scholarly journals The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model

2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Control Group ◽  
Blood Products

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.

Effects of chronic inhibition of inducible nitric oxide synthase in hyperthyroid rats

2005 ◽  
Vol 288 (6) ◽  
pp. E1252-E1257 ◽  
Author(s):  
Isabel Rodríguez-Gómez ◽  
Rosemary Wangensteen ◽  
Juan Manuel Moreno ◽  
Virginia Chamorro ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Control Group ◽  
Hemodynamic Variable ◽  
Male Wistar Rats ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Inducible Nitric Oxide

We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphological and renal variables in hyperthyroid rats were analyzed. The following four groups ( n = 8 each) of male Wistar rats were used: control group and groups treated with AG (50 mg·kg−1·day−1, via drinking water), thyroxine (T4, 50 μg·rat−1·day−1), or AG + T4. All treatments were maintained for 3 wk. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats and morphological, plasma, and renal variables. T4 administration produced a small BP (125 ± 2, P < 0.05) increase vs. control (115 ± 2) rats. AG administration to normal rats did not modify BP (109 ± 3) or any other hemodynamic variable. However, coadministration of T4 and AG produced a marked increase in BP (140 ± 3, P < 0.01 vs. T4). Pulse pressure and HR were increased in both T4- and T4 + AG -treated groups without differences between them. Plasma NOx (μmol/l) were increased in the T4 group (10.02 ± 0.15, P < 0.05 vs. controls 6.1 ± 0.10), and AG reduced this variable in T4-treated rats (6.81 ± 0.14, P < 0.05 vs. T4) but not in normal rats (5.78 ± 0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T4.

The nitric oxide synthase inhibitor, N-monomethyl-L-arginine blocks induction of a long-term potentiation-like phenomenon in rat medial frontal cortical neurons in vitro

1993 ◽  
Vol 70 (3) ◽  
pp. 1255-1259 ◽  
Author(s):  
A. V. Nowicky ◽  
L. J. Bindman
Keyword(s):  
Nitric Oxide ◽  
Cortical Neurons ◽  
Long Term Potentiation ◽  
Control Group ◽  
Term Potentiation ◽  
The Mean ◽  
Synthase Inhibitor ◽  
Stimulation Of

1. Nitric oxide has been implicated in the production of long-term depression (LTD) in the cerebellum and in the production of long-term potentiation (LTP) and LTD in the hippocampus. We now provide evidence of its involvement in the induction of long-term synaptic potentiation in in vitro slices in the cerebral cortex of the rat. 2. Intracellular recordings were made from layer V neurons in the medial frontal cortex, and excitatory synaptic potentials (EPSPs) were evoked by electrical stimulation of layers II/III. Tetanic stimulation of this pathway may induce LTD or LTP or no change at these synapses. First we established experimental conditions under which a long lasting potentiation could be induced with a high incidence (> 60%), namely perfusion of slices with 1 microM bicuculline methiodide, second the use of increased shock duration in the tetanic conditioning stimuli, third and most important the addition of QX-314 to the microelectrode to reduce potassium conductances. Because the potentiation of the mean EPSP slope was significantly greater than the control at 40-min postconditioning, but was declining throughout this period, we refer to it for brevity as LTP, but strictly class it as an LTP-like phenomenon. 3. The nitric oxide (NO) synthase inhibitor interfered with the production of LTP. In the control group of neurons (n = 13) the mean depolarizing slope of the EPSP at 30-min post-conditioning was 142.7 +/- 2% (mean +/- SE) of the prestimulation control.(ABSTRACT TRUNCATED AT 250 WORDS)

Pre-gestational overweight in guinea pig sows induces fetal vascular dysfunction and increased rate of large and small fetuses

2015 ◽  
Vol 7 (3) ◽  
pp. 237-243 ◽  
Author(s):  
B. J. Krause ◽  
E. A. Herrera ◽  
F. A. Díaz-López ◽  
M. Farías ◽  
R. Uauy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Risk ◽  
Guinea Pig ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Fetal Weight ◽  
Control Group ◽  
Umbilical Arteries ◽  
Oxide Synthase

