Cardiovascular “Patterns” of H2S and SSNO−-Mix Evaluated from 35 Rat Hemodynamic Parameters

This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H2S, NO donor S-nitrosoglutathione (GSNO) and their H2S/GSNO products (SSNO−-mix) have numerous biological actions, we aimed to...

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Published inBiomolecules (Basel, Switzerland) Vol. 11; no. 2; p. 293
Main Authors Tomasova, Lenka, Grman, Marian, Misak, Anton, Kurakova, Lucia, Ondriasova, Elena, Ondrias, Karol
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 16.02.2021
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Abstract This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H2S, NO donor S-nitrosoglutathione (GSNO) and their H2S/GSNO products (SSNO−-mix) have numerous biological actions, we aimed to compare their effects on APW and to find characteristic “patterns” of their actions. The right jugular vein of anesthetized rats was cannulated for i.v. administration of the compounds. The left carotid artery was cannulated to detect APW. From APW, 35 hemodynamic parameters (HPs) were evaluated. H2S transiently influenced all 35 HPs and from their cross-relationships to systolic blood pressure “patterns” and direct/indirect signaling pathways of the H2S effect were proposed. The observed “patterns” were mostly different from the published ones for GSNO. Effect of SSNO−-mix (≤32 nmol kg−1) on blood pressure in the presence or absence of a nitric oxide synthase inhibitor (L-NAME) was minor in comparison to GSNO, suggesting that the formation of SSNO−-mix in blood diminished the hemodynamic effect of NO. The observed time-dependent changes of 35 HPs, their cross-relationships and non-hysteresis/hysteresis profiles may serve as “patterns” for the conditions of a transient decrease/increase of blood pressure caused by H2S.
AbstractList This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H2S, NO donor S-nitrosoglutathione (GSNO) and their H2S/GSNO products (SSNO−-mix) have numerous biological actions, we aimed to compare their effects on APW and to find characteristic “patterns” of their actions. The right jugular vein of anesthetized rats was cannulated for i.v. administration of the compounds. The left carotid artery was cannulated to detect APW. From APW, 35 hemodynamic parameters (HPs) were evaluated. H2S transiently influenced all 35 HPs and from their cross-relationships to systolic blood pressure “patterns” and direct/indirect signaling pathways of the H2S effect were proposed. The observed “patterns” were mostly different from the published ones for GSNO. Effect of SSNO−-mix (≤32 nmol kg−1) on blood pressure in the presence or absence of a nitric oxide synthase inhibitor (L-NAME) was minor in comparison to GSNO, suggesting that the formation of SSNO−-mix in blood diminished the hemodynamic effect of NO. The observed time-dependent changes of 35 HPs, their cross-relationships and non-hysteresis/hysteresis profiles may serve as “patterns” for the conditions of a transient decrease/increase of blood pressure caused by H2S.
This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H 2 S, NO donor S-nitrosoglutathione (GSNO) and their H 2 S/GSNO products (SSNO − -mix) have numerous biological actions, we aimed to compare their effects on APW and to find characteristic “patterns” of their actions. The right jugular vein of anesthetized rats was cannulated for i.v. administration of the compounds. The left carotid artery was cannulated to detect APW. From APW, 35 hemodynamic parameters (HPs) were evaluated. H 2 S transiently influenced all 35 HPs and from their cross-relationships to systolic blood pressure “patterns” and direct/indirect signaling pathways of the H 2 S effect were proposed. The observed “patterns” were mostly different from the published ones for GSNO. Effect of SSNO − -mix (≤32 nmol kg −1 ) on blood pressure in the presence or absence of a nitric oxide synthase inhibitor (L-NAME) was minor in comparison to GSNO, suggesting that the formation of SSNO − -mix in blood diminished the hemodynamic effect of NO. The observed time-dependent changes of 35 HPs, their cross-relationships and non-hysteresis/hysteresis profiles may serve as “patterns” for the conditions of a transient decrease/increase of blood pressure caused by H 2 S.
Author Tomasova, Lenka
Grman, Marian
Kurakova, Lucia
Misak, Anton
Ondriasova, Elena
Ondrias, Karol
AuthorAffiliation 1 Biomedical Research Center, Institute of Clinical and Translational Research, Slovak Academy of Sciences, 811 04 Bratislava, Slovakia; lenka.tomasova@savba.sk (L.T.); marian.grman@savba.sk (M.G.); anton.misak@savba.sk (A.M.)
2 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, 814 99 Bratislava, Slovakia; kurakova4@uniba.sk (L.K.); ondriasova@fpharm.uniba.sk (E.O.)
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– name: 2 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, 814 99 Bratislava, Slovakia; kurakova4@uniba.sk (L.K.); ondriasova@fpharm.uniba.sk (E.O.)
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CitedBy_id crossref_primary_10_1007_s12011_024_04196_3
crossref_primary_10_3390_molecules28124826
crossref_primary_10_1002_ame2_12354
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Snippet This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform...
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StartPage 293
SubjectTerms Anesthesia
arterial pulse waveform
Bioavailability
Blood pressure
Cardiovascular system
Carotid artery
Experiments
hemodynamic parameters
Hydrogen sulfide
Hysteresis
Jugular vein
Laboratory animals
NG-Nitroarginine methyl ester
Nitric oxide
Nitric-oxide synthase
nitrosopersulfide
Physiology
sulfide
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Title Cardiovascular “Patterns” of H2S and SSNO−-Mix Evaluated from 35 Rat Hemodynamic Parameters
URI https://www.proquest.com/docview/2491725614
https://pubmed.ncbi.nlm.nih.gov/PMC7920056
https://doaj.org/article/f9275fa5f3404b4a929f3672b49a0aaa
Volume 11
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