project into the dilated end of its corresponding renal tubule, from which it is separated by a thin layer of cells called glome—rular (Bowman' s) capsule; glomerulus plus capsule form a renal (Nalpighian) corpuscle. The cortex contains multitudes of such corpuscles, each giving rise to a tubule which passes down into the medul la and back again in the so—called loop of Henle. Back in, the cortex loop ends in a functional tubule which joins а larger collecting tube. Ultimately, a number of collecting tubes combine to form an excretory tube, which opens at the ареx of a papilla into a renal calyx. The efferent vessel from the glomerulus accompanies the loop of Henle, supply ing the tubule on the way and finally ends in a small vein. A renal corpuscule plus its complement of tubules and blood vessels is called a renal unit, or nephron; there are said to be one million such units in each kidney, their tubing totaling a length of some twenty miles.
New words
bean—shaped organ – орган в форме боба
four inches long – 4 дюйма в длину
two inches wide – 2 дюйма в ширину
peritoneum – брюшина
lumbar – поясничный
renal cortex – корковый слой
renal medulla – мозговой слой
fibrous – волокнистая
dilated – расширенный
to be separated – быть разделенным
loop of henle – петля Генле
52. Acute renal failure
The two major mechanisms may participate in association between intratubular hemorrage and nephron damage in acute renal failure. The first mechanism is direct nephrotoxicity from hemoglobin, because intratubular degradation of erythrocytes releases heme and iron which are toxic to cells. The second mechanism is hypoxic damage induced by regional vasoconstriction because heme avidly binds the potent vasodilator nitric oxide.
Intratubular degradation of hemoglobin releases heme containing molecules and eventually free iron. These breakdown products, also elaborated from myoglobin, probably play an important role in the pathogenesis of acute tubular necrosis. Endocytic reabsorption from the tubular him en of filtered free hemoglobin or myoglobin may be a major pathway to proximal tubular damage in pigment nephropathy. In addition, free iron promotes the formation of oxygen free radicals, lipid peroxidation and cell death Another source of toxic iron is from the breakdown of intracellular cytochrom P–450 under hypoxic condition. One of the most potent intrarenal vasodilator system is nitric oxide, produced from L—arginine in vascular endothelium. smooth muscle and tubular calls, causing Vascular smooth muscle relaxation through the induction of intracellular cyclic GMP. Blocking nitric oxide synthesis causes profound vascular constriction, systemic hypertension and a marked decline in renal blood flow. Endothelial dysfunction with reduced nitric oxid production may underlie the defective regional vasodilation in diabetes and atherosclerosis, predisposing to renal ischemia and nephrotoxic insult.
Hemoglobin avidly binds nitric oxide and ingibits nitrovasodilation. The presence of large pool of hemoglo bin in the tubular lumen could therefore affect the vasomotor balance of kidney circulation: intrarenal vasoconstriction is likely to be most pronounced and most significant in the medulla., because the ratio of tubular mass to vessels surface may be particularly high in this region. The medulla normally functions at low oxygen tension, because of limited medulla blood flow and counter—current exchange of oxygen. Inhibinion of nitric oxide synthesis induces severe and prolonged outer medullary hypoxia and predisposes to tubular necrosis Unfortunately, biopsy specimens of glomerulonephritis associated with acute tubular necrosis do not provide the precise distribution of the tubular lesions.
In chronic glomerulonephritis tubulo—interstitiaJ damage has often been reported as correlate of kidney function and also its best prognostic marker. Glomerular obsolescence deprives the renal parenchyma from nutritional blood flow, leading to tubule—interstitial fibrosis in medullary rays and outer medulla. Proteinuria imposes to the proximal tubules a constant burden of reabsorption and catabolism of albumin and other proteins from the tubular lumen, which have been suggested to cause cellular injury.
New words
nephron – нефрон
intratubular – внутриканальцевый
heme – гем
tubular necrosis – канапьцевый некроз
reabsorption – реабсорбция
proteinuria – протеннурия
53. Iron in the body
It is accepted that the total amount of iron in the body is between 2 and 5 g., varying with body— weight and hemoglobin level; about two—thirds of this is in the form of hemoglobin and about 30 % is storage iron; iron in 1 т1уо– globin and enzymes makes up the small remaining fraction together with iron in transport, which is only 0,12 %. There is a big difference between the sexes: in the adult male the total iron is about 50 mg. per kg. body—weight. But in the adult female the figure is only 35 mg. per kg., mainly be cause the normal blood —level of hemoglobin is lower than in the male. Iron exists in the body mainly in two forms: firstly, as heme in hemoglobin, and cytochrome concerned with the utilization of oxygen; and secondly, bound to a protein without heme formation, as storage and transport iron. Iron in the body has a very rapid turnover, since some 3 million red blood cells are broken down per second and the greater part of the iron released is returned to the bone marrow and re—formed into fresh hemoglobin; some 6,3 g. of hemoglobin containing 21 mg. of iron is handled this way every 24 hours.
The amount of iron in the body is regulated by control of absorption, since excretion is very small. The amount of iron absorbed from food differs with different foodstuffs, so the com position of the diet is important. Absorption can be increased in the normal Individual when the blood—hemoglobin is lower than normal and is the iron stores are low. Iron stores are normally lower in women than men and so they tend to absorb more iron. Iron absorption can decrease in older persons, especially in those over 60. Many estimates have agreed that the average Western diet pro vides between 10 and 15 mg. of iron daily, of which only 5—10 % is absorbed.
Iron absorption takes place mainly in the upper jejunum, though some is absorbed in all parts of the small intestine and even in the colon. Iron in food is mostly in ferric form and must b е reduced to the ferrous form before it can be absorbed; this reduction begins in the stomach – though very little is absorbed there – and continues in the small intestine. The iron is absorbed via the brush—border of the intestine and then may take one of two paths; it is either passed into the blood, where it combines with a globulin, and passes to the marrow or to storage sites; or it combines with the protein, which is then deposited in the intes tinal cells.
Iron is lost mostly through the gastrointestinal tract by way of red cells and intestinal cells containing iron lost in the constant desquamation from the intestinal mucosa.
New words
iron – железо
varying – изменение
hemoglobin – гемоглобин
storage – хранение
mioglobin – миоглобин
fraction – фракция
together – вместе
body—weight – масса тела
desquamation – десквамация
54. Atherosclerotic mechanisms
Pivotal mechanisms involved in atherogenesis include.
1. Focal intimal influx and accumulation of plasma lipoproteins at lesion—prone sites.
2. Focal intimal monocyte—macrophage recruitment.
3. Generation within the intima of reactive oxygen species of free radicals by smooth muscle cells,
