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Hypertrophy

Pancrease Pancreatectomy Pancreatic a-amylase Pancreatic dornase Pancreatic elastase Pancreatic hypertrophy Pancreatic lipase Pancreatin [8049-47-6]... [Pg.719]

The growth of animals can be defined as an increase in mass of whole body, tissue(s), organ(s), or ceU(s) with time. This type of growth can be characterized by morphometric measurements eg, skeletal muscle or adipose tissue growth can be described by observing temporal changes in ceU number, ie, hyperplasia, and ceU size, ie, hypertrophy. Growth also includes developmental aspects of function and metaboHsm of cells and tissues from conception to maturity. [Pg.408]

One possible mechanism responsible for the abiHty of trenbolone acetate to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satelHte ceUs as the result of increased sensitivity to insuHn-Hke growth factor-I (IGE-1) and fibroblast growth factor (43). [Pg.409]

Mechanism of Action. P-Agonists stimulate skeletal muscle growth by accelerating rates of fiber hypertrophy and protein synthesis, but generally do not alter muscle DNA content in parallel with the increases in protein accretion (133—135). This is in contrast to the effects of anaboHc steroids and ST on skeletal muscle growth. Both of the latter stimulate fiber hypertrophy and muscle protein synthesis, but also increase muscle DNA content coincident with increased protein accretion. Whether the P-agonists decrease muscle protein degradation is equivocal. [Pg.414]

Pea.nuts, The proteins of peanuts are low in lysine, threonine, cystine plus methionine, and tryptophan when compared to the amino acid requirements for children but meet the requirements for adults (see Table 3). Peanut flour can be used to increase the nutritive value of cereals such as cornmeal but further improvement is noted by the addition of lysine (71). The trypsin inhibitor content of raw peanuts is about one-fifth that of raw soybeans, but this concentration is sufficient to cause hypertrophy (enlargement) of the pancreas in rats. The inhibitors of peanuts are largely inactivated by moist heat treatment (48). As for cottonseed, peanuts are prone to contamination by aflatoxin. FDA regulations limit aflatoxin levels of peanuts and meals to 100 ppb for breeding beef catde, breeding swine, or poultry 200 ppb for finishing swine 300 ppb for finishing beef catde 20 ppb for immature animals and dairy animals and 20 ppb for humans. [Pg.301]

ACE inhibitors lower the elevated blood pressure in humans with a concomitant decrease in total peripheral resistance. Cardiac output is increased or unchanged heart rate is unchanged urinary sodium excretion is unchanged and potassium excretion is decreased. ACE inhibitors promote reduction of left ventricular hypertrophy. [Pg.140]

Methyldopa. Methyldopa reduces arterial blood pressure by decreasing adrenergic outflow and decreasing total peripheral resistance and heart rate having no change in cardiac output. Blood flow to the kidneys is not changed and that to the heart is increased. It causes regression of myocardial hypertrophy. [Pg.142]

Methyldopa is effective in mild, moderate, and severe hypertension but a thiazide-type diuretic is needed to overcome the fluid retaining side effect. Methyldopa has been shown to prevent and induce regression of ventricular hypertrophy in hypertensive patients. The principal side effects are sedation, drowsiness, nasal congestion, fluid retention, and in rare occasions, hemolytic anemia. [Pg.142]

ACE inhibitors inhibit the degradation of bradykinin and potentiate the effects of bradykinin by about 50-100-fold. The prevention of bradykinin degradation by ACE inhibitors is particularly protective for the heart. Increased bradykinin levels prevent postischemic reperfusion arrhythmia, delays manifestations of cardiac ischemia, prevents platelet aggregation, and probably also reduces the degree of arteriosclerosis and the development of cardiac hypertrophy. The role of bradykinin and bradykinin-induced NO release for the improvement of cardiac functions by converting enzyme inhibitors has been demonstrated convincingly with use of a specific bradykinin receptor antagonist and inhibitors of NO-synthase. [Pg.10]

ACE inhibitors are approved for the treatment of hypertension and cardiac failure [5]. For cardiac failure, many studies have demonstrated increased survival rates independently of the initial degree of failure. They effectively decrease work load of the heart as well as cardiac hypertrophy and relieve the patients symptoms. In contrast to previous assumptions, ACE inhibitors do not inhibit aldosterone production on a long-term scale sufficiently. Correspondingly, additional inhibition of aldosterone effects significantly reduces cardiac failure and increases survival even further in patients already receiving diuretics and ACE inhibitors. This can be achieved by coadministration of spironolactone, which inhibits binding of aldosterone to its receptor. [Pg.10]

Calcineurin is involved in cardiac hypertrophy and in cognitive and behavioral defects in the brain. Inhibitors of calcineurin such as cyclosporine A and FK 506 are used clinically in transplant rejection and autoimmune diseases. [Pg.294]

