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Biomedical subjects

I F Ueki

Publications and source records attributed to I F Ueki.

46 records · Page 3Linked to original sources

Micropipette measurement of airway submucosal gland secretion: laryngeal reflex.

We used our microcollection technique to study the effect of mechanical stimulationof the larynx on tracheobrochial gland secretion. The basal secretory rate of 8 glands in 5 cats rose from 18.6 +/- 2.0 nl/min (mean +/- SE) to a maximum of 47.8 +/- 4.0 nl/min within 1 min of mechanical stimulationof the laryngeal mucosa(p < 0.005) and returned to prestimulation levels within 4 to 5 min after cessation of the stimulus. The effect of laryngeal stimulation on gland secretion was prevented by cooling both cerevical vagi to - 3 degrees C before and during stimulation, and was restored by warming both vagito 37 degrees C before stimulaltion. Atropine sulfate (0.5 mg/kg given intravaenously) also prevented the secretory response to laryngeal stimulation. Transsection of the sensory nerves to the larynx blocked this response as well. Electrical stimulation (7 V, 20 Hz, 15 s) of the central end of the cut superior layyngeal nerve increased the rate of secretion of 6 glands in 5 cats from 10.0 +/- 2.0 nl/min to 26.0 +/- 3.0 nl/min (p < 0.01); atropine also prevented this effect.

Animals↗

The effects of sodium substitution and ouabain on ion transport by dog tracheal epithelium.

Using ouabain and sodium removal, we studied the mechanism of chloride transport by dog tracheal epithelium. When applied to the submucosal side of the tissue, 2 x 10(-4) M ouabain decreased the short-circuit current, the net chloride flux toward the lumen, and the net sodium flux toward the submucosa to zero after 30 min. Applied to the luminal side, ouabain had little effect. Potassium-free medium, like ouabain, decreased the short-circuit current when present in the submucosal bath; on the luminal side ti produced a slight increase (7.0 +/- 1.5 per cent; n = 6) in short-circuit current. Replacement of sodium in the submucosal bathing medium by choline led to a decrease in net chloride flux of 84 per cent. Sodium replacement in the luminal bath produced no change in net chloride flux. It is proposed that chloride secretion by this tissue depends on active basolateral sodium pumps, and that a component of chloride entry into the transporting cells from the submucosal medium may be sodium-linked.

Animals↗

Permeability of renal peritubular capillaries to neutral dextrans dextrans and endogenous albumin.

Renal lymph-to-renal vein concentration ratios (CL/CV) for neutral dextrans (18-42 A effective radii) and endogenous serum albumin were measured in rats before and during acute colume expansion with isoncotic plasma or Ringer solution. Under all conditions studied, CL/CV decreased with increasing dextran size, in normal hydropenia falling from 0.93 +/- 0.03 SE at 18 A to 0.24 +/- 0.02 a 42 A (n = 12). Albumin (36 A pradius) behaved in a manner similar to a 40 A dextran, CL/CV averaging 0.33 +/- 0.03 (n = 12) in hydropenia. For all dextran sizes studied and for albumin, CL/CV decreased markedly during either form of volume expansion. Ringer loading produced significantly greater decreases in CL/CV for the larger dextrans and albumin than did plasma loading, and also resulted in much greater increases in renal lymph flow, while causing increases in whole kidney fluid reabsorption similar to those with plasma loading. With a compartmental model in which diffusion of dextrans and albumin from capillary lumen to interstitium is opposed by capillary uptake of tubule reabsorbate, these results are interpreted to indicate that connective reflection coefficients for dextrans with radii great than or equal to 36 A and albumin are essentially equal to 1. Indirect evidence is therefore provided that albumin and the larger globulins exert their full osmotic pressures across the walls of peritubular capillaries.

Animals↗

Permselectivity of of the glomerular capillary wall. Studies of experimental glomerulonephritis in the rat using neutral dextran.

Polydisperse [3h] dextran was infused into eight Munich-Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN), thereby permitting direct measurements of pressures and flows in surface glomeruli and fractional clearances for dextrans [(U/P) dextran/(U/P) inulin] ranging in radius from 18 to 42 A. Despite glomerular injury, evidenced morphologically and by a marked reduction in the glomerular capillary ultrafiltration coefficient, the glomerular filtration rate remained normal because of a compensating increase in the mean net ultrafiltration pressure. In NSN rats, as in normal controls, inulin was found to permeate the glomerular capillary wall without measurable restriction, and dextrans were shown to be neither secreted nor reabsorbed. For dextran radii of 18, 22, 26, 30, 34, 38, and 42 A, (U/P) dextran/(U/P) inulin in NSN and control rats, respectively, averaged 0.90 vs. 0.99, 0.81 vs. 0.97, 0.63 vs. 0.83, 0.38 vs 0.55, 0.20 vs. 0.30, 0.08 vs. 0.11, and 0.02 vs. 0.03. Using a theory based on macromolecular transport through pores, the results indicate that in NSN rats, effective pore radius is the same as in controls, approximately 50 A. In NSN, however, the ratio of total pore surface area to pore length, a measure of the number of pores, is reduced to approximately 1/3 that of control, probably due to a reduction in capillary surface area. These results suggest that proteinuria in glomerular disease is not due simply to increases in effective pore radius or number of pores, as previously believed. Using a second theoretical approach, based on the Kedem-Katchalsky flux equations, dextran permeability across glomerular capillaries was found to be slightly lower, and reflection coefficient slightly higher in NSN than in control rats.

