Autoregulatory action

Models have been developed that consider these influences and examine feedforward and feedback autoregulatory action to simulate the transient responses of brain tissue to oxygen tension upsets. Controller dynamics are being proposed that give essentially the same responses as those obtained from in vivo cat experiments. 

Because of discrepancies between experimental tests and predicted tissue oxygen response by convection-diffusion models, the influence of physiological control mechanisms was considered. It is proposed that a minimum of two autoregulatory actions (at least conceptually) are functional in helping prevent neuron damage when low blood oxygen tensions are encountered. 

Autoregulatory action helps to reduce nerve cell destruction resulting from brain tissue anoxia. Two possible mechanisms include flow controller dynamics in the form of pure delays and time constant lags and oxygen consumption control with Michaelis-Menten behavior. Response curves also suggest the possibility of facilitated or active transport of oxygen in tissue and resistance to the diffusion of oxygen from the tissue into the blood stream. 

Changes in constructive metabolism and ultrastructural organization of Bacillus cereus cells under the action of a specific autoregulatory factor. Microbiology, Vol.48, No.2, (February 1979), pp.240-244, ISSN 1350-0872... 

In usual therapeutic doses, Epi has little constrictor action on cerebral arterioles. The cerebral circulation does not constrict in response to activation of the sympathetic nervous system by stressful stimuli indeed, autoregulatory mechanisms tend to limit the increase in cerebral blood flow caused by increased blood pressure. 

The long-term fall in systemic blood pressure observed in hypertensive individuals treated with ACE inhibitors is accompanied by a leftward shift in the renal pressure-natriuresis curve (Figure 30-5) and a reduction in total peripheral resistance that varies in different vascular beds. Vasodilation in the kidney is a relatively constant finding that is explained by the exquisite sensitivity of renal vessels to the vasoconstrictor actions of Angll. Increased renal blood flow occurs without an increase in GFR thus, the filtration fraction is reduced. Both the afferent and efferent arterioles are dilated. Blood flows in the cerebral and coronary beds, where autoregulatory mechanisms are powerful, generally are well maintained. 

Hemodynamic stress can be mimicked by using a tolerance test such as acetazolamide administration in conjunction with quantitative measurement of CBF. Although the exact mechanism of action is uncertain, acetazolamide causes vasodilatation of normal cerebral arteries and an increase in CBF in the corresponding territory. Patients with impaired cerebrovascular reserve, however, are aheady maximally vasodilated due to the response of cerebral autoregulatory mechanisms, and thus cannot respond further to acetazolamide. CBF does not increase, but remains stable or even decreases, because of a steal phenomenon by the healthy arteries (Nariai et al. 1995). Acetazolamide is generally well tolerated, with the most common side effects being cir-cumoral numbness, paresthesias, and headache. One case of acetazolamide-associated reversible ischemia has been reported (Komiyama et al. 1997). 

To the autoregulatory processes of this t3rpe can be added the action of specialized regulators such as the hormones which have been developed by organisms in the course of biochemical evolution. 

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