Pregnancy hypertension-associated endothelial dysfunction is attenuated by isoflurane anesthesia: Evidence of protective effect related to increases in nitric oxide

Pregnancy hypertension-induced endothelial dysfunction associated with impairment of nitric oxide (NO) bioavailability and hemodynamic derangements is a challenging for urgent procedures requiring maternal anesthesia. The volatile anesthetic isoflurane has demonstrated NO-associated protective effec...

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Veröffentlicht in:Life sciences (1973) 2023-10, Vol.331, p.122039-122039, Article 122039
Hauptverfasser: Rodrigues, Serginara David, da Silva, Maria Luiza Santos, Martins, Laisla Zanetoni, Gomes, Sáskia Estela Biasotti, Mariani, Noemia A.P., Silva, Erick J.R., Kushima, Hélio, Mattos, Bruna Rahal, Rizzi, Elen, Dias-Junior, Carlos Alan
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container_end_page 122039
container_issue
container_start_page 122039
container_title Life sciences (1973)
container_volume 331
creator Rodrigues, Serginara David
da Silva, Maria Luiza Santos
Martins, Laisla Zanetoni
Gomes, Sáskia Estela Biasotti
Mariani, Noemia A.P.
Silva, Erick J.R.
Kushima, Hélio
Mattos, Bruna Rahal
Rizzi, Elen
Dias-Junior, Carlos Alan
description Pregnancy hypertension-induced endothelial dysfunction associated with impairment of nitric oxide (NO) bioavailability and hemodynamic derangements is a challenging for urgent procedures requiring maternal anesthesia. The volatile anesthetic isoflurane has demonstrated NO-associated protective effects. However, this isoflurane-induced effect is still unclear in pregnancy hypertension. Therefore, the present study examined the potential protective effects of isoflurane anesthesia on endothelial dysfunction and hemodynamic changes induced by hypertensive pregnancy associated with fetal and placental growth restrictions. Animals were distributed into four groups: normotensive pregnant rats (Preg), anesthetized pregnant rats (Preg+Iso), hypertensive pregnant rats (HTN-Preg), and anesthetized hypertensive pregnant rats (HTN-Preg+Iso). Systolic and diastolic pressures, mean arterial pressure (MAP), heart rate, fetal and placental weights, vascular contraction, endothelium-derived NO-dependent vasodilation, and NO levels were assessed. The vascular endothelial growth factor (VEGF) levels and endothelial NO synthase (eNOS) Serine (1177) phosphorylation (p-eNOS) expression were also examined. Isoflurane produced more expressive hypotensive effects in the HTN-Preg+Iso versus Preg+Iso group, with respective reductions in MAP by 50 ± 13 versus 25 ± 4 mmHg (P 
doi_str_mv 10.1016/j.lfs.2023.122039
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The volatile anesthetic isoflurane has demonstrated NO-associated protective effects. However, this isoflurane-induced effect is still unclear in pregnancy hypertension. Therefore, the present study examined the potential protective effects of isoflurane anesthesia on endothelial dysfunction and hemodynamic changes induced by hypertensive pregnancy associated with fetal and placental growth restrictions. Animals were distributed into four groups: normotensive pregnant rats (Preg), anesthetized pregnant rats (Preg+Iso), hypertensive pregnant rats (HTN-Preg), and anesthetized hypertensive pregnant rats (HTN-Preg+Iso). Systolic and diastolic pressures, mean arterial pressure (MAP), heart rate, fetal and placental weights, vascular contraction, endothelium-derived NO-dependent vasodilation, and NO levels were assessed. The vascular endothelial growth factor (VEGF) levels and endothelial NO synthase (eNOS) Serine (1177) phosphorylation (p-eNOS) expression were also examined. Isoflurane produced more expressive hypotensive effects in the HTN-Preg+Iso versus Preg+Iso group, with respective reductions in MAP by 