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.

Neuronal NO promotes cerebral cortical hyperemia during cortical spreading depression in rabbits

1997 ◽  
Vol 272 (3) ◽  
pp. H1315-H1322 ◽  
Author(s):  
D. M. Colonna ◽  
W. Meng ◽  
D. D. Deal ◽  
M. Gowda ◽  
D. W. Busija
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Repeated Measures ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Repeated Measures Analysis ◽  
Nos Inhibitor

Temporary elevations in cortical cerebral blood flow (CBF) accompany cortical spreading depression (CSD) in anesthetized animals. We tested the hypothesis that nitric oxide (NO) is an important promotor of CSD-induced cortical hyperemia in urethan-anesthetized rabbits. CBF was measured at four time points by administration of 15-microm microspheres with the reference withdrawal technique. Intravenous administration of the nonspecific NO synthase (NOS) inhibitor N(omega)-nitro-L-arginine increased mean arterial blood pressure and resting cerebrovascular resistance and attenuated CSD-induced hyperemia. Cortical CBF before intraperitoneal 7-nitroindazole (7-NI), a neuronal NOS inhibitor, was 42 +/- 8 and 124 +/- 19 ml x 100 g(-1) x min(-1) at baseline and during CSD, respectively (P < 0.05 by repeated-measures analysis of variance). After 7-NI administration, mean arterial blood pressure, CBF, and cerebrovascular resistance were unchanged from baseline values; cortical CBF was 38 +/- 4 and 90 +/- 8 ml x 100 g(-1) x min(-1) post-7-NI at rest and during a second CSD, respectively. Similar to N(omega)-nitro-L-arginine, 7-NI decreased the cortical hyperemic response during CSD (P < 0.05 by repeated-measures analysis of variance). We conclude that neuronal NOS promotes the temporary cortical hyperemia observed during CSD.

scholarly journals Effects of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor, in L-NAME-induced hypertension in rats

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 57-59 ◽  
Author(s):  
Marcio Wilker Soares Campelo ◽  
Ana Paula Bomfim Soares Campelo ◽  
Luiz Gonzaga de França Lopes ◽  
Armenio Aguiar dos Santos ◽  
Sergio Botelho Guimarães ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Arterial Blood Pressure ◽  
Wistar Rats ◽  
Nitric Oxide Donor ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Male Wistar Rats

PURPOSE: To evaluate the effect of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor in Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. METHODS: Twenty-four male Wistar rats were randomly assigned to four groups (n=6), named according to the treatment applied (G1-Saline, G2-Rut-bpy, G3-L-NAME and G4-L-NAME+Rut-bpy). L-NAME (30 mg/Kg) was injected intraperitoneally 30 minutes before the administration of Rut-bpy (100 mg/Kg). Mean abdominal aorta arterial blood pressure (MAP) was continuously monitored. RESULTS: Mean arterial blood pressure (MAP) in G3 rats rose progressively, reaching 147±16 mmHg compared with 100±19 mm Hg in G1 rats (p<0.05). In G4 rats, treated with L-NAME+Rut-bpy, MAP reached 149+11 mm Hg while in G2 rats, treated with Rut-bpy, MAP values were 106±11 mm Hg. In G1 rats these values decreased progressively reaching 87+14 mm Hg after 30 minutes. An important finding was the maintenance of the MAP throughout the experiment in G2 rats. CONCLUSION: Rut-bpy does not decrease the MAP in L-Name induced hypertensive rats. However, when it is used in anesthetized hypotensive rats a stable blood pressure is obtained.

scholarly journals Increased nitric oxide activity in a rat model of acute pancreatitis

Gut ◽  
1998 ◽  
Vol 43 (4) ◽  
pp. 564-570 ◽  
Author(s):  
R A Al-Mufti ◽  
R C N Williamson ◽  
R T Mathie
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Acute Pancreatitis ◽  
Arterial Blood Pressure ◽  
Tissue Damage ◽  
No Synthase ◽  
Arterial Blood ◽  
Inducible No Synthase ◽  
Cellular Localisation ◽  
Male Wistar Rats

