Biomedical subjects

G R Marchand

Publications and source records attributed to G R Marchand.

29 records · Page 2Linked to original sources

PubMed1976

Determinants of glomerular filtration rate in the dog.

Micropuncture techniques were used to evaluate the determinants of glomerular filtration in hydropenic dogs. Stop-flow and servo-null techniques were used to estimate the glomerular capillary and proximal tubule hydrostatic pressures. The validity of stop-flow estimates was verified by comparisons with direct puncture of glomerular capillaries in Munich-Wistar rats. Efferent arteriolar oncotic pressure was calculated from the filtration fraction and systemic protein concentrations. This calculation was verified in separate experiments by measurement of the protein concentration in blood collected directly from efferent arterioles. In 14 dogs, estimated glomerular capillary pressure (GCP) averaged 65.8 +/- 2.9 mmHg and proximal tubule pressure (PT) averaged 20.5 +/- 1.3 mmHg. The net hydrostatic filtration pressure (GCP - PT) of 45.3 +/- 2.7 mmHg was significantly higher than the efferent arteriolar oncotic pressure (piEA) of 33.2 +/- 2.8 mmHg (P less than .001). These findings indicate that filtration dynamics in the dog are characterized by filtration pressure disequilibrium.

Animals↗

PubMed1976

Comparison of proximal tubule fluid-to-plasma ultrafiltrate chloride ratio in rats and dogs.

Previous studies in rats have demonstrated that the concentration of chloride in proximal tubule fluid is greater than that in plasma. The gradient reaches a free-flow steady-state level in the early proximal tubule and is maintained throughout the accessible proximal tubule. On the other hand, studies in dogs are in conflict regarding either the existence of a gradient or the development of a free-flow steady-state level. Since a species difference of tubule fluid to plasma chloride (TF/PC1) may exist, the present study was done to systematically compare the tubule fluid to ultrafiltrate chloride ratio (TF/UFC1) in hydropenic rats and dogs during normal acid-base balance. Chloride was analyzed by microelectrometric titration. In the rat the TFC1 and UFC1 concentrations were 139 +/- 1.4 and 120 +/- 1.2 meq/1, respectively. In the dog the TFC1 and UFC1 concentrations were 138 +/- 1.3 and 121 +/- 1.5 meq/1, respectively. Thus, there was no significant difference in the TF/UFC1 ratio between the rat (1.17 +/- 0.02) and the dog (1.14 +/- 0.01). Furthermore, regression analysis indicates that there is no correlation between TF/UFC1 and TF/PIn in either the rat or dog, which suggests that the gradient originates early in the proximal tubule and is maintained throughout the accessible proximal tubule in both species.

Animals↗

PubMed1976

Phosphaturic effect of dopamine in dogs. Possible role of intrarenally produced dopamine in phosphate regulation.

A possible role for dopamine in phosphate handling by the dog kidney was investigated by intrarenal artery infusions of dopamine. Dopamine increased fractional phosphate excretion both in the presence and absence of control of parathyroid hormone and calcitonin. In addition, dopamine increased both renal blood flow and sodium excretion, however, the phosphaturia was independent of these changes; since 30 min after completion of dopamine infusion, renal blood flow and sodium excretion returned to control levels and phosphate excretion remained elevated. For comparison, the vasodilator isoproterenol increased renal blood flow and sodium excretion without a significant change in fractional phosphate excretion. Thus, the phosphaturic effect of dopamine is probably independent of its vasodilator effect. The phosphaturic effect of dopamine could not be accounted for by subsequent conversion to norepinephrine, since norepinephrine was antiphosphaturic in the dog. The effect of endogenous dopamine on renal phosphate excretion was investigated by intrarenal infusion of the precursor dopa. Dopa was phosphaturic both in the presence and absence of parathyroid hormone and calcitonin. In dogs pretreated with carbidopa, which blocks conversion of dopa to dopamine, dopa was no longer phosphaturic, although the kidney remained responsive to dopamine. It is postulated that dopamine may play a role in the intrarenal regulation of phosphate excretion.

Animals↗

PubMed1976

Lack of effect of hypocalcemia on renal phosphate handling.

A possible effect of decreased plasma ionized calcium concentration on renal phosphate handling was investigated in dogs with control of parathyroid hormone. Intrarenal artery infusion of either EDTA or sodium citrate decreased ionized calcium concentration 25 per cent in renal vein blood but had no significant effect on fractional phosphate excretion. Similarly, intravenous infusion of chelators had no significant effect on fractional phosphate excretion. It is concluded that acute decreases in ionized calcium have no significant effect on the renal handling of phosphate.

Animals↗

PubMed1975

Effects of extracellular fluid volume contraction and expansion on the bicarbonaturia of parathyroid hormone.

To evaluate the effect of extracellular fluid volume alterations on the bicarbonaturia of parathyroid hormone, thyroparathyroidectomized dogs were made alkalotic and volume-contracted or expanded through hemodialysis. Clearance studies were performed before and after infusion of purified bovine parathyroid extract (PTE). Glomerular filtration rate and blood bicarbonate concentrations were kept constant throughout the experiments. A significant increase in fractional bicarbonate excretion was observed following PTE infusion in both the volume-contracted (8.67 +/- 3.25 to 14.70 +/- 3.63%, P less than 0.010) and the volume-expanded state (22.80 +/- 3.04 to 37.26 +/- 3.38%, P less than 0.050). It is concluded that PTE decreases reabsorption of bicarbonate independent of the volume state of the animal.

Alkalosis↗

PubMed1975

Furosemide induced release of prostaglandin E to increase renal blood flow.

Levels of PGE in renal venous blood were found to be significantly elevated at the time RBF was increased by furosemide. Following indomethacin, a second dose of furosemide failed to increase RBF and levels of PGE in renal venous blood were not elevated. Levels of PGF and PGA were not affected by furosemide. The increase of PGE in renal venous blood at the time of renal dilation supports the hypothesis that furosemide increases RBF by releasing PGE. An intrarenal action of the released PGE is implied by this mechanism.

Animals↗

PubMed1974