Intracortical Distribution of Renal Blood Flow in Hemorrhagic Shock in Dogs

Logan, Alexander G.; José, Pedro A.; Eisner, Gilbert M.; Lilienfield, Lawrence S.; Slotkoff, Lawrence M.

doi:10.1161/01.res.29.3.257

Cited by 38 publications

(21 citation statements)

References 22 publications

(34 reference statements)

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“…Recent studies from this and other laboratories have demonstrated that hemorrhagic hypotension is associ-ated with a marked decrease in the fractional distribution of renal cortical blood flow to outer cortical nephrons (1)(2)(3). This alteration in intrarenal hemodynamics may be related to one or more of the following changes known to occur during hemorrhage: (a) increased humoral release of norepinephrine (4), (b) increased humoral release of angiotensin (5), (c) enhanced adrenergic stimulation (6), and (d) diminished renal perfusion pressure.…”

Section: Introductionmentioning

confidence: 86%

Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

Stein¹,

Boonjarern²,

Mauk³

et al. 1973

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 86%

Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

Stein¹,

Boonjarern²,

Mauk³

et al. 1973

J. Clin. Invest.

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“…Logan, Jose, Eisner, Lilienfield & Slotkoff, 1971;Shirley, MacRae & Walker, 1991). A number of hormones whose release is stimulated by haemorrhage can account, at least in part, for the renal vasoconstriction.…”

Section: Introductionmentioning

confidence: 99%

A micropuncture study of the renal response to haemorrhage in rats: assessment of the role of vasopressin

Shirley¹,

Walter²

1995

Experimental Physiology

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SUMMARYThe acute effects of haemorrhage (15 ml (kg body wt)-') on renal function at whole-kidney and single-nephron levels were studied in Inactin-anaesthetized rats. In order to assess the role of vasopressin in mediating the haemodynamic effects, responses in untreated Long-Evans rats were compared with those in Brattleboro rats (which lack circulating vasopressin) and in Long-Evans rats treated with a V1 receptor antagonist. In time-control animals, there were no significant changes in mean arterial pressure (MAP), excretion rates, glomerular filtration rate (GFR), superficial-nephron GFR (SNGFR) or fluid reabsorption in the superficial proximal tubules during the course of the experiment. Following haemorrhage, the immediate reduction in MAP was followed in each group by partial recovery for 30 min; thereafter, MAP was stable. In untreated Long-Evans rats, haemorrhage was followed by a 26 % reduction in GFR (P < 0-001, measured 60-150 min post-haemorrhage) and a larger reduction (45 %, P < 0.001) in SNGFR, so that the SNGFR/GFR ratio fell significantly ((27.9 + 1.9) x 10-6, control period; (20.2 + 2-2) x 10-6, post-haemorrhage, P <0.01). Slightly greater reductions in GFR and SNGFR were seen in Brattleboro rats and V, antagonist-treated Long-Evans rats, which corresponded to slightly greater haemorrhage-induced reductions in blood pressure in these groups; the falls in the SNGFR/GFR ratio were similar to that in untreated Long-Evans rats. In all three groups of bled rats, fractional reabsorption by the proximal convoluted tubule increased slightly 30-60 min after haemorrhage, but during the subsequent period (60-150 min) returned to values indistinguishable from those during the control period. The results suggest that the renal haemodynamic changes that follow moderate haemorrhage include a preferential reduction in the GFR of superficial nephrons. Vasopressin appears to play no role in this response. Increases in fractional reabsorption in the proximal tubules are seen only during the immediate post-haemorrhage period.

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“…The studies of Logan e t al. (14) also demonstrate the effect of nonspecific stress on renal blood flow distribution. These authors showed that simple cannulation of the external carotid artery in dogs could result in a redistribution of intrarenal blood flow.…”

mentioning

confidence: 79%

“…Many conditions have been reported to result in a redistribution of renal blood flow. These include hemorrhage (14), acidosis (2), changes in hematocrit (17), and external perfusion of a kidney (I 9). Carriere and Biron (5) and Carriere and Friborg (6) have studied intrarenal blood flow distribution during angiotensin infusion.…”

mentioning

confidence: 99%

Effects of Positive Pressure Ventilation on Intrarenal Blood Flow in Infant Primates

et al. 1974

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Extractcortical flow rates in patients with acute failure. Horster and Measurement of intrarenal distribution of renal blood flow by injection of radionuclides in 3-5-day-old infant monkeys showed a preponderance of outer cortical over inner cortical " flow with flow rates of 4.23 and 2.54 ml/min/g, respectively.Intermit tent positive pressure ventilation (IPPV) causes a reversal of this flow pattern. The theoretical difference in nephron function in these two areas suggests that this reversal in intrarenal flow induced by IPPV may have important clinical implications. SpeculationExtrarenal stimuli such as IPPV causes a redistribution of intrarenal blood flow in infant primates. Any stimuli that results in increased production of epinephrine or similar compounds may be responsible for this redistribution by a local effect on outer cortical blood vessels. Our data further suggest that antidiuretic hormone may influence intrarenal blood flow in addition to altering tubular membrane permeability.

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Intracortical Distribution of Renal Blood Flow in Hemorrhagic Shock in Dogs

Cited by 38 publications

References 22 publications

Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

Mechanism of the Redistribution of Renal Cortical Blood Flow during Hemorrhagic Hypotension in the Dog

A micropuncture study of the renal response to haemorrhage in rats: assessment of the role of vasopressin

Effects of Positive Pressure Ventilation on Intrarenal Blood Flow in Infant Primates

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