50 ± 13 versus 25 ± 4 mmHg (P < 0.05). Also, HTN-Preg+Iso compared to the HTN-Preg group showed (respectively) preventions against the weight loss of the fetuses (4.0 ± 0.6 versus 2.8 ± 0.6 g, P < 0.05) and placentas (0.37 ± 0.06 versus 0.30 ± 0.06 mg, P < 0.05), hyper-reactive vasocontraction response (1.8 ± 0.4 versus 2.8 ± 0.6 g, P < 0.05), impaired endothelium-derived NO-dependent vasodilation (84 ± 8 versus 50 ± 17 %, P < 0.05), reduced VEGF levels (147 ± 46 versus 25 ± 13 pg/mL, P < 0.05), and decreased p-eNOS expression (0.24 ± 0.07 versus 0.09 ± 0.05 arbitrary units, P < 0.05). Isoflurane anesthesia protects maternal endothelial function in pregnancy hypertension, and possibly endothelium-derived NO is involved. 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The volatile anesthetic isoflurane has demonstrated NO-associated protective effects. However, this isoflurane-induced effect is still unclear in pregnancy hypertension. Therefore, the present study examined the potential protective effects of isoflurane anesthesia on endothelial dysfunction and hemodynamic changes induced by hypertensive pregnancy associated with fetal and placental growth restrictions. Animals were distributed into four groups: normotensive pregnant rats (Preg), anesthetized pregnant rats (Preg+Iso), hypertensive pregnant rats (HTN-Preg), and anesthetized hypertensive pregnant rats (HTN-Preg+Iso). Systolic and diastolic pressures, mean arterial pressure (MAP), heart rate, fetal and placental weights, vascular contraction, endothelium-derived NO-dependent vasodilation, and NO levels were assessed. The vascular endothelial growth factor (VEGF) levels and endothelial NO synthase (eNOS) Serine (1177) phosphorylation (p-eNOS) expression were also examined. Isoflurane produced more expressive hypotensive effects in the HTN-Preg+Iso versus Preg+Iso group, with respective reductions in MAP by 50 ± 13 versus 25 ± 4 mmHg (P < 0.05). Also, HTN-Preg+Iso compared to the HTN-Preg group showed (respectively) preventions against the weight loss of the fetuses (4.0 ± 0.6 versus 2.8 ± 0.6 g, P < 0.05) and placentas (0.37 ± 0.06 versus 0.30 ± 0.06 mg, P < 0.05), hyper-reactive vasocontraction response (1.8 ± 0.4 versus 2.8 ± 0.6 g, P < 0.05), impaired endothelium-derived NO-dependent vasodilation (84 ± 8 versus 50 ± 17 %, P < 0.05), reduced VEGF levels (147 ± 46 versus 25 ± 13 pg/mL, P < 0.05), and decreased p-eNOS expression (0.24 ± 0.07 versus 0.09 ± 0.05 arbitrary units, P < 0.05). Isoflurane anesthesia protects maternal endothelial function in pregnancy hypertension, and possibly endothelium-derived NO is involved. 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da Silva, Maria Luiza Santos ; Martins, Laisla Zanetoni ; Gomes, Sáskia Estela Biasotti ; Mariani, Noemia A.P. ; Silva, Erick J.R. ; Kushima, Hélio ; Mattos, Bruna Rahal ; Rizzi, Elen ; Dias-Junior, Carlos Alan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c363t-7e811ddb0ad78c7595d95e8302ce31380fddf3757f0354253380582a2515e6693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Anesthesia</topic><topic>bioavailability</topic><topic>Endothelial dysfunction</topic><topic>Gestational hypertension</topic><topic>heart rate</topic><topic>Hemodynamic derangements</topic><topic>hypertension</topic><topic>Isoflurane</topic><topic>Nitric oxide</topic><topic>phosphorylation</topic><topic>pregnancy</topic><topic>protective effect</topic><topic>serine</topic><topic>vascular endothelial growth factors</topic><topic>vasodilation</topic><topic>weight loss</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rodrigues, Serginara David</creatorcontrib><creatorcontrib>da Silva, Maria Luiza Santos</creatorcontrib><creatorcontrib>Martins, Laisla Zanetoni</creatorcontrib><creatorcontrib>Gomes, Sáskia Estela Biasotti</creatorcontrib><creatorcontrib>Mariani, Noemia A.P.