scholarly journals Hemodynamic evaluation of chemical mediators of sepsis during systemic inflammatory response in an experimental animal model

2021 ◽  
Author(s):  
GUILHERME DE SOUZA VIEIRA ◽  
Fernanda Antunes ◽  
Josias Alves Machado ◽  
Isabella Cristina Morales ◽  
Priscilla Olivieri Benck de Jesus ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Inflammatory Response ◽  
Arterial Blood Pressure ◽  
Cecal Ligation ◽  
Systemic Inflammatory Response ◽  
Arterial Blood ◽  
Time Period ◽  
Sepsis Induction ◽  
Surgical Manipulation

The early diagnosis of sepsis increases the chances of its successful treatment. Biomarkers are able to distinguish between systemic inflammatory response syndrome and sepsis and are used to monitor pro- and anti-inflammatory changes associated with the host response to pathogens. A total of 11 rats underwent sepsis induction and measured systolic, diastolic and mean arterial blood pressure. Leukocyte counts, procalcitonin, and nitric oxide also were measured 0, 2, and 4 hours after the induction of sepsis using the cecal ligation and puncture method. The animals were divided into two groups: control (SHAM) and induced. Procalcitonin levels remained within the normal range for an inflammatory response throughout the experiment. There was a statistically insignificant increase in nitric oxide levels. All animals showed increased diastolic arterial blood pressure; however, the increase in the induced animals was even more pronounced. Procalcitonin and nitric oxide levels can increase due to surgical manipulation, while arterial blood pressure was not a good predictor for the onset of sepsis during the time period studied here.

scholarly journals Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2382-2387 ◽  
Author(s):  
Karim Sabrane ◽  
Markus-N. Kruse ◽  
Alexandra Gazinski ◽  
Michaela Kuhn
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

scholarly journals Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

1994 ◽  
Vol 14 (6) ◽  
pp. 939-943 ◽  
Author(s):  
Zheng Gang Zhang ◽  
Michael Chopp ◽  
Kenneth I. Maynard ◽  
Michael A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Arterial Blood ◽  
Nos Inhibitors ◽  
Before And After ◽  
Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

scholarly journals Arterial Blood Pressure Responses to Cell-free Hemoglobin Solutions and the Reaction with Nitric Oxide

1998 ◽  
Vol 273 (20) ◽  
pp. 12128-12134 ◽  
Author(s):  
Ronald J. Rohlfs ◽  
Eric Bruner ◽  
Albert Chiu ◽  
Armando Gonzales ◽  
Maria L. Gonzales ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Free Hemoglobin ◽  
Arterial Blood ◽  
Blood Pressure Responses

Does nitric oxide buffer arterial blood pressure variability in humans?

2002 ◽  
Vol 93 (4) ◽  
pp. 1466-1470 ◽  
Author(s):  
William H. Cooke ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Jian Cui ◽  
Thad E. Wilson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Animal Studies ◽  
Transfer Functions ◽  
Body Position ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Arterial Blood

Animal studies suggest that nitric oxide (NO) plays an important role in buffering short-term arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G-monomethyl-l-arginine (l-NMMA). Electrocardiogram and beat-by-beat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after l-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05–0.15 Hz) and high-frequency (HF; 0.15–0.35 Hz) ranges.l-NMMA infusion increased supine BP (systolic, 109 ± 4 vs. 122 ± 3 mmHg, P = 0.03; diastolic, 68 ± 2 vs. 78 ± 3 mmHg, P = 0.002), but it did not affect supine R-R interval or BP variability. Beforel-NMMA, HUT decreased HF R-R variability ( P= 0.03), decreased transfer function gain (LF, 12 ± 2 vs. 5 ± 1 ms/mmHg, P = 0.007; HF, 18 ± 3 vs. 3 ± 1 ms/mmHg, P = 0.002), and increased LF BP variability ( P < 0.0001). After l-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without l-NMMA. Increased supine BP afterl-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans.

scholarly journals Inhibition of Nitric Oxide Synthesis: Effects on Cerebral Blood Flow and Glucose Utilisation in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 985-992 ◽  
Author(s):  
I. M. Macrae ◽  
D. A. Dawson ◽  
J. D. Norrie ◽  
J. McCulloch
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Bolus Administration ◽  
Nitric Oxide Synthesis ◽  
Conscious Rat ◽  
Nitric Oxide Synthase Inhibitor ◽  
Glucose Utilisation ◽  
Arterial Blood

