199 research outputs found

    Some Biochemical Properties of Pemphigoid Antigen Bound to the Surface of Dissociated Epidermal Basal Cells

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    Bullous pemphigoid antigen (BP Ag) is a cell surface marker of epidermal basal cells. The functional role of this molecule is unknown. Epidermal cell suspensions obtained by trypsinization of skin show a population of epidermal basal cells with a polar rim of antigen as demonstrated by indirect immunofluorescence technique. This study shows that treatment of these cells suspensions with a variety of proteolytic and glycosidic enzymes failed to remove the antigen from these basal cells. BP Ag was also stable upon incubation with distilled water, Triton X-100, PBS, and 1 m NaCl. Treatment of epidermal basal cells with 2 n NaSCN, 1% periodic acid, and 4 m urea, as well as acidic pH or 56°C temperature, abolished the reactivity of these cells with BP antibodies

    Paradoxical response of plasma atrial natriuretic hormone to pericardiocentesis in cardiac tamponade

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26804/1/0000360.pd

    Clinical syndromes associated with disorders of renal tubular chloride transport: Excess and deficiency of a circulating factor?

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    Two contrasting patients are described, one with pseudo-Bartter's syndrome induced by frusemide abuse and the other a case of hyporeninaemic hypoaldosteronism.The clinical and biochemical features of these two conditions are the opposite of each other and, in the first patient, the effects of frusemide were antagonised by treatment with indomethacin while in the second frusemide itself corrected the syndrome.The decreased pressor sensitivity to infused angiotensin II seen in the patient with pseudo-Bartter's syndrome was corrected with indomethacin and the enhanced pressor sensitivity seen in hyporeninaemic hypoaldosteronism was reversed with frusemide.Frusemide, an agent which blocks chloride transport at the ascending limb of Henle's loop, was respectively thus the cause and the cure of these conditions. On the basis of this the suggestion is made that Bartter's syndrome and hyporeninaemic hypoaldosteronism represent respectively an excess and a deficiency of a circulating factor similar to frusemide capable of blocking renal tubular chloride transport.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24748/1/0000170.pd

    Natriuresis associated with elevated plasma atrial natriuretic hormone during supraventricular tachycardia

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    Elevated plasma levels of atrial natriuretic hormone (ANH) have been found in patients during paroxysmal supraventricular tachycardia (SVT) and other clinical syndromes. However, physiologic effects of this endogenous ANH have not been demonstrated. To determine whether the rise in ANH during SVT is associated with either a natriuresis or kalluresis, urine sodium and potassium levels were measured in five patients at baseline and during SVT simulated by rapid atrioventricular pacing. Plasma ANH levels increased from 149 +/- 35 pmol/L at baseline to 387 +/- 31 pmol/L (p = 0.007) during SVT. Plasma vasopressin and renin levels were unchanged. Urine sodium levels increased 49% from 1.54 +/- 0.66 mEq/hr at baseline to 2.29 +/- 0.89 mEq/hr (p = 0.044) during SVT, and urine potassium levels increased 22% from 4.14 +/- 0.10 mEq/hr to 5.04 +/- 1.25 mEq/hr (p = 0.018). Urine sodium and potassium levels returned to baseline values 1 hour after pacing. Thus elevated plasma levels of ANH during SVT are associated with both a natriuresis and kalluresis, which may represent physiologic effects of the endogenously secreted hormone.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28078/1/0000523.pd

    Plasma levels of immunoreactive atrial natriuretic factor increase during supraventricular tachycardia

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    A significant diuretic and natriuretic response occurs during paroxysmal supraventricular tachycardia (SVT). Although the diuresis may be secondary to suppression of vasopressin secretion, the etiology of the natriuresis remains unexplained. To determine if atrial natriuretic factor (ANF) could contribute to the polyuric response during SVT, 10 patients were studied: five during spontaneous SVT and five during simulated SVT produced by rapid simultaneous atrial and ventricular pacing. Plasma immunoreactive ANF (IR-ANF) levels measured by radioimmunoassay were obtained at baseline (before and/or 24 to 48 hours after SVT) and after at least 15 minutes of SVT in all patients. During spontaneous and simulated SVT, IR-ANF was significantly elevated (mean +/- SE; 275 +/- 68 pmol/L) compared to baseline (28 +/- 7 pmol/L; P = 0.0036). Similar increases in IR-ANF were noted during both simulated and spontaneous SVT. To determine if this IR-ANF release was related to the increase in heart rate or the rise in right atrial pressure during SVT, IR-ANF levels were also measured in five patients with sinus tachycardia and in six patients with congestive heart failure, IR-ANF was significantly related to right atrial pressure (r = 0.93; P = 0.0009) but not to heart rate (r = 0.46). Thus, IR-ANF is elevated during SVT and may contribute to the natriuretic response. The stimulus to IR-ANF secretion during SVT appears to be related to the rise in right atrial pressure rather than to the increase in heart rate.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26001/1/0000067.pd
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