</creatorcontrib><creatorcontrib>Silva, Erick J.R.</creatorcontrib><creatorcontrib>Kushima, Hélio</creatorcontrib><creatorcontrib>Mattos, Bruna Rahal</creatorcontrib><creatorcontrib>Rizzi, Elen</creatorcontrib><creatorcontrib>Dias-Junior, Carlos Alan</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodrigues, Serginara David</au><au>da Silva, Maria Luiza Santos</au><au>Martins, Laisla Zanetoni</au><au>Gomes, Sáskia Estela Biasotti</au><au>Mariani, Noemia A.P.</au><au>Silva, Erick J.R.</au><au>Kushima, Hélio</au><au>Mattos, Bruna Rahal</au><au>Rizzi, Elen</au><au>Dias-Junior, Carlos Alan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pregnancy hypertension-associated endothelial dysfunction is attenuated by isoflurane anesthesia: Evidence of protective effect related to increases in nitric oxide</atitle><jtitle>Life sciences (1973)</jtitle><date>2023-10-15</date><risdate>2023</risdate><volume>331</volume><spage>122039</spage><epage>122039</epage><pages>122039-122039</pages><artnum>122039</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract><![CDATA[Pregnancy hypertension-induced endothelial dysfunction associated with impairment of nitric oxide (NO) bioavailability and hemodynamic derangements is a challenging for urgent procedures requiring maternal anesthesia. The volatile anesthetic isoflurane has demonstrated NO-associated protective effects. However, this isoflurane-induced effect is still unclear in pregnancy hypertension. Therefore, the present study examined the potential protective effects of isoflurane anesthesia on endothelial dysfunction and hemodynamic changes induced by hypertensive pregnancy associated with fetal and placental growth restrictions. Animals were distributed into four groups: normotensive pregnant rats (Preg), anesthetized pregnant rats (Preg+Iso), hypertensive pregnant rats (HTN-Preg), and anesthetized hypertensive pregnant rats (HTN-Preg+Iso). Systolic and diastolic pressures, mean arterial pressure (MAP), heart rate, fetal and placental weights, vascular contraction, endothelium-derived NO-dependent vasodilation, and NO levels were assessed. The vascular endothelial growth factor (VEGF) levels and endothelial NO synthase (eNOS) Serine (1177) phosphorylation (p-eNOS) expression were also examined. Isoflurane produced more expressive hypotensive effects in the HTN-Preg+Iso versus Preg+Iso group, with respective reductions in MAP by 50 ± 13 versus 25 ± 4 mmHg (P < 0.05). Also, HTN-Preg+Iso compared to the HTN-Preg group showed (respectively) preventions against the weight loss of the fetuses (4.0 ± 0.6 versus 2.8 ± 0.6 g, P < 0.05) and placentas (0.37 ± 0.06 versus 0.30 ± 0.06 mg, P < 0.05), hyper-reactive vasocontraction response (1.8 ± 0.4 versus 2.8 ± 0.6 g, P < 0.05), impaired endothelium-derived NO-dependent vasodilation (84 ± 8 versus 50 ± 17 %, P < 0.05), reduced VEGF levels (147 ± 46 versus 25 ± 13 pg/mL, P < 0.05), and decreased p-eNOS expression (0.24 ± 0.07 versus 0.09 ± 0.05 arbitrary units, P < 0.05). Isoflurane anesthesia protects maternal endothelial function in pregnancy hypertension, and possibly endothelium-derived NO is involved. [Display omitted]]]></abstract><pub>Elsevier Inc</pub><doi>10.1016/j.lfs.2023.122039</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0348-6144</orcidid></addata></record>
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subjects Anesthesia
bioavailability
Endothelial dysfunction
Gestational hypertension
heart rate
Hemodynamic derangements
hypertension
Isoflurane
Nitric oxide
phosphorylation
pregnancy
protective effect
serine
vascular endothelial growth factors
vasodilation
weight loss
title Pregnancy hypertension-associated endothelial dysfunction is attenuated by isoflurane anesthesia: Evidence of protective effect related to increases in nitric oxide
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