Osteoarthritis is a noninflammatory degenerative joint disease marked by degeneration of the articular cartilage, changes in the synovial membrane, and hypertrophy of the bone at the margins. [Pg.186]

These drugp are contraindicated in those with a hypersensitivity to the anticholinergic dragp, those with glaucoma (angle-closure), pyloric or duodenal obstruction, peptic ulcers, prostatic hypertrophy, achalasia (failure of... [Pg.268]

As with all antidepressants, the TCAs are used cautiously in patients witii hepatic or renal impairment. The tricyclics are used cautiously in patients witii heart disease, angina, paroxysmal tachycardia, increased intraocular pressure, prostatic hypertrophy, or a history of seizures. [Pg.285]

The antipsychotic dru are used cautiously in patients exposed to extreme heat or phosphorous insecticides and in those with respiratory disorders, glaucoma, prostatic hypertrophy, epilepsy, decreased renal function, lactation, or peptic ulcer. The antipsychotic drags are used cautiously in elderly and debilitated patients because these patients are more sensitive to the antipsychotic dragp. lithium is used cautiously in patients who are in situations in which they may sweat profusely and those who are suicidal, have diarrhea, or who have an infection or fever. [Pg.299]

Antiemetics and antivertigo drag s are used cautiously in patients with glaucoma or obstructive disease of the gastrointestinal or genitourinary system, those with renal or hepatic dysfunction, and in older men with possible prostatic hypertrophy. Piromethazine is used cautiously in patients with hypertension, sleep apnea, or epilepsy. Trimethobenzamide is used cautiously in children with a viral illness because it may increase the risk of Reye s syndrome... [Pg.311]

Preanesthetic drugs may be omitted in those 60 years or older because many of the medical disorders for which these drugsare contraindicated are seen in older individuals For example, atropine and glycopyrrolate, drugs that can be used to decrease secretions of the upper respiratory tract, are contraindicated in certain medical disorders such as prostatic hypertrophy, glaucoma, and myocardial ischemia. Other preanesthetic drugs that depress the central nervous astern (CN, such as narcotics barbiturates and antianxiety drugs with or without antiemetic properties may be contraindicated in the older individual. [Pg.319]

The antihistamines are used cautiously in patients with bronchial asthma, cardiovascular disease, narrow-angle glaucoma, symptomatic prostatic hypertrophy, hypertension, impaired kidney function, peptic ulcer, urinary... [Pg.326]


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A Client with Benign Prostatic Hypertrophy and Spinal Anesthesia

Antihistamines prostatic hypertrophy

Benign prostate hypertrophy

Benign prostatic hypertrophy

Biomarkers cardiac hypertrophy

Biomarkers of Cardiac Hypertrophy

Biventricular hypertrophy

Bladder hypertrophy

Cardiac hypertrophy

Cardiac hypertrophy biomarker

Cardiac hypertrophy diagnosis

Cardiac hypertrophy echocardiography

Cardiac hypertrophy induction

Cardiac hypertrophy natriuretic peptides

Cardiac hypertrophy pathological

Cardiac hypertrophy physiologic

Cardiac hypertrophy physiological

Cardiac hypertrophy, animal models

Cardiomyopathy left ventricular hypertrophy

Cardiovascular hypertrophy

Cardiovascular system hypertrophy

Cellular hypertrophy

Compensatory hypertrophy

Concentric cardiac hypertrophy

Drug development hypertrophy

Eccentric cardiac hypertrophy

Finasteride benign prostatic hypertrophy treatment

Hepatocellular hypertrophy

Hepatocyte hypertrophy

Hepatocytic hypertrophy

Hypertrophied Elbow

Hypertrophied Rheumatoid Arthritis

Hypertrophied Synovium

Hypertrophied endothelial cells

Hypertrophy, after compensatory

Hypertrophy, cardiac left ventricular

Hypertrophy, muscle

Hypertrophy, papillary

Intimal Hypertrophy

Left atrial hypertrophy

Left ventricular hypertrophy

Left ventricular hypertrophy and

Leptin hypertrophy

Liver cell hypertrophy

Mesenteric hypertrophy

Metabolism) hypertrophy

Muscle hypertrophy, protein synthesis

Muscle hypertrophy, protein synthesis increase

Muscular hypertrophy

Myocardial hypertrophy

Pancreatic hypertrophy

Peroneal Tubercle Hypertrophy

Predictive Cardiac Hypertrophy Biomarkers in Nonclinical Studies

Proliferation, cell hypertrophy

Prostate hypertrophy

Prostate hypertrophy/hyperplasia

Prostate prostatic hypertrophy, benign

Prostatic hypertrophy

Regeneration Hypertrophy

Renal tubular hypertrophy

Right Ventricular Hypertrophy (RVH)

Right ventricular hypertrophy

Septal hypertrophy

Thyroid hypertrophy

Ventricular Hypertrophy (LVH)

Ventricular hypertrophy

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