In humans, obesity before and during pregnancy is associated with both fetal macrosomia and growth restriction, and long-term cardiovascular risk in the offspring. We aimed to determine whether overweighted pregnant guinea pig sows results in an increased fetal weight at term and the effects on the vascular reactivity in fetal systemic and umbilical arteries. Pregnant guinea pigs were classified as control (n=4) or high weight (HWS, n=5) according to their pre-mating weight, and their fetuses extracted at 0.9 gestation (~60 days). Segments of fetal femoral and umbilical arteries were mounted in a wire myograph, where the contractile response to KCl (5–125 mM), and the relaxation to nitric oxide synthase-dependent agents (insulin, 10−10–10−7 and acetylcholine, 10−10–10−5) and nitric oxide [sodium nitroprusside (SNP), 10−10–10−5] were determined. Fetuses from HWS (HWSF) were grouped according to their body weight as low (<76 g) or high (>85 g) fetal weight, based on the confidence interval (76.5–84.9 g) of the control group. No HWSF were observed in the normal range. Umbilical arteries from HWSF showed a lower response to KCl and insulin compared with controls, but a comparable response with SNP. Conversely, femoral arteries from HWSF showed an increased response to KCl and acetylcholine, along with a decreased sensitivity to SNP. These data show that overweight sows have altered fetal growth along gestation. Further, large and small fetuses from obese guinea pig sows showed altered vascular reactivity at umbilical and systemic vessels, which potentially associates with long-term cardiovascular risk.

scholarly journals Non-compliant and compliant balloons for endovascular rescue therapy of cerebral vasospasm after spontaneous subarachnoid haemorrhage: experiences of a single-centre institution with radiological follow-up of the treated vessel segments

2020 ◽  
pp. svn-2020-000410
Author(s):  
Alexander Neumann ◽  
Jan Küchler ◽  
Claudia Ditz ◽  
Kara Krajewski ◽  
Jan Leppert ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Rescue Therapy ◽  
Catheter Angiography ◽  
Single Centre ◽  
Vessel Injury ◽  
Valid Data ◽  
Risk Treatment

BackgroundFor endovascular rescue therapy (ERT) of cerebral vasospasm (CVS) due to spontaneous subarachnoid haemorrhage (sSAH), non-compliant (NCB) and compliant (CB) balloons are used with both balloon types bearing the risk of vessel injury due to specific mechanical properties. Although severe delayed arterial narrowing after transluminal balloon angioplasty (TBA) for CVS has sporadically been described, valid data concerning incidence and relevance are missing. Our aim was to analyse the radiological follow-up (RFU) of differently TBA-treated arteries (CB or NCB).MethodsTwelve patients with utilisation of either NCB or CB for CVS were retrospectively analysed for clinical characteristics, ERT, functional outcome after 3 months and RFU. Compared with the initial angiogram, we classified delayed arterial narrowing as mild, moderate and severe (<30%, 30%–60%, respectively >60% calibre reduction).ResultsTwenty-three arteries were treated with CB, seven with NCB. The median first RFU was 11 months after TBA with CB and 10 after NCB. RFU was performed with catheter angiography in 18 arteries (78%) treated with CB and in five (71%) after NCB; magnetic resonance angiography was acquired in five vessels (22%) treated with CB and in two (29%) after NCB. Mild arterial narrowing was detected in three arteries (13%) after CB and in one (14%) after NCB. Moderate or severe findings were neither detected after use of CB nor NCB.ConclusionWe found no relevant delayed arterial narrowing after TBA for CVS after sSAH. Despite previous assumptions that CB provides for more dilatation in segments adjacent to CVS, we observed no disadvantages concerning long-term adverse effects. Our data support TBA as a low-risk treatment option.

Inhaled nitric oxide prevents left ventricular impairment during endotoxemia

1998 ◽  
Vol 85 (6) ◽  
pp. 2018-2024 ◽  
Author(s):  
Satoshi Ishihara ◽  
John A. Ward ◽  
Osamu Tasaki ◽  
Basil A. Pruitt ◽  
Cleon W. Goodwin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Left Ventricle ◽  
Cardiac Contractility ◽  
Ringer Solution ◽  
Left Ventricular ◽  
Control Group ◽  
Baseline Levels ◽  
Lv Volume

We evaluated the effect of long-term inhalation of nitric oxide (NO) on cardiac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to measure LV volume and a micromanometer to measure LV pressure. One week later, the animals were divided into a control group ( n = 6) or a NO group ( n = 6). All animals received intravenous Escherichia coliendotoxin (10 μg ⋅ kg−1 ⋅ h−1) and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The end-systolic elastance in the control group was significantly decreased beyond 7 h. NO inhalation maintained the end-systolic elastance at baseline levels and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.

