Effects of Asphyxia on Renal Function in the Newborn Piglet

Alward, Charles T; Hook, Jerry B.; Helmrath, Thomas A.; Bailie, Michael D.

doi:10.1203/00006450-197803000-00013

Cited by 32 publications

(20 citation statements)

References 14 publications

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“…In the present study the significant increase in filtration fraction associated with absence of changes in GFR suggest that during fetal hypoxemia the renal vasoconstriction is more important at the efferent than at the afferent arteriolar level and that fetal GFR is not necessarily plasma flow dependent. Similar findings also have been made by Alward et al (1978) in newborn piglets following the simultaneous production of hypoxemia, hypercarbia, and acidosis.…”

Section: Influence Of Hypoxemia On Fetal Renal Hemodynamics and Circusupporting

confidence: 85%

“…In previous experiments, Alward et al (1978) demonstrated in newborn piglets that production of hypoxemia associated with hypercarbia and acidosis increased absolute sodium excretion. In the present study, factors that could have contributed to the increase in electrolytes excretion during hypoxemia, and especially after hypoxemia, were not investigated.…”

Section: Influence Of Hypoxemia On Water and Electrolyte Excretion Bymentioning

confidence: 93%

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Developmental aspects of the renal response to hypoxemia in the lamb fetus.

Robillard¹,

Weitzman²,

Burmeister

et al. 1981

Circulation Research

128

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SUMMARY The effects of fetal hypoxemia on renal hemodynamics and renal function were studied in two groups of chronically catheterized young (<120 days of gestation) and near-term lamb fetuses (>130 days). Fetal hypoxemia produced, in both groups, a significant decrease in renal blood flow (RBF) and a significant increase in the filtration fraction. However, the glomerular filtration rate (GFR) did not change significantly, suggesting that the renal vasoconstriction associated with fetal hypoxemia was more important at the efferent than at the afferent arteriolar level. In the group of near-term fetuses, the decrease in RBF correlated closely with changes in plasma renin activity (PRA) (r = -0.77). No changes in PRA were observed during hypoxemia in the group of young fetuses. After hypoxemia, reactive hyperemia associated with a significant increase in urinary prostaglandin excretion (PGE and PGF 2a ) was observed in near-term fetuses but not in young fetuses. It also was demonstrated that fetal hypoxemia produced a significant increase in fetal plasma concentrations of vasopressin associated with an antidiuresis in all but one near-term fetus and in 50% of the young fetuses, suggesting that the ability of the fetal kidney to reabsorb free water is more developed in near-term fetuses. Finally, fetal hypoxemia had no effect on mean arterial pressure and heart rate in young fetuses; however, in nearterm fetuses, a significant increase in blood pressure and a decrease in heart rate were observed. In summary, it appears that the response of the fetal kidney to hypoxemia depends on the degree of fetal maturation. Circ Res 48: 128-138. 1981

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Section: Influence Of Hypoxemia On Fetal Renal Hemodynamics and Circusupporting

confidence: 85%

Section: Influence Of Hypoxemia On Water and Electrolyte Excretion Bymentioning

confidence: 93%

Developmental aspects of the renal response to hypoxemia in the lamb fetus.

Robillard¹,

Weitzman²,

Burmeister

et al. 1981

Circulation Research

128

View full text Add to dashboard Cite

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“…The renin-angiotensin-aldosterone (RAA) system has been suggested as a possible regulator of hemodynamic responses to pathophysiological conditions such as hypoxemia (Mattioli et al, 1975;Alward et al, 1978;Robillard et al, 1981). Furthermore, activity of the RAA system varies with postnatal age, including postnatal age-related differences in production of, and response to, angiotensin II, the vasoconstrictor product of angiotensin-converting enzyme activity (Skeggs et al, 1976;Pipkin et al, 1974;Mott, 1975;Siegel and Fisher, 1977;Siegel and Fisher, 1980;Wallace et al, 1980aWallace et al, , 1980bSiegel, 1981).…”

mentioning

confidence: 99%

Renal and adrenal responses to hypoxemia during angiotensin-converting enzyme inhibition in lambs.

