Abstract
To evaluate the effects of intravenously administered ritodrine hydrochloride on sodium and water metabolism, a pregnant baboon model was studied. Animals given ritodrine retained significantly more sodium (p < 0.001) and administered fluids (p < 0.002) compared with control animals. Although plasma volume did not change significantly within or between the two groups, extracellular volume increased by a mean of 1,480 ml in those given ritodrine compared with 790 ml in the control animals. There was no significant difference between animals given ritodrine and their controls regarding serial hematocrits, serum sodium, or colloid oncotic pressures. From this we conclude that the retained sodium and water was in the interstitial space. Since plasma volume was unaltered by ritodrine administration it seems unlikely that pure volume overload can explain the pulmonary edema induced by β-mimetics. Combined with the prior observation that direct pulmonary capillary membrane toxicity does not occur, the likely pathophysiology of β-agonist-induced pulmonary edema invclves left ventricular failure.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 254-259 |
| Number of pages | 6 |
| Journal | American Journal of Obstetrics and Gynecology |
| Volume | 147 |
| Issue number | 3 |
| State | Published - Oct 1 1983 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
- Obstetrics and Gynecology
Cite this
Ritodrine hydrochloride infusion in pregnant baboons. II. Sodium and water compartment alterations. / Hankins, Gary; Hauth, John C.; Kuehl, Thomas J.; Brans, Yves W.; Cunningham, F. Gary; Pierson, Wayne.
In: American Journal of Obstetrics and Gynecology, Vol. 147, No. 3, 01.10.1983, p. 254-259.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ritodrine hydrochloride infusion in pregnant baboons. II. Sodium and water compartment alterations
AU - Hankins, Gary
AU - Hauth, John C.
AU - Kuehl, Thomas J.
AU - Brans, Yves W.
AU - Cunningham, F. Gary
AU - Pierson, Wayne
PY - 1983/10/1
Y1 - 1983/10/1
N2 - To evaluate the effects of intravenously administered ritodrine hydrochloride on sodium and water metabolism, a pregnant baboon model was studied. Animals given ritodrine retained significantly more sodium (p < 0.001) and administered fluids (p < 0.002) compared with control animals. Although plasma volume did not change significantly within or between the two groups, extracellular volume increased by a mean of 1,480 ml in those given ritodrine compared with 790 ml in the control animals. There was no significant difference between animals given ritodrine and their controls regarding serial hematocrits, serum sodium, or colloid oncotic pressures. From this we conclude that the retained sodium and water was in the interstitial space. Since plasma volume was unaltered by ritodrine administration it seems unlikely that pure volume overload can explain the pulmonary edema induced by β-mimetics. Combined with the prior observation that direct pulmonary capillary membrane toxicity does not occur, the likely pathophysiology of β-agonist-induced pulmonary edema invclves left ventricular failure.
AB - To evaluate the effects of intravenously administered ritodrine hydrochloride on sodium and water metabolism, a pregnant baboon model was studied. Animals given ritodrine retained significantly more sodium (p < 0.001) and administered fluids (p < 0.002) compared with control animals. Although plasma volume did not change significantly within or between the two groups, extracellular volume increased by a mean of 1,480 ml in those given ritodrine compared with 790 ml in the control animals. There was no significant difference between animals given ritodrine and their controls regarding serial hematocrits, serum sodium, or colloid oncotic pressures. From this we conclude that the retained sodium and water was in the interstitial space. Since plasma volume was unaltered by ritodrine administration it seems unlikely that pure volume overload can explain the pulmonary edema induced by β-mimetics. Combined with the prior observation that direct pulmonary capillary membrane toxicity does not occur, the likely pathophysiology of β-agonist-induced pulmonary edema invclves left ventricular failure.
UR - http://www.scopus.com/inward/record.url?scp=0020639653&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020639653&partnerID=8YFLogxK
M3 - Article
C2 - 6624791
AN - SCOPUS:0020639653
VL - 147
SP - 254
EP - 259
JO - American Journal of Obstetrics and Gynecology
JF - American Journal of Obstetrics and Gynecology
SN - 0002-9378
IS - 3
ER -