The effect of intraumbilical fetal nutrition via a subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses

2017 ◽  
Vol 45 (2) ◽  
Author(s):  
Michael Tchirikov ◽  
Zhaxybay Sh. Zhumadilov ◽  
Gauri Bapayeva ◽  
Michael Bergner ◽  
Michael Entezami
Keyword(s):  
Cerebral Arteries ◽  
Control Group ◽  
Human Fetuses ◽  
Fetal Plasma ◽  
Fetal Nutrition ◽  
Placental Blood ◽  
Port System ◽  
Intravascular Treatment ◽  
Glucose Supplementation

AbstractObjective:To determine if intrauterine intraumbilical supplementation with amino acids (AA) and glucose can improve neonatal outcome of severe growth restricted human fetuses (IUGR).Methods:Prospective pilot study of intrauterine treatment of severe IUGR fetuses [n=14, 27 weeks of gestation (range 23–31)] with cerebroplacental ratio <1, with long-term intraumbilical AA and glucose supplementation (10% of feto-placental blood volume/day) using a perinatal port system alone (n=5) or combined with hyperbaric oxygenation (n=1, HBO) vs. control group (n=8).Results:The duration of continuous intraumbilical AA/glucose supplementation was 11 (6–13) days. Daily intravascular fetal nutrition significantly prolonged the brain sparing to delivery interval by 24 (14–33) days vs. 5.6 (2–12) days in controls. Fetal nutrition reduced blood flow resistance in the placental circulation but did not affect the Doppler profile of cerebral arteries. Higher weight gain of 113.5 (36–539) g was observed following supplementation compared to 33.3 (8–98) g in the control group (P<0.05). In spite of this, fetuses below 28 weeks of gestation did not sufficiently benefit from infused commercial AA. We found a reduced fetal plasma concentration of the essential AA histidine, threonine, lysine and arginine, and non-essential AA taurine, in severe IUGR fetuses in both groups. Long-term supplementation with a commercial AA formula led to a slight, but not significant, reduction of histidine, threonine, lysine, arginine, asparagine and glutamine. However, the concentration of tryptophan and glutamic acid slightly increased. HBO can be combined with AA supplementation via a port system. In one case, the port system was also successfully used for fetal blood transfusion.Conclusions:Intravascular treatment of IUGR with fetal nutrition can prolong pregnancy with severe placental insufficiency and brain sparing for many weeks. However, rather than normalizing AA concentrations, an enhanced AA imbalance was observed in IUGR fetuses following supplementation. These deviations in AA concentrations prevent the recommendation for use of commercial AA solutions for prenatal treatment of extreme preterm IUGR fetuses.

Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake

1997 ◽  
Vol 272 (4) ◽  
pp. R1162-R1169 ◽  
Author(s):  
R. D. Manning ◽  
L. Hu ◽  
J. F. Reckelhoff
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Control Group ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
High Sodium Intake

The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure.

scholarly journals Long-Term Effects of Maternal Deprivation on the Neuronal Soma Area in the Rat Neocortex

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Milan Aksić ◽  
Nevena V. Radonjić ◽  
Dubravka Aleksić ◽  
Gordana Jevtić ◽  
Branka Marković ◽  
...  
Keyword(s):  
Animal Model ◽  
Morphological Changes ◽  
Maternal Deprivation ◽  
Retrosplenial Cortex ◽  
Control Group ◽  
Long Term Effects ◽  
Adult Rats ◽  
Adult Age ◽  
Neuronal Soma

Early separation of rat pups from their mothers (separatio a matrem) is considered and accepted as an animal model of perinatal stress. Adult rats, separated early postnatally from their mothers, are developing long-lasting changes in the brain and neuroendocrine system, corresponding to the findings observed in schizophrenia and affective disorders. With the aim to investigate the morphological changes in this animal model we exposed 9-day-old (P9) Wistar rats to a 24 h maternal deprivation (MD). At young adult age rats were sacrificed for morphometric analysis and their brains were compared with the control group bred under the same conditions, but without MD. Rats exposed to MD had a 28% smaller cell soma area in the prefrontal cortex (PFCX), 30% in retrosplenial cortex (RSCX), and 15% in motor cortex (MCX) compared to the controls. No difference was observed in the expression of glial fibrillary acidic protein in the neocortex of MD rats compared to the control group. The results of this study demonstrate that stress in early life has a long-term effect on neuronal soma size in cingulate and retrosplenial cortex and is potentially interesting as these structures play an important role in cognition.

