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Biomedical subjects

T F Ferris

Publications and source records attributed to T F Ferris.

At least 37 records · Page 2Linked to original sources
PubMed1982

Urinary concentrating ability and antidiuretic hormone responsiveness in the potassium-depleted dog.

The effects of potassium depletion on urine concentration ability, renal PGE2 excretion, and ADH release were studied in 28 female dogs made K depleted by oral K-exalate and a K-free diet. After K depletion was established (serum K 2.9 +/- 0.1 mEq/L), urine volume increased from control measurements, 596.4 +/- 34.0 to 1201.5 +/- 96.9 ml/24 hr (p less than 0.001); urine PGE2 excretion increased, 985.4 +/- 91.1 to 2122.0 +/- 328.5 ng/24 hr, (p less than 0.001); and Umax decreased, 2006 +/- 74.0 to 1186 +/- 71.9 mOsm/kg H2) (p less than 0.001). Indomethacin (5 mg/kg/day, s.c.) administered on 3 consecutive days after K depletion had been established, resulted in no significant improvement in Umax, 1186.8 +/- 71.9 to 1341.8 +/- 105.6 mOsm/kg H2O. Release of ADH from the neurohypophysis was evaluated by measuring plasma ADH during graded increases in serum tonicity with intravenous hypertonic saline before and after K depletion. Although ADH increased with increasing serum tonicity during both control and K depletion periods, there was a blunting of ADH release during K depletion. The regression coefficient of plasma ADH and serum tonicity was significantly lower during K depletion, 0.24, than in the control period, 0.65, (p less than 0.01). After 3 days of indomethacin (5 mg/kg/day, s.c.) ADH release from the neurohypophysis in response to graded increases in serum tonicity was partially normalized in the K-depleted animals without changes in serum K (regression coefficient, 0.53). K depletion in dogs therefore leads to an increase in the urine volume and an increase in renal PGE synthesis associated with a decrease in Umax. The increase in PGE2 synthesis is not responsible for the defect in Umax, since it is not corrected with indomethacin. The release of ADH in response to raising serum tonicity is blunted during K depletion, which is partially corrected by indomethacin. These data suggest an inhibiting role for PGE2 in the release of ADH from the neurohypophysis during K depletion.

Animals↗
PubMed1979

The effect of prostaglandin-synthesis stimulation and blockade on sodium excretion at a fixed renal perfusion pressure.

PGE synthesis was increased by an infusion of AA and decreased with indomethacin or carpofen. Intrarenal infusions of arachidonate increased RBF from 222 +/- 37 to 275 +/- 51 ml/min (p less than 0.05) and UNaV from 85 +/- 23 to 121 +/- 32 muEq/min (p less than 0.05), with renal vein PGE increasing from 0.41 +/- 0.08 to 1.81 +/- 0.69 ng/ml (p less than 0.05). However, when renal perfusion pressure was reduced and maintained constant at 82 +/- 4 mm Hg during the AA infusion, RBF, and UNaV did not change, 185 +/- 26 vs. 178 +/- 21 ml/min and 10 +/- 3 vs 8 +/- 3 muEq/min, respectively, although renal vein PGE increased from 0.8 +/- 0.2 to 1.95 +/- 0.52 ng/ml (p less than 0.05. During Pl with indomethacin, 2 mg/kg, RBF fell from 210 +/- 27 to 120 +/- 16 ml/min (p less than 0.05), and UNaV diminished from 39 +/- 6 to 22 +/- 10 muEq/min (p less than 0.05), as renal vein PGE decreased from 0.37 +/- 0.04 to 0.19 +/- 0.03 ng/ml (p less than 0.05). When renal perfusion pressure was reduced and maintained constant at 90 +/- 2 mm Hg, renal vein PGE fell from 0.72 +/- 0.29 to 0.20 +/- 0.08 ng/ml (p less than 0.05), whereas RBF and UNaV were unchanged during Pl, 172 +/- 20 vs. 166 +/- 30 and 33 +/- 15 vs. 28 +/- 11, respectively. The results indicate that the change in sodium excretion with variation in prostaglandin synthesis is best explained by concomitant changes in RBF.

Animals↗
PubMed1977

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was presented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

Animals↗
PubMed1977

The hemodynamic effects of potassium deficiency in the dog.

Potassium deficiency for 3 weeks in dogs caused 374 +/- 38 mEq of sodium retention with increase in body weight, plasma volume, and inulin space. Cardiac output increased from 3.7 +/- 0.6 to 5 +/- 0.6 liters/min (P less than 0.02) and systemic vascular resistance decreased from 3,050 +/- 590 to 2,000 +/- 286 dynes/cm per sec2 (P less than 0.05). Plasma renin activity (PRA) increased from 0.4 +/- 0.1 to 17.2 +/- 0.9 ng/ml per hour (P less than 0.01) without change in plasma aldosterone. Angiotensin sensitivity decreased from a rise of 37 +/- 4 mm Hg in mean arterial pressure (MAP) to 10 ng/kg per min before potassium depletion to a rise of 10 +/- 2 mm Hg after hypokalemia. Urinary prostaglandin E (PGE) excretion increased from control values of 1,224 to 1,556 ng/day to 9,352 +/- 3,670 after 21 days of hypokalemia (P less than 0.01). Indomethacin, 150 mg a day for 3 days, decreased urinary PGE to control values as PRA decreased from 17.2 +/- 5.9 to 1.1 +/- .3 ng/ml per hour and angiotensin sensitivity was partially restored. These findings indicate that hypokalemia increased urinary PGE with extracellular fluid volume expansion, decreased sensitivity to angiotensin and increase in PRA.