Animals↗

Permselectivity of the glomerular capillary wall to macromolecules. II. Experimental studies in rats using neutral dextran.

To determine the permselectivity characteristics of the glomerular capillary wall, known molecular size fractions of [3H]dextran, prepared by gel chromatography, were infused into normally hydrated Wistar rats, thus permitting simultaneous measurement of Bowman's space/plasma water (BS/P) and urine/plasma water (U/P) concentration ratios, along with glomerular pressures and flows. Since (BS/P)inulin = 1.01 +/- 0.01 SE(n = 34, radius = approximately 14 A) and since (BS/P)dextran/(BS/P)inulin equaled (U/P)dextran/(U/P)inulin for dextrans ranging in molecular radius from 21 to 35 A, these findings validate that dextrans are neither secreted nor reabsorbed. For dextran radii of 20, 24, 28, 32, 36, 40, and 44 A, (U/P)dextran/(U/P)inulin averaged 0.99, 0.92, 0.69, 0.42, 0.19, 0.06, and 0.01, respectively. In accord with theoretical predictions that these fractional dextran clearances should vary appreciably with changes in glomerular transcapillary pressures and flows, an increase in glomerular plasma flow rate, induced in these same rats by plasma volume expansion, resulted in a highly significant lowering of fractional clearance of all but the smallest and largest dextrans studied. These findings emphasize that fractional solute clearances alone are inadequate to describe the permselective properties of the glomerular capillary wall unless glomerular pressures and flows are also known. This sensitivity of fractional dextran clearance to changes in plasma flow indicates that dextrans are transported across the capillary not only by bulk flow but also to an important extent by diffusion.

Animals↗

Dynamics of glomerular ultrafiltration in the rat. V. Response to ischemic injury.

An experimental model of postischemic, acute renal failure has been developed in Wistar rats with surface glomeruli, thereby making possible a direct assessment of the mechanisms responsible for the fall in glomerular filtration rate that characterizes this disorder. Whole kidney and cortical single nephron filtration rates were reduced proportionately, on average by approximately 40%, after 3 h of nearly complete occlusion of the ipsilateral renal artery. The possibility of a significant transtubular leak of inulin was excluded. This decline in filtration rate occurred in the absence of measured changes in mean arterial pressure, mean glomerular transcapillary hydrostatic pressure, or net ultrafiltration pressure at afferent and efferent ends of the glomerular capillary. Net ultrafiltration pressure at the efferent end of the capillary approached zero both before and after ischemic injury, demonstrating that filtration pressure equilibrium was achieved throughout this study. Single nephron filtration fraction remained unchanged, indicating that the fall in filtration rate was accompanied by a proportional decline in glomerular plasma flow. The results indicate that the fall in filtration rate was solely the consequence of this fall in glomerular plasma flow. Since filtration rate per nephron is equal to the product of the ultrafiltration coefficient and mean ultrafiltration pressure, this product must also have fallen in proportion to the decline in glomerular plasma flow. Evidence is presented to indicate that a change in ultrafiltration coefficient is not required to account for the observed fall in filtration rate. The reduction in glomerular plasma flow, occuring in the absence of a concomitant decline in mean glomerular capillary hydrostatic pressure, resulted from large and proportional increases in afferent and efferent arteriolar resistances. These resistance changes appear to play a fundamental role in the pathogenesis of this form of acute renal failure.

Acute Kidney Injury↗

Renal response to chronic intravenous salt loading in the rat.

The natriuresis of acute Ringer's loading is associated with a rise in the rate of delivery of fluid beyond the proximal tubule due both to a rise in glomerular filtration and a fall in absolute reabsorption, the latter being causally mediated, at least in part, by the accompanying fall in postglomerular vascular [protein]. To determine whether these factors also contribute to the renal response to chronic Ringer's loading, nine rats given continuous infusions, 30% body weight/day over 5-14 days, were studied using free-flow micro-puncture techniques. Results were compared with data from 10 chronic control rats given less than 1.5% body wt/day. Late proximal tubule fluid-to-plasma [inulin] ratios, (TF/P)(IN), single nephron glomerular filtration rate (SNGFR), absolute proximal reabsorption, and postglomerular vascular [protein] in chronic control rats and chronically loaded rats averaged 2.2+/-SE 0.1 (n = 35) and 1.5+/-0 (35), P<0.001; 37+/-2 (35) and 47+/-4 nl/min (35), P<0.05; 19+/-1 (35) and 16+/-2 nl/min (35), P>0.2; and 9.5+/-0.3 (8) and 8.6+/-0.3 g/100 ml (8), P>0.05, respectively. Thus the fall in (TF/P)(IN) and the rise in distal delivery during chronic Ringer's loading were due almost entirely to the rise in SNGFR, and not to any large fall in absolute reabsorption. Hence chronic and acute Ringer's loading increase delivery of proximal tubule fluid by different mechanisms, with chronic sodium homeostasis being governed overwhelmingly by adjustments in GFR. When, however, an acute Ringer's load was infused into chronically loaded rats, we observed significant and parallel reductions in absolute proximal reabsorption and postglomerular vascular [protein]. These findings suggest that the difference between the effects of chronic vs. acute Ringer's loading on absolute proximal reabsorption may have been due, at least in part, to the corresponding difference in the effects these two loading procedures have on postglomerular vascular [protein].

Aminohippuric Acids↗