Compensatory mechanism

Flucytosine-resistant strains can develop very rapidly. These mutants may have a disturbed 5-FC-metabohsm, or a compensatory mechanism for the disturbed nucleic acid functions. No cytosine permease was found in a resistant Cyptococcus neoformans strain, whereas cytosine deaminase was absent in resistant C. albicans strains. A deficiency of uridine monophosphate pyrophosphorylase occurs frequently in resistant C. albicans strains (1). 

The cardiac effects of the calcium antagonists, ie, slowed rate (negative chronotropy) and decreased contractile force (negative inotropy), are prominent in isolated cardiac preparations. However, in the intact circulation, these effects may be masked by reflex compensatory adjustments to the hypotension that these agents produce. The negative inotropic activity of the calcium antagonists may be a problem in patients having heart failure, where contractility is already depressed, or in patients on concomitant -adrenoceptor blockers where reflex compensatory mechanisms are reduced. 

Diuretics are needed to return to normal the expanded extracellular volume that other antihypertensive agents produce, such as fluid retention and blood volume expansion, via compensatory mechanisms of the body. The loss of efficacy of antihypertensive agents can be restored if a diuretic is used concomitandy. In the treatment of hypertension, high ceiling or loop diuretics, such as furosemide, ethacrynic acid, and bumetanide, are no more efficacious than the thiazide-type of diuretics. In fact, these agents cause more side effects, such as dehydration, metaboHc alkalosis, etc, and therefore, should not be used except in situations where rapid elimination of duid volume is cleady indicated. 

Mice lacking the al subunit have also been generated, as well as mice lacking the (32 subunit. Given the fact that these are the most abundant a and (3 subunits respectively, it is surprizing that these animals survive, presumably indicating the presence of compensatory mechanisms. 

The adrenergic dragp are important in the care and treatment of patients in shock. Shock is defined as a life-threatening condition of inadequate perfusion. In shock, there is an inadequate supply of arterial blood flow and oxygen delivery to the cells and tissues. The body initiates compensatory mechanisms to counteract the symptoms of shock (eg, the release of epinephrine and norepinephrine), hi some situations, the body is able to compensate and blood pressure is maintained. However, if shock is untreated and compensatory mechanisms of the body fail, irreversible shock occurs and... 

Various clinical manifestations may be present in a patient in shock. For example, in the early stages of shock the extremities may be warm because compensatory mechanisms are initiated and the blood flow to the skin and extremities is maintained. If the condition is untreated, the skin and extremities become cool and clammy because of the failure of the compensatory mechanisms and the progression of shock. Thus, more advanced shock may be referred to as... 

The body activates the neurohormonal compensatory mechanisms, which result in ... 

By necessity, herbivores have evolved GIT and systemic compensatory mechanisms that allow them to subsist on plant-based diets that have limited nutrient quality and include phytochemicals. Still, herbivores remain susceptible to some of the anti-nutrient and toxic phytochemicals. For example, several herbivores are sensitive to the phytotoxins associated with autumn crocus, which include colchicine (Yamada et al, 2000). As a consequence, herbivores tend to select species and portions of plants based on a combination of nutrient quality and concentrations of phytochemicals (Yeager et al, 1997), and this has an impact on habitat selection and plant ecology (Duncan and Gordon, 1999). Carnivorous species have not been under selective pressure to develop similar compensatory mechanisms, generally have only limited abilities to subsist on plant-based diets, and in many cases are less tolerant of phytochemicals. 

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... 

Urine leakage with physical activity (volume is proportional to activity level). No Ul with physical inactivity, especially when supine (no nocturia). May develop urgency and frequency as a compensatory mechanism (or as a separate component of bladder overactivity). 

Hypercapnia (abnormally high concentration of carbon dioxide in the blood) can develop as a result of overfeeding with both dextrose and total calories.1,37 Excess carbon dioxide production and retention can lead to acute respiratory acidosis. The excess carbon dioxide also will stimulate compensatory mechanisms, resulting in an increase in respiratory rate in order to eliminate the excess carbon dioxide via the lungs. This increase in respiratory workload can cause respiratory insufficiency that may require mechanical ventilation. Reducing total calorie and dextrose intake would result in resolution of hypercapnia if due to overfeeding. 

Compensatory mechanisms in the circulatory system are needed to counteract the effects of gravity. Two important mechanisms include ... 

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. 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

Compensatory mechanisms in HF stimulate excessive sodium and water retention, often leading to systemic and pulmonary congestion. Consequently, diuretic therapy (in addition to sodium restriction) is recommended in all patients with clinical evidence of fluid retention. However, because they do not alter disease progression or prolong survival, they are not considered mandatory therapy for patients without fluid retention. 

The primary compensatory mechanism is to decrease PaCC>2 by increasing the respiratory rate. 

Arterial blood gases are the primary tools for evaluation of therapeutic outcome. They should be monitored closely to ensure resolution of simple acid-base disorders without deterioration to mixed disorders due to compensatory mechanisms. For example, arterial blood gases should be obtained every 2 to 4 hours during the acute phase of respiratory acidosis and then every 12 to 24 hours as acidosis improves. 

The large scale adoption of PHEVs (or BEVs) in Europe might create a regulatory issue as electric vehicles will shift C02 emissions from the transport sector to the electric power sector, which - unlike road transport - is covered by the European Emissions Trading Scheme (ETS), a compensatory mechanism or the inclusion of road transportation within the scheme would be required. 

Arrow b This represents an increased Pc. If only the arteriolar pressure rises, the gradient of the line will increase, whereas if the venous pressure rises in tandem the line will undergo a parallel shift. The net result is again filtration. This occurs clinically in vasodilatation. The opposite scenario is seen in shock, where the arterial pressure at the capillaries drops. This results in net reabsorption of fluid into the capillaries and is one of the compensatory mechanisms to blood loss. 

The Davenport diagram shows the relationships between pH, Pco2 and HC03. It can be used to explain the compensatory mechanisms that occur in acid-base balance. At first glance it appears complicated because of the number of lines but if it is drawn methodically it becomes easier to understand. 

Draw and label the axes as shown. Note that the x axis is usually drawn without any numerical markers. Normal intracranial volume is assumed to be at the left side of the curve and should be in keeping with an ICP of 5-10 mmHg. Draw a curve similar in shape to a positive tear-away exponential. Demonstrate on your curve that compensation for a rise in the volume of one intracranial component maintains the ICP < 20 mmHg. However, when these limited compensatory mechanisms are exhausted, ICP rises rapidly, causing focal ischaemia (ICP 20-45 mmHg) followed by global ischaemia (ICP > 45 mmHg). 

Interestingly, upon extended observation, the changes induced by overexpression of either of the two variants of HI become neutralized by a compensatory mechanism which adjusted all cellular parameters to a normal level [132]. 

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... 

Although much has been learned ftom in vitro assays, we do not yet fully understand the predominant migratory mechanisms used by cancer cells in vivo. It is important that any molecular mediators (or their inhibitors) identified in one assay are tested in complementary assays and validated in appropriate in vivo models before they can be assumed to play a significant role in invasion and metastasis. There are several examples where a molecule can have either positive or negative regulatory roles in key cellular functions depending on the cellular/microenvironmental context (e.g., tissue inhibitors of matrix metalloproteinases TIMPs (12)). Thus, care needs to be taken to avoid undesirable activities or, as in the example of some angiogenic inhibitors, compensatory mechanisms that result in adverse events (13). 

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