Control compensatory

In addition to excess sodium intake, abnormal renal sodium retention may be the primary event in the development of hypertension, and it includes abnormalities in the pressure-natriuresis mechanism. In hypertensive individuals, this theory proposes a shift in the control mechanism preventing the normalization of blood pressure. The mechanisms behind the resetting of the pressure-natriuresis curve may include afferent arteriolar vasoconstriction, decreased glomerular ultrafiltration, or an increase in tubular sodium reabsorption.4 Other theories supporting abnormal renal sodium retention suggest a congenital reduction in the number of nephrons, enhanced renin secretion from nephrons that are ischemic, or an acquired compensatory mechanism for renal sodium retention.9... 

Respiratory acidosis is characterized by a reduced arterial pH, a primary increase in the arterial PaC02 and, when present for sufficient time, a compensatory rise in the HCOf concentration. Because increased C02 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in C02 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 25-6. 

Some evidence supports a hypothesis that the POA hypnogenic system also plays a role in homeostatic control of sleep. Homeostatic control of NREM sleep refers to compensatory increases in sleep amounts and particularly in EEG slow wave activity (SWA, usually 0.5-4 Hz) after sleep deprivation. SWA is the hallmark of homeostatic control. SWA gradually declines within sustained sleep, as homeostatic drive for sleep is satisfied. A role for the POA in homeostasis is suggested by the following observations. 

The spreader most commonly found in the rubber industry has a working width across the application roller/blade of 1.5 metres. Wider spreaders (up to 4 metres) exist for very wide cloth coating but they require special control of the bending of the doctor blade and have compensatory mechanisms to overcome this problem. 

Overproduction of free radicals by erythrocytes and leukocytes and iron overload result in a sharp increase in free radical damage in T1 patients. Thus, Livrea et al. [385] found a twofold increase in the levels of conjugated dienes, MDA, and protein carbonyls with respect to control in serum from 42 (3-thalassemic patients. Simultaneously, there was a decrease in the content of antioxidant vitamins C (44%) and E (42%). It was suggested that the iron-induced liver damage in thalassemia may play a major role in the depletion of antioxidant vitamins. Plasma thiobarbituric acid-reactive substances (TBARS) and conjugated dienes were elevated in (3-thalassemic children compared to controls together with compensatory increase in SOD activity [386]. The development of lipid peroxidation in thalassemic erythrocytes probably depends on a decrease in reduced glutathione level and decreased catalase activity [387]. 

Abstract For more than a half century, tobacco manufacturers have conducted sophisticated internal research to evaluate nicotine delivery, and modified their products to ensure availability of nicotine to smokers and to optimize its effects. Tobacco has proven to be a particularly effective vehicle for nicotine, enabling manipulation of smoke chemistry and of mechanisms of delivery, and providing sensory cues that critically inform patterns of smoking behavior as well as reinforce the impact of nicotine. A range of physical and chemical product design changes provide precise control over the quantity, form, and perception of nicotine dose, and support compensatory behavior, which is driven by the smoker s addiction to nicotine. Cigarette... 

Signal transduction pathways and protein regulatory networks are not linear (26) but contain branches, negative feedback loops, and common points of connection between seemingly parallel pathways known as nodes. Furthermore, these pathways and networks are tightly controlled within cells so that disruption of any point has a rippling effect often activating compensatory mechanisms... 

The a-blocker phentolamine (83-3) was used fairly extensively as an antihypertensive agent prior to the availability of more effective and far better tolerated drugs. Some of the most important side effects from use of this drug, such as fluid retention and tachycardia, were at that time attributed to compensatory mechanisms, casting a cloud on all a-blockers. The use of this class of agents for controlling elevated blood... 

Enflurane produces a dose-related decrease in systemic arterial blood pressure secondary to reductions in cardiac output and systemic vascular resistance. There is evidence that cardiac output is partially maintained by a compensatory increase in heart rate. This effect seems dependent on a degree of hypercardia and does not occur during controlled ventilation. Enflurane and halothane depress myocardial contractility to a similar extent and less than isoflurane. Enflurane does not sensitise the heart to the effects of catecholamines to any significant extent and adrenaline (epinephrine) may be given subcutaneously for control of bleeding. 

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