Hemodynamic coupling

In vitro, urotensin II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where urotensin II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. In vivo, urotensin II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. The extent to which the peptide is involved in the regulation of vascular tone and blood pressure in humans is not clear recent studies have produced conflicting results. The actions of urotensin II are mediated by G protein-coupled receptors that are widely distributed in the brain, spinal cord, heart, vascular smooth muscle, skeletal muscle, and pancreas. Some effects of the peptide including vasoconstriction are mediated by the phospholipase C/IP3/DAG signal transduction pathway. 

The molecular pathways that couple increased hemodynamic load to cardiac hypertrophy, cardiac fibrosis, and heart failure are multiplex and incompletely understood, despite intense recent investigation (Hunter and Chien 1999 MacLellan and Schneider 2000). Although TGF-pj initiates multiple modes of signal activation, including the recently discovered TPRII/TAK1 pathway (Watkins et al. 2006),... 

Our next problem concerns the dynamic response of the arteriolar system to the signal from the mascula densa cells. This response is restricted to that part of the afferent arteriole that is closest to the glomerulus. Hence, the afferent arteriole is divided into two serially coupled sections of which the first (representing a fraction (3 of the total length) is assumed to have a constant flow (or hemodynamic) resistance, while the second (closer to the glomerulus) is capable of varying its diameter and hence the flow resistance in dependence of the tubuloglomerular feedback activation ... 

The parameters y and e relate to the model of nephron-nephron interaction to be discussed in Section 12.5. In order to represent the hemodynamic coupling it is necessary to also introduce a parameter Cgj0 that describes the elastic response of... 

Arrows point to couples of nephrons that share a piece of common arteriole. We suppose that hemodynamic coupling can be important for such nephrons. For other nephrons, the vascularly propagated coupling is likely to dominate. 

To implement the hemodynamic coupling in our model, a piece of common afferent arteriole is included into the system, and the total length of the incoming blood vessel is hereafter divided into a fraction s < that is common to the two interacting nephrons, a fraction 1 — that is affected by the TGF signal, and a remaining fraction — e for which the flow resistance is considered to remain constant As compared with the equilibrium resistance of the separate arterioles, the piece of shared arteriole is assumed to have half the flow resistance per unit length. 

Here, Rao denotes the total flow resistance for each of the two nephrons in equilibrium. ri and ri are the normalized radii of the active parts of the afferent arterioles for nephron 1 and nephron 2, respectively, and Pg and Pg2 are the corresponding glomerular pressures. As a base value of the hemodynamic coupling parameter we shall use s = 0.2. This parameter measures the fraction of the arteriolar length that is shared between the two nephrons. 

In order to examine the synchronization phenomena that can arise in larger ensembles of nephrons, we recently developed a model of a vascular-coupled nephron tree [35], focusing on the effect of the hemodynamic coupling. As explained above, the idea is here that, as one nephron reduces its arterioler diameter to lower the incoming blood flow, more blood is distributed to the other nephrons in accordance with the flow resistances in the network. An interesting aspect of this particular coupling is that the nephrons interact both via the blood flow that controls their tendency to oscillate and via the oscillations in this blood flow that control their tendency to synchronize. We refer to such a structure as a resource distribution chain, and we have shown that phenomena similar to those that we describe here... 

Three significant developments move us closer to the capability of safely acquiring regional in vivo biochemical information in the human brain. First, the appearance within the medical environment of apparatus for nuclear bombardment, such as cyclotrons and linear accelerators, coupled with ingenious techniques for rapid synthesis of radiopharmaceuticals, have provided many radiopharmaceuticals suitable for in vivo regional hemodynamic and metabolic studies (9). Second, the parallel development of appropriate mathematical models has provided... 

The same ventricle may be coupled to a pathological arterial system, for example, one with doubled peripheral resistance R. As expected, increased peripheral resistance raises arterial pulse pressure (to 140/95 mmHg) and impedes the ventricle s ability to eject blood (Figure 8.6). The ejection fraction decreases to 50% in this experiment. Other experiments, such as altered arterial stiffness, may be performed. The model s flexibility allows description of heart pathology as well as changes in blood vessels. This one equation (Equation 8.8) with one set of measured parameters is able to describe the wide range of hemodynamics observed experimentally [11],... 

In this study, we applied non-invasive approach for evaluating focal cerebral ischemia. The pattern of SSEP response shows that the Pl-Nl amplitude was sipiflcant attenuated but the PI latency was not significant decayed. The hemodynamic response was detected when somatosensory evoke potential was measured from surface recording region. The result of time frequency analysis shows that the high frequency shifts in the initial of the SSEPs. Several studies have also indicated that phenomenon may be caused by brain injury. The results of neurovascular coupling are consistent with previous studies [9]. 

Franceschini M, Nissila 1, Wu W, Diamond S, Bonmassar G, Boas D. Coupling between somatosensory evoked potentials and hemodynamic response in the rat. Neuroimage. 2008 41 189-203. 

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