scholarly journals A case report on the management of severe vasospasm in subarachnoid hemorrhagic patients using intra-arterial nimodipine, intrathecal sodium nitroprusside and intra-arterial papaverine

2020 ◽  
Vol 11 (4) ◽  
pp. 7334-7337
Author(s):  
Sheen Reynold ◽  
Jiya Marium George ◽  
Athul Gopan ◽  
Anila KN ◽  
Sreehari NR ◽  
...  
Keyword(s):  
Subarachnoid Haemorrhage ◽  
Sodium Nitroprusside ◽  
Cerebral Vasospasm ◽  
Side Effect ◽  
Cerebral Arteries ◽  
Treatment Strategies ◽  
Intrathecal Administration ◽  
Aneurysmal Subarachnoid Haemorrhage ◽  
Multimodality Approach ◽  
Effective Drugs

Management and prevention of vasospasm in subarachnoid haemorrhage are one of the complex dictums so far. Aneurysmal subarachnoid haemorrhage (aSAH) is the condition in which bleeding occurs in subarachnoid space. Vasospasm is a complex immunologically active phenomenon which requires a multimodality approach in the treatment of established vasospasm. Various treatment strategies for vasospasm and related disabilities include vasodilators such as nimodipine, sodium nitroprusside and papaverine. Intra-arterial nimodipine shows drastic improvement in several patients by resolving and preventing vasospasm. Intra-arterial administration of nimodipine can cause hypotension which can be easily managed. Papaverine is also an efficient drug-producing vasodilatory action on cerebral arteries. Papaverine is considered as the first intraarterial agent to reduce angiographic cerebral vasospasm which has the side effect of elevated intracranial pressure. Besides, the intrathecal administration of sodium nitroprusside has also demonstrated the effect in ischemic vasospasm after subarachnoid haemorrhage. Intraarterial administration of this drug can induce arterial hypotension which is not a recommended method. Vomiting is the main side effect of sodium nitroprusside, which can be managed with antiemetics such as ondansetron. Here we present a case of management of cerebral vasospasm in subarachnoid patients using the combination of these three effective drugs which showed a remarkable improvement in the resolution of aneurysmal vasospasm.

Loss of nitric oxide synthase immunoreactivity in cerebral vasospasm

1996 ◽  
Vol 84 (4) ◽  
pp. 648-654 ◽  
Author(s):  
Ryszard M. Pluta ◽  
B. Gregory Thompson ◽  
Ted M. Dawson ◽  
Solomon H. Snyder ◽  
Robert J. Boock ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cerebral Vasospasm ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Nerve Fibers ◽  
Content Type ◽  
The Right ◽  
Oxide Synthase ◽  
Fine Print

✓ To determine the distribution of nitric oxide synthase (NOS) in the primate cerebral artery nervi vasorum and to examine the potential role of NOS in cerebral vasospasm after subarachnoid hemorrhage (SAH) in primates, the distribution of NOS immunoreactivity (NOS-IR) in the major cerebral arteries was examined immunohistochemically in cynomolgus monkeys by the use of whole, mounted preparations of the circle of Willis. In four normal monkeys, NOS-IR was localized to the endothelial and adventitial layers of the large cerebral arteries. On the abluminal side, NOS-IR staining was densely concentrated in perivascular nerve fibers (nervi vasorum) of the anterior circulation. Staining was less prominent in the posterior circulation. In six monkeys with vasospasm on Day 7 after placement of preclotted arterial blood to form an SAH around the right middle cerebral artery (MCA) (42% ± 8.3% decrease of MCA area, mean ± standard deviation), NOS-IR was virtually absent in nerve fibers around the spastic right MCA but was normal on the contralateral side. In five monkeys in which vasospasm resolved by Day 14 after SAH (36% ± 14% decrease of right MCA area on Day 7, and 5% ± 14% decrease on Day 14), NOS-IR was also absent in the right MCA adventitial nerve fibers and remained normal in the left MCA. Adventitial NOS-IR was also normal in cerebral vessels of a sham-operated, nonspastic monkey