Weismann¹,

Herrig²,

McWeeny³

et al. 1983

Circulation Research

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SUMMARY. Chronically catheterized lambs (4-37 days postnatal age) (n =35) were studied to test the hypothesis that the products of angiotensin-converting enzyme activity are involved in renal and adrenal responses to normocapnic hypoxemia in immature lambs. Arterial angiotensin II (from 111.0 ± 38.8 to 71.0 ± 38.8 pg/ml, P < 0.01) and aldosterone (from 128.0 ± 98.0 to 62.1 ± 27.9 pg/ml, P < 0.01) concentrations were significantly decreased and vasopressor responses to angiotensin I were greater than 90% inhibited by continuous intravenous infusion of angiotensin-converting enzyme inhibitor (captopril, 2.5 /ig/kg/min, n =16). Baseline mean arterial pressure (64 ± 14 vs. 78 ± 9 mmHg) and urinary sodium excretion rate (UN 8 V 3.04 ± 2.83 vs. 15.00 ± 20.00 fiEq//min) were significantly (P < 0.05) decreased in captopril-treated lambs vs. control lambs. Baseline arterial plasma renin activity was significantly (P < 0.01) increased in captopril-treated vs. control lambs (8.6 ± 9.0 vs. 100.0 ± 64.0 ng/ml per hr). Normocapnic hypoxemia (P02 38 ± 6 torr for 30 minutes) during captopril infusion was associated with no significant (P > 0.05) changes in renal hemodynamics and function, including glomerular filtration rate (from 0.34 ± 0.24 to 0.35 ± 0.25 ml/min per g). Urinary prostaglandin E excretion rate (from 0.655 ± 0.703 to 1.310 ± 1.020 ng/min) and adrenal blood flow (from 2.67 ± 1.69 to 6.24 ± 3.73 ml/min per g) increased significantly (P < 0.05) under these conditions. Arterial epinephrine (from 0.11 ± 0.07 to 1.1 ± 1.8 ng/ml), norepinephrine (0.48 ± 0.38 to 3.2 ± 5.4 ng/ml), and arginine vasopressin (from 5.11 ± 2.20 to 10.70 ± 8.61 jiU/ml) also increased significantly (P < 0.05) in response to hypoxemia during angiotensin-converting enzyme inhibition with captopril. None of these responses to hypoxemia were significantly different from that of uninhibited (control) lambs (n=19). In contrast, cortisol response to hypoxemia was significantly (P < 0.05) less in captopril-treated lambs (captopril vs. control, -1.00 ± 1.90 vs. 3.40 ± 3.30 /ig/dl). These data suggest that the products of angiotensin-converting enzyme activity are not important regulators of renal responses to hypoxemia, but may be involved in cortisol responses to normocapnic hypoxemia in immature lambs. (Circ Res 52: 179-187, 1983)

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“…In animal models as in humans, hypoxemia can lead to functional renal insufficiency (5)(6)(7). In the newborn rabbit, acute normocapnic hypoxemia induces renal hypoperfusion with decreased GFR and RBF (4,(7)(8)(9).…”

mentioning

confidence: 99%

Renal Effects of Adenosine A1-Receptor Blockade with 8-Cyclopentyl-1,3-Dipropylxanthine in Hypoxemic Newborn Rabbits

et al. 2003

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The key role of intrarenal adenosine in mediating the hypoxemic acute renal insufficiency in newborn rabbits has been well demonstrated using the nonspecific adenosine antagonist theophylline. The present study was designed to define the role of adenosine A 1 receptors during systemic hypoxemia by using the specific A 1 -receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Renal function parameters were assessed in 31 anesthetized and mechanically ventilated newborn rabbits. In normoxia, DPCPX infusion induced a significant increase in diuresis (ϩ44%) and GFR (ϩ19%), despite a significant decrease in renal blood flow (RBF) (Ϫ22%) and an increase in renal vascular resistance (RVR) (ϩ37%). In hypoxemic conditions, diuresis (Ϫ19%), GFR (Ϫ26%), and RBF (Ϫ35%) were decreased, whereas RVR increased (ϩ33%). DPCPX administration hindered the hypoxemia-induced decrease in GFR and diuresis. However, RBF was still significantly decreased (Ϫ27%), whereas RVR increased (ϩ22%). In all groups, the filtration fraction increased significantly. The overall results support the hypothesis that, in physiologic conditions, intrarenal adenosine plays a key role in regulating glomerular filtration in the neonatal period through preferential A 1 -mediated afferent vasoconstriction. During a hypoxemic stress, the A 1 -specific antagonist DPCPX only partially prevented the hypoxemiainduced changes, as illustrated by the elevated RVR and drop in RBF. These findings imply that the contribution of intrarenal adenosine to the acute adverse effects of hypoxemia might not be solely mediated via the A 1 receptor. Adenosine is ubiquitous in the kidney. Intrarenal adenosine vasoconstricts the preglomerular vessels via the A 1 receptors, while dilating the efferent arterioles via the A 2 receptors. It thus affects GFR as well as RBF and its distribution within the kidney. In addition to its vascular actions, intrarenal adenosine modulates renal mechanisms, including TGF, renin release, and the tubular handling of electrolytes and water. Intrarenal adenosine also appears to be an important hemodynamic mediator in some models of vasomotor nephropathy, such as those induced by intramuscular glycerol injection (1), contrast media (2), cisplatin (3), or hypoxemia (4).In animal models as in humans, hypoxemia can lead to functional renal insufficiency (5-7). In the newborn rabbit, acute normocapnic hypoxemia induces renal hypoperfusion with decreased GFR and RBF (4, 7-9). The underlying mechanism of this hypoxemia-induced vasomotor nephropathy still remains controversial. The chemoreceptor-mediated reflex and/or the activation of vasoactive factors such as angiotensin II (AII) (9), endothelin (10), nitric oxide (8), or bradykinin (11) have been suggested to play a role.We previously demonstrated that the administration of theophylline, a nonspecific antagonist to adenosine receptors, ameliorates the hypoxemia-induced renal hemodynamic changes seen in the newborn rabbit model (4). Moreover, in neonates with respiratory distress syndrome (12)

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Effects of Asphyxia on Renal Function in the Newborn Piglet

Cited by 32 publications

References 14 publications

Developmental aspects of the renal response to hypoxemia in the lamb fetus.

Developmental aspects of the renal response to hypoxemia in the lamb fetus.

Renal and adrenal responses to hypoxemia during angiotensin-converting enzyme inhibition in lambs.

Renal Effects of Adenosine A1-Receptor Blockade with 8-Cyclopentyl-1,3-Dipropylxanthine in Hypoxemic Newborn Rabbits

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