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

• Published in: Biomolecules (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
• Language: English
• Published: Basel MDPI AG 16.02.2021; MDPI
• Subjects: 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; Germany; Slovakia
• ISSN: 2218-273X; 2218-273X
• DOI: 10.3390/biom11020293

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.