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Schölzel2015 - Modelica implementation of the Seidel-Herzel model of the human baroreflex (v1.6)

ABSTRACT: This project contains a Modelica implementation of the model of the human baroreflex developed by H. Seidel in his PhD thesis (Seidel 1997) under the supervision of H. Herzel. We published and presented this implementation at the 2015 International Modelica Conference. The Seidel-Herzel model (SHM) describes the autonomic control of the heart rate in humans at a high level of abstraction as a hybrid (discrete and continuous), deterministic, quantitative, macro-level model. All effects are described on the organ level, including the time course of systemic arterial blood pressure generated by the pumping of the heart; the Windkessel effect of the expanding arteries dampening the initial rise in blood pressure; the arterial baroreceptors generating a neural signal depending on the absolute value and the increase in blood pressure; the autonomic nervous system emitting norepinephrine and acetylcholine as hormone and neurotransmitter based on signals from the baroreceptor and the lungs; and the cardiac conduction system with the SA node as main pacemaker and the AV node as a fallback system. The model is able to simulate several relevant disease conditions such as first and second degree atrioventricular block (Seidel 1997), carotid sinus hypersensitivity (Seidel and Herzel 1998), congestive heart failure (Kotani et al. 2005), and primary autonomic failure (Kotani et al. 2005) as well as treatment options such as the administration of atropine or metoprolol (Kotani et al. 2005). It is also especially interesting with regard to its dynamical properties such as the emergence of Mayer waves (Seidel 1997), bifurcations (Seidel and Herzel 1998) and cardiorespiratory synchronization (Kotani et al. 2002). The current version of the model can also be found at https://github.com/CSchoel/shm.

SUBMITTER: Christopher Schölzel

PROVIDER: MODEL2101280001 | BioModels | 2021-01-29

REPOSITORIES: BioModels

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Project description:In patients with severe kidney disease AVF are surgically placed in order to create good access for hemodialysis. In these dialysis patients the failure rates of AVF can be as high as 24% within 6 months after surgery, causing ineffective dialysis and necessitating additional clinical interventions. The pathological processes known to lead to AVF failure are beginning to be unravelled include the formation of venous neointimal hyperplasia (VNIH), thrombosis (Chang et al. PMID 16105066), and venous stenosis (Kanterman et al. PMID7892454, Tang et al. 1998), resulting in a reduced blood flow through the fistula. We established a rat model for AVF failure in human kidney dialysis patients. The characterization of this model has been previously described (Globerman et al. 2011, PubmedID:22002501). In this model the AVFs are surgically constructed in the right leg by connecting the superficial epigastric vein SEV to the common femoral artery (CFA), resulting in exposure of the SEV to arterial pressure with pulsatile and low resistant flow patterns (Globerman et al. 2011, PMID22002501). In the present study we utilized this AVF model in order to assess the effects of arterialized flow, with consequent pathological changes of the vessel wall due to surgical AVF instalment, on the transcriptome of endothelium from the SEV. Within the SEV these pathologies of the vessel wall include the formation of NIH in the main branch, and stenosis in the side branches. By employing this rat model we assessed the changes of the endothelial transcriptome in relation to these pathologies in order to gain mechanistic understanding of the potential roles of venous endothelium in AVF failure, as well as to identify potential biomarkers preceding AVF failure. AVF surgery was performed on N=6 rats, and 13-14 days after surgery the rats were sacrificed. AVFs were extracted from the rats, and microarray transcriptome analyses were performed on luminal endothelial cells that isolated from four different sites of the AVF by employing Laser Capture Microdissection (LCM). These sites included (i) N=5 AVF sections of the superficial epigastric vein (SEV) with neointimal hyperplasia (NIH), (ii) N=3 AVF sections of SEV side branches with luminal stenosis, (iii), N=6 sections of the SEV located distally from a ligation thereby omitting exposure to arterialized flow and consequently preventing the development of NIH or stenosis, and (iv) N=3 sections of the AVF common femoral artery without signs of NIH or stenosis.

Project description:We have compared the gene-expression in cerebral arteries from rats after experimental SAH with the expression in cerebral vessels from sham operated animals. The model is well characterised (Prunell et al. 2003; Prunell et al. 2004) regarding the physiological changes but not regarding the gene expression pattern. Male Sprague-Dawley rats (350-400 g) were anaesthetized using 5% halothane (Halocarbon Laboratories, River Edge, New Jersey) in N2O/O2 (30:70). The rat was intubated and artificially ventilated with inhalation of 0.5-1.5% halothane in N2O/O2 (70:30) during the surgical procedure. The depth of anaesthesia was carefully monitored and the respiration checked by regularly withdrawing arterial blood samples for blood gas analysis (Radiometer, Copenhagen, Denmark). An arterial catheter to measure blood pressure was placed in the tail artery and a catheter to monitor intracranial pressure (ICP) was placed in the subocciptal membrane. At either side of the skull, 3 mm from the midline and 4 mm anteriorly from the bregma, holes were drilled through the skull bone down to dura mater (without perforation) allowing the placement of two laser-Doppler flow probes to measure CBF. Finally, a 27G blunt canula with side hole was introduced stereotactically 6.5 mm anterior to bregma in the midline at an angle of 30 degrees to the vertical. After 30 minutes of equilibration 250 ul blood was withdrawn from the tail catheter and injected intracranially at a pressure equal to the mean arterial blood pressure (80-100 mmHg). Subsequently the rat was kept under anaesthesia for another 60 minutes to allow recovery from the cerebral insult after which catheters were removed and the incisions closed. The rat was then revitalized and extubated. A subcutaneous injection of carprofen (4.0 mg/kg) (Pfizer, Denmark) was administered and the rat was hydrated subcutaneously using 40 ml isotonic sodium chloride at the end of the operation and at day one. During the period of observation the rat was monitored regularly, and if showing severe distress the animal was prematurely killed. In addition, a series of sham-operated rats were prepared. They went through the same procedure with the exception that no blood was injected intracisternally.

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Schölzel2015 - Modelica implementation of the Seidel-Herzel model of the human baroreflex (v1.6)

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