The consequences of inhibition of nitric oxide synthesis on local CBF and glucose utilisation have been studied in the conscious rat using the specific nitric oxide synthase inhibitor Ng-nitro-l-arginine methyl ester (l-NAME; 30 mg kg−1 i.v.). Local CBF and glucose utilisation were assessed with the [14C]iodoantipyrine and the 2-deoxy-d-[14C]glucose autoradiographic techniques, respectively. l-NAME induced prolonged (>3 h) reductions in local CBF throughout the CNS with concomitant increases in arterial blood pressure. For example, 1 h post l-NAME, CBF dropped from 79 ± 4 to 45 ± 1 ml 100 g−1 min−1 in cerebellum, from 76 ± 4 to 47 ± 2 ml 100 g−1 min−1 in medulla oblongata, and from 117 ± 6 to 72 ± 2 ml 100 g−1 min−1 in cortex. l-NAME produced sustained elevations (e.g., 46 ± 2 mm Hg at 1 h after bolus administration) in mean arterial blood pressure throughout the period evaluated. Despite evidence implicating nitric oxide in neuronal signalling, l-NAME did not significantly influence CNS functional activity, as measured by local rates of glucose utilisation, in any neuroanatomical region examined. Consequently, the normal ratio of blood flow to glucose use throughout the brain was significantly reduced in the presence of l-NAME, although the hierarchy of blood flow levels in different neuroanatomical regions was preserved. These results are consistent with the involvement of nitric oxide in the tonic control of cerebral tissue perfusion.

scholarly journals Role of Endogeneous Nitric Oxide (NO) in Arterial Blood Pressure (ABP) Regulation in Preterm Neonates

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 42A-42A
Author(s):  
Tannette G Krediet ◽  
Leonieke Valk ◽  
Ingrid Hempenius ◽  
Johannes Egberts ◽  
Frank Van Bel
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Preterm Neonates ◽  
Arterial Blood

Nitric Oxide-Dependent Vasodilation and the Regulation of Arterial Blood Pressure

2001 ◽  
Vol 38 ◽  
pp. S19-S22 ◽  
Author(s):  
Alberto U Ferrari ◽  
Alberto Radaelli ◽  
Ileana Mori ◽  
Luca Mircoli ◽  
Stefano Perlini ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Arterial Blood

Cortical NOS inhibition raises the lower limit of cerebral blood flow-arterial pressure autoregulation

1999 ◽  
Vol 276 (4) ◽  
pp. H1253-H1262 ◽  
Author(s):  
Stephen C. Jones ◽  
Carol R. Radinsky ◽  
Anthony J. Furlan ◽  
Douglas Chyatte ◽  
Alejandro D. Perez-Trepichio
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Blood Withdrawal ◽  
Arterial Blood ◽  
Pressure Autoregulation

The maintenance of constant cerebral blood flow (CBF) as arterial blood pressure is reduced, commonly referred to as CBF-pressure autoregulation, is typically characterized by a plateau until the vasodilatory capacity is exhausted at the lower limit, after which flow falls linearly with pressure. We investigated the effect of cortical, as opposed to systemic, nitric oxide synthase (NOS) inhibition on the lower limit of CBF-pressure autoregulation. Forty-four Sprague-Dawley rats were anesthetized with halothane and N2O in O2. With a closed cranial window placed the previous day in a ventilated and physiologically stable preparation, we determined the CBF using laser-Doppler flowmetry. Animals with low reactivity to inhaled CO2 and suffused ADP or ACh were excluded. Five arterial pressures from 100 to 40 mmHg were obtained with controlled hemorrhagic hypotension under cortical suffusion with artificial cerebrospinal fluid (aCSF) and then again after suffusion for 35 ( n = 5) and 105 min ( n = 10) with aCSF, 10−3 M N ω-nitro-l-arginine (l-NNA; n = 12), or 10−3 M N ω-nitro-d-arginine (d-NNA; n = 5). An additional group ( n = 7) was studied after a 105-min suffusion of l-NNA followed by a single blood withdrawal procedure. The lower limit of autoregulation was identified visually by four blinded reviewers as a change in the slope of the five-point plot of CBF vs. mean arterial blood pressure. The lower limit of 90 ± 4.3 mmHg after 105 min of 1 mMl-NNA suffusion was increased compared with the value in the time-control group of 75 ± 5.3 mmHg ( P < 0.01; ANOVA) and the initial value of 67 ± 3.7 mmHg ( P < 0.001). The lower limit of 84 ± 5.9 mmHg in seven animals with 105 min of suffusion of 1 mM l-NNA without previous blood withdrawal was significantly increased ( P < 0.01) in comparison with 70 ± 1.9 mmHg from those with just aCSF suffusion ( n = 37). No changes in lower limit for the other agents or conditions, including 105 or 35 min of aCSF or 35 min of l-NNA suffusion, were detected. The lack of effect on the lower limit withd-NNA suffusion suggests an enzymatic mechanism, and the lengthyl-NNA exposure of 105 min, but not 35 min, suggests inhibition of a diffusionally distant NOS source that mediates autoregulation. Thus cortical suffusion ofl-NNA raises the lower limit of autoregulation, strongly suggesting that nitric oxide is at least one of the vasodilators active during hypotension as arterial pressure is reduced from normal.

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