that the ANS responses to perturbations in SCD patients are more biased toward parasympathetic withdrawal and sympathetic activation, compared to normal controls. The complete mechanism is still a topic of investigation. Thus far, we have shown a relationship between the degree of this abnormality and the degree of both the anemia and infection/inflammation. We suspect that a mechanism related to the inflammatory reflex might play an important role in the ANS impairment in this group of patients.; In conclusion, this study draws attention to an enhanced ANS-mediated peripheral sympathetic driven vasoconstriction in SCD that could increase red cell retention in the microvasculature, promoting vaso-occlusion. This cascade of events could be the mechanism which triggers the VOC. |
| Keyword | autonomic nervous system; heart rate variability; respiration; sickle cell disease; physiological system modeling; sympathetic; parasympathetic; minimal model; baroreflex; respiratory-cardiac coupling; hypoxia; sigh; cold face test; cardiovascular autonomic control |
| Geographic subject | medical facilities: Childrens' Hospital Los Angeles |
| Geographic subject (city or populated place) | Los Angeles |
| Geographic subject (state) | California |
| Geographic subject (country) | USA |
| Coverage date | 2005/2010 |
| Language | English |
| Part of collection | University of Southern California dissertations and theses |
| Publisher (of the original version) | University of Southern California |
| Place of publication (of the original version) | Los Angeles, California |
| Publisher (of the digital version) | University of Southern California. Libraries |
| Provenance | Electronically uploaded by the author |
| Type | texts |
| Legacy record ID | usctheses-m3781 |
| Contributing entity | University of Southern California |
| Rights | Sangkatumvong, Suvimol "Ming" |
| Repository name | Libraries, University of Southern California |
| Repository address | Los Angeles, California |
| Repository email | cisadmin@lib.usc.edu |
| Filename | etd-Sangkatumvong-4436 |
| Archival file | uscthesesreloadpub_Volume23/etd-Sangkatumvong-4436.pdf |
Description
| Title | Page 199 |
| Contributing entity | University of Southern California |
| Repository email | cisadmin@lib.usc.edu |
| Full text | 181 between ΔSBP and ΔPU (hSymp) on this side represents the resistance of the vessels. In the other words, the changes in pressure applying to the resistance will cause a change in current or perfusion. This resistance can be altered when smooth muscles on the wall of large capillaries or arterioles constrict, in response to changes of the firing rate of the peripheral sympathetic neurons. This relationship is also assumed to be present on the ipsi-lateral side. In addition, on this side, the effect of the change in peripheral resistance due to the NO effect is modeled as another additive input to ΔPU. We use ΔSBP as the driving force for this part, and the impulse response which relates ΔSBP to ΔPU is denoted as hEndo. The stochastic and other influences on ΔSBP are denoted as ωPUcontra and ωPUcontra for contra-lateral ΔPU and ipsi-lateral ΔPU, respectively. To obtain both impulse responses, we will first use the measurement from the contra lateral side to quantify hSymp(t): ΔPUcontra t hSymp iΔSBPt i TSymp M1 i0 ωPUcontra t Equation 6.1 Substitute hSymp(t) into Equation 6.2 for the ipsi-lateral side, we can obtain the impulse response for the endothelial effect, hEndo(t). ΔPUipsi t hSymp iΔSBPt i TSymp M1 i0 Σ hEndo iΔSBPt i TEndo M1 i0 ωPUipsi t Equation 6.2 |