Background—Overproduction of nitric oxide (NO) via induction of the inducible NO synthase (iNOS) is an important factor in the haemodynamic disturbances of several inflammatory states.Aims—To identify the role of NO in a caerulein induced model of acute pancreatitis in the rat.Methods—Arterial blood pressure and plasma NO metabolites were measured at zero and seven hours in adult male Wistar rats administered caerulein (n=10) or saline (n=10). Pancreatic activity of NOS (inducible and constitutive) was assayed biochemically. The pancreatic expression and cellular localisation of NOS and nitrotyrosine (a marker of peroxynitrite induced oxidative tissue damage) were characterised immunohistochemically.Results—Compared with controls at seven hours, the pancreatitis group displayed raised plasma NO metabolites (mean (SEM) 70.2 (5.9) versus 22.7 (2.2) μmol/l, p<0.0001) and reduced mean arterial blood pressure (88.7 (4.6) versus 112.8 (4.1) mm Hg, p=0.008). There was notable iNOS activity in the pancreatitis group (3.1 (0.34) versus 0.1 (0.01) pmol/mg protein/min, p<0.0001) with reduced constitutive NOS activity (0.62 (0.12) versus 0.96 (0.08) pmol/mg protein/min, p=0.031). The increased expression of iNOS was mainly localised within vascular smooth muscle cells (p=0.003 versus controls), with positive perivascular staining for nitrotyrosine (p=0.0012 versus controls).Conclusions—In this experimental model of acute pancreatitis, iNOS induction and oxidative tissue damage in the pancreas is associated with raised systemic NO and arterial hypotension. Excess production of NO arising from the inducible NO synthase may be an important factor in the systemic and local haemodynamic disturbances associated with acute pancreatitis.

Cardiovascular Effects of Micromeria graeca (L.) Benth. ex Rchb in Normotensive and Hypertensive Rats

2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Arterial Blood

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.

The Study of Dynamic Response to Acute Hemorrhage by Pulse Spectrum Analysis

2006 ◽  
Vol 34 (03) ◽  
pp. 449-460 ◽  
Author(s):  
Yu Hsin Chang ◽  
Chia I Tsai ◽  
Jaung Geng Lin ◽  
Yue Der Lin ◽  
Tsai Chung Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spectrum Analysis ◽  
Pulse Spectrum ◽  
Acute Hemorrhage ◽  
Arterial Blood ◽  
Percentage Difference ◽  
Before And After

Traditional Chinese Medicine (TCM) holds that Blood and Qi are fundamental substances in the human body for sustaining normal vital activity. The theory of Qi, Blood and Zang-Fu contribute the most important theoretical basis of human physiology in TCM. An animal model using conscious rats was employed in this study to further comprehend how organisms survive during acute hemorrhage by maintaining the functionalities of Qi and Blood through dynamically regulating visceral physiological conditions. Pulse waves of arterial blood pressure before and after the hemorrhage were taken in parallel to pulse spectrum analysis. Percentage differences of mean arterial blood pressure and harmonics were recorded in subsequent 5-minute intervals following the hemorrhage. Data were analyzed using a one-way analysis of variance (ANOVA) with Duncan's test for pairwise comparisons. Results showed that, within 30 minutes following the onset of acute hemorrhage,the reduction of mean arterial blood pressure was improved from 62% to 20%. Throughout the process, changes to the pulse spectrum appeared to result in a new balance over time. The percentage differences of the second and third harmonics, which were related to kidney and spleen, both increased significantly than baseline and towards another steady state. Apart from the steady state resulting from the previous stage, the percentage difference of the 4th harmonic decreased significantly to another steady state. The observed change could be attributed to the induction of functional Qi, and is a result of Qi-Blood balancing activity that organisms hold to survive against acute bleeding.

