Flow rate-perfusion pressure relationships in situ in the uterine circulation of pregnant rats.

Eva E. Fulep, Yuri P. Vedernikov, George Saade, Robert E. Garfield

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

OBJECTIVE: Our purpose was to study the effects of inhibition of nitric oxide synthesis on perfusion pressure and flow rate-perfusion pressure relationships in the rat uterine circulation in situ. STUDY DESIGN: Nonpregnant, midpregnant (day 14), and late pregnant (day 21) Sprague-Dawley rats were studied. The vascular bed of the intact uterus and its contents were isolated and perfused with Krebs buffer (37 degrees C, pH approximately 7.4, 2% dextran and indomethacin, 10(-5) mol/L) through a cannula inserted into the abdominal aorta close to the iliac artery bifurcation, and perfusion pressure was monitored. After equilibration, the flow rate was increased from 1 mL/min to 8 or 16 mL/min, in the absence and presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), phenylephrine, or both. RESULTS: The flow rate-perfusion pressure relationship in midpregnant rats (n = 9) was not significantly different from that in late pregnant rats (n = 12), but the latter was significantly greater than the relationship in nonpregnant animals (n = 5). L-NAME did not influence perfusion pressure and flow rate-perfusion pressure relationships in any of the groups. However, L-NAME enhanced the phenylephrine-induced and flow rate-induced increase in perfusion pressure in the vascular beds from nonpregnant and midpregnant animals, and to a lesser extent in late pregnant rats. L-arginine did not influence perfusion pressure or the flow rate-perfusion pressure relationship in any group. CONCLUSIONS: Vasoconstriction produced by phenylephrine uncovers basal release of endothelium derived nitric oxide. Vasoconstriction increases perfusion pressure responses to increases in flow rate in the uterine vascular beds of nonpregnant, midpregnant, and late pregnant rats. The release of endothelial nitric oxide in the uterine vascular beds depends on the basal contractile state of the vasculature.

Original languageEnglish (US)
Pages (from-to)1022-1026
Number of pages5
JournalAmerican Journal of Obstetrics and Gynecology
Volume186
Issue number5
StatePublished - May 2002

Fingerprint

Perfusion
Pressure
NG-Nitroarginine Methyl Ester
Blood Vessels
Phenylephrine
Nitric Oxide
Vasoconstriction
Iliac Artery
Abdominal Aorta
Dextrans
Indomethacin
Uterus
Sprague Dawley Rats
Arginine
Buffers

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Flow rate-perfusion pressure relationships in situ in the uterine circulation of pregnant rats. / Fulep, Eva E.; Vedernikov, Yuri P.; Saade, George; Garfield, Robert E.

In: American Journal of Obstetrics and Gynecology, Vol. 186, No. 5, 05.2002, p. 1022-1026.