Angiotensin II↗
PubMed1976

The effect of changes in perfusion pressure on uteroplacental blood flow in the pregnant rabbit.

The effect of perfusion pressure on uteroplacental blood flow was determined in pregnant rabbits utilizing the radioactive microsphere method. Control mean arterial pressure, 93 mm Hg +/- 2.6 SEM, was raised by carotid ligation to 109 +/- 4.1 mm Hg and then reduced with antihypertensive drugs to 74 +/- 1.3 mm Hg. Over this range of pressure there was no significant change in cardiac output, 605 +/- 36, 523 +/- 37, and 540 +/- 39 ml/min; or uteroplacental blood flow, 30 +/- 3.2, 27 +/- 5.2, and 29 +/- 4.5 ml/min, respectively. When prostaglandin synthesis was inhibited with either indomethacin or meclofenamate (2 mg/kg), uterine vascular resistance was higher but maintenance of uteroplacental flow occurred over a perfusion pressure of 89 +/- 6.7-115 +/- 9.3 mm Hg. With more severe hypotension induced with trimethaphan, control arterial pressure fell from 92 +/- 2.4 to 39 +/- 0.9 mm Hg, cardiac output fell from 514 +/- 17 to 407 +/- 22 ml/min (P less than 0.025) and uteroplacental blood flow fell from 6.1 +/- 0.9 to 2.5 +/- 0.9% of cardiac output (P less than 0.05), which represented an absolute fall from 32.4 +/- 5 to 10.6 +/- 3 ml/min (P less than 0.025). There was no significant change in renal blood flow expressed as percentage of cardiac output, 14.9 +/- 2 and 13 +/- 1.5%, or in absolute flow, 75 +/- 7.7 and 54 +/- 7 ml/min with trimethaphan-induced hypotension. These studies indicate that uteroplacental blood flow is maintained relatively constant over a range of perfusion pressure of 60-140 mm Hg in both normal and prostaglandin-inhibited pregnant rabbits. However, with reduction in pressure to 36-42 mm Hg, uteroplacental blood flow falls, expressed as a percentage of cardiac output and in absolute flow.

Animals↗
PubMed1975

Plasma renin and aldosterone in an abdominal pregnancy with toxemia.

The first reported measurement of plasma renin and aldosterone in toxemia with an abdominal pregnancy is presented. In contrast to toxemia where plasma renin and aldosterone are either normal or low, extraordinarily high levels of both were found in this patient which returned to normal after delivery. The role of extrarenal renin in the hypertension of toxemia is discussed and the possibility raised that the elevated renin in this case was of placental origin.

Adult↗
PubMed1975

Prostaglandins and renal function. II. The effect of prostaglandin inhibition on autoregulation of blood flow in the intact kidney of the dog.

In order to evaluate the effect of prostaglandin release on renal autoregulation in the intact kidney of the dog, pressure-flow curves were obtained before and after the administration of either indomethacin or meclofenamate, two potent prostaglandin synthetase inhibitors. After drug administration renal venous prostaglandin E decreased in each of eight studies with a mean change from 286 to 141 pg/ml (p less than .001). In addition, prostaglandin inhibition was associated with a 31 percent decrease in renal blood flow and 58 percent increase in renal resistance. Yet, as renal perfusion pressure was decreased by aortic constriction, the change in flow per pressure reduction and the percent change in renal resistance were not significantly different after prostaglandin inhibition when compared to control values in the same animals. The magnitude of the pressure range over which autoregulation was maintained was also similar in the two groups although both the initial and lowest level of autoregulation were slightly higher after prostaglandin inhibition. It is concluded that the administration of these prostaglandin synthetase inhibitors does not significantly impair renal autoregulation in the intact dog kidney.

Animals↗
PubMed1975

Pathophysiology of a nephrotoxic model of acute renal failure.

Studies were performed in the dog to determine the mechanism of the renal functional impairment which follows the administration of the nephrotoxic agent, uranyl nitrate. In the first series of 28 experiments, total renal blood flow was determined with the radioactive microsphere method before and after uranyl nitrate administration, 10 mg/kg. Total blood flow fell from 199 to 121 ml/min 6 hr after administration of uranyl nitrate (P less than 0.001) but was unchanged 48 hr after administration of the drug. Yet the blood urea nitrogen concentration had increased from a control value of 13 to 120 mg/100 ml at 48 hr (P less than 0.001). Since renal blood flow was normal at 48 hr, micropuncture studies were performed to further evaluate the mechanism of the renal impairment. In the first group of nine studies using a 10 mg/kg dose of uranyl nitrate, nephron glomerular filtration rate (GFR) was reduced 37% while total kidney GFR averaged less than 1% of normal. A similar disparity between superficial and total GFR was noted after a 5 mg/kg dose even though urine flow was comparable to values found in normal hydropenic dogs. Proximal tubular transit time and intratubular pressure were normal. The recovery of 3H-inulin injected into the proximal tubule was 97% in normal dogs and 14% in uranyl nitrate dogs (P less than 0.001). Since there was no difference between early and late proximal tubular nephron GFR, it was suggested that the pars recta, the segment most severely involved histologically, was the main site of inulin leak. Scanning electron microscopy revealed an alteration in epithelial architecture which may have accounted, at least in part, for the diminution in nephron GFR. These studies are interpreted to indicate that the impairment in renal function in this model is due to both leakage of filtrate across damaged tubular epithelium and a modest decrease in nephron GFR.

Acute Kidney Injury↗