scholarly journals Interrelationships between pulse arrival time and arterial blood pressure during postural transitions before and after spaceflight

2019 ◽  
Vol 127 (4) ◽  
pp. 1050-1057
Author(s):  
Katelyn N. Wood ◽  
Danielle K. Greaves ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Arrival Time ◽  
Standing Posture ◽  
Pulse Arrival Time ◽  
Arterial Blood ◽  
Increased Risk ◽  
Before And After ◽  
Acute Changes ◽  
Pulse Arrival

We tested the hypothesis that acute changes in arterial blood pressure (BP) when astronauts moved between supine and standing posture before and after spaceflight can be tracked by beat-to-beat changes in pulse arrival time (PAT). Nine male crewmembers (45 ± 7 yr of age; mean mission length: 165 ± 13 days) participated in a standardized supine-to-sit-to-stand test (5 min-30 s-3 min) before flight and 1 day following return to Earth with continuous monitoring of ECG and finger arterial BP. PAT was determined from the R-wave of the ECG to the foot of the BP waveform. On average, modest cardiovascular deconditioning was detected by ~10 beats/min increase in heart rate in supine and standing posture after spaceflight ( P < 0.05). When looking across the full data collection period, the r2 values between inverse of PAT (1/PAT) and systolic (SBP) and diastolic BP (DBP) varied considerably between individuals (SBP preflight 0.142 ± 0.186, postflight 0.262 ± 0.243). Individual variability was consistent during periods of transition (SBP preflight 0.284 ± 0.324, postflight 0.297 ± 0.269); however, when SBP dropped >20 mmHg, r2 was significant in 5 of 5 preflight tests and 5 of 7 postflight tests. The standard error of the estimate based on a simple linear model during both pre- and postflight testing was 9–11 mmHg for SBP and 6–7 mmHg for DBP. Overall, the results support the hypothesis that PAT tracked dynamic changes in BP. PAT as a noninvasive, nonintrusive surrogate for changes in BP could be developed as an indicator of risk for syncope on return from spaceflight or other Earth-based applications. NEW & NOTEWORTHY Astronauts returning to Earth’s gravity are at increased risk of low blood pressure on standing. Arterial pulse arrival time tracked the decrease in arterial blood pressure on moving from supine to upright posture. Nonintrusive technology providing indicators sensitive to acute changes in blood pressure could act as an early warning system to identify risk for hypotension that place astronauts, or people on Earth, at risk of impaired cognitive performance, fainting, and falls.

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

1977 ◽  
Vol 232 (3) ◽  
pp. H283-H287
Author(s):  
D. J. Loegering
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Liver Slice ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Shed Blood ◽  
Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

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.

Ouabain prevents loss of autoregulation in rat pial arterioles caused by reoxygenation after a brief hypoxic episode

1989 ◽  
Vol 67 (5) ◽  
pp. 423-427 ◽  
Author(s):  
J. Kettler ◽  
B. Y. Ong ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Protective Effects ◽  
Cranial Window ◽  
Arterial Blood ◽  
Hypoxic Episode ◽  
Electrogenic Sodium Pump ◽  
Before And After ◽  
Pressure Changes ◽  
Arteriolar Diameter

Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the changes in pial arteriolar diameters during blood pressure changes in rats induced by hemorrhage and reinfusion of blood, before and after a brief period of hypoxia. The slopes of the changes in pial arteriolar diameter as a function of mean arterial blood pressure were −0.47 ± 0.26 μm/mmHg (mean ± SD; 1 mmHg = 133.3 Pa) before hypoxia and −0.11 ± 0.23 μm/mmHg after hypoxia in the untreated rats. In ouabain-treated rats, corresponding slopes were −0.42 ± 0.24 and −0.46 ± 0.22 μm/mmHg. The observed protective effects of ouabain might be a blockade of the Na–K pump in the sarcolemma of the vascular smooth muscle.Key words: vascular smooth muscle, electrogenic sodium pump, metabolic inhibition.

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