Research output: Contribution to journalArticle

Fulep, Eva E. ; Vedernikov, Yuri P. ; Saade, George ; Garfield, Robert E. / Flow rate-perfusion pressure relationships in situ in the uterine circulation of pregnant rats. In: American Journal of Obstetrics and Gynecology. 2002 ; Vol. 186, No. 5. pp. 1022-1026.
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abstract = "OBJECTIVE: Our purpose was to study the effects of inhibition of nitric oxide synthesis on perfusion pressure and flow rate-perfusion pressure relationships in the rat uterine circulation in situ. STUDY DESIGN: Nonpregnant, midpregnant (day 14), and late pregnant (day 21) Sprague-Dawley rats were studied. The vascular bed of the intact uterus and its contents were isolated and perfused with Krebs buffer (37 degrees C, pH approximately 7.4, 2{\%} dextran and indomethacin, 10(-5) mol/L) through a cannula inserted into the abdominal aorta close to the iliac artery bifurcation, and perfusion pressure was monitored. After equilibration, the flow rate was increased from 1 mL/min to 8 or 16 mL/min, in the absence and presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), phenylephrine, or both. RESULTS: The flow rate-perfusion pressure relationship in midpregnant rats (n = 9) was not significantly different from that in late pregnant rats (n = 12), but the latter was significantly greater than the relationship in nonpregnant animals (n = 5). L-NAME did not influence perfusion pressure and flow rate-perfusion pressure relationships in any of the groups. However, L-NAME enhanced the phenylephrine-induced and flow rate-induced increase in perfusion pressure in the vascular beds from nonpregnant and midpregnant animals, and to a lesser extent in late pregnant rats. L-arginine did not influence perfusion pressure or the flow rate-perfusion pressure relationship in any group. CONCLUSIONS: Vasoconstriction produced by phenylephrine uncovers basal release of endothelium derived nitric oxide. Vasoconstriction increases perfusion pressure responses to increases in flow rate in the uterine vascular beds of nonpregnant, midpregnant, and late pregnant rats. The release of endothelial nitric oxide in the uterine vascular beds depends on the basal contractile state of the vasculature.",
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N2 - OBJECTIVE: Our purpose was to study the effects of inhibition of nitric oxide synthesis on perfusion pressure and flow rate-perfusion pressure relationships in the rat uterine circulation in situ. STUDY DESIGN: Nonpregnant, midpregnant (day 14), and late pregnant (day 21) Sprague-Dawley rats were studied. The vascular bed of the intact uterus and its contents were isolated and perfused with Krebs buffer (37 degrees C, pH approximately 7.4, 2% dextran and indomethacin, 10(-5) mol/L) through a cannula inserted into the abdominal aorta close to the iliac artery bifurcation, and perfusion pressure was monitored. After equilibration, the flow rate was increased from 1 mL/min to 8 or 16 mL/min, in the absence and presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), phenylephrine, or both. RESULTS: The flow rate-perfusion pressure relationship in midpregnant rats (n = 9) was not significantly different from that in late pregnant rats (n = 12), but the latter was significantly greater than the relationship in nonpregnant animals (n = 5). L-NAME did not influence perfusion pressure and flow rate-perfusion pressure relationships in any of the groups. However, L-NAME enhanced the phenylephrine-induced and flow rate-induced increase in perfusion pressure in the vascular beds from nonpregnant and midpregnant animals, and to a lesser extent in late pregnant rats. L-arginine did not influence perfusion pressure or the flow rate-perfusion pressure relationship in any group. CONCLUSIONS: Vasoconstriction produced by phenylephrine uncovers basal release of endothelium derived nitric oxide. Vasoconstriction increases perfusion pressure responses to increases in flow rate in the uterine vascular beds of nonpregnant, midpregnant, and late pregnant rats. The release of endothelial nitric oxide in the uterine vascular beds depends on the basal contractile state of the vasculature.

AB - OBJECTIVE: Our purpose was to study the effects of inhibition of nitric oxide synthesis on perfusion pressure and flow rate-perfusion pressure relationships in the rat uterine circulation in situ. STUDY DESIGN: Nonpregnant, midpregnant (day 14), and late pregnant (day 21) Sprague-Dawley rats were studied. The vascular bed of the intact uterus and its contents were isolated and perfused with Krebs buffer (37 degrees C, pH approximately 7.4, 2% dextran and indomethacin, 10(-5) mol/L) through a cannula inserted into the abdominal aorta close to the iliac artery bifurcation, and perfusion pressure was monitored. After equilibration, the flow rate was increased from 1 mL/min to 8 or 16 mL/min, in the absence and presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), phenylephrine, or both. RESULTS: The flow rate-perfusion pressure relationship in midpregnant rats (n = 9) was not significantly different from that in late pregnant rats (n = 12), but the latter was significantly greater than the relationship in nonpregnant animals (n = 5). L-NAME did not influence perfusion pressure and flow rate-perfusion pressure relationships in any of the groups. However, L-NAME enhanced the phenylephrine-induced and flow rate-induced increase in perfusion pressure in the vascular beds from nonpregnant and midpregnant animals, and to a lesser extent in late pregnant rats. L-arginine did not influence perfusion pressure or the flow rate-perfusion pressure relationship in any group. CONCLUSIONS: Vasoconstriction produced by phenylephrine uncovers basal release of endothelium derived nitric oxide. Vasoconstriction increases perfusion pressure responses to increases in flow rate in the uterine vascular beds of nonpregnant, midpregnant, and late pregnant rats. The release of endothelial nitric oxide in the uterine vascular beds depends on the basal contractile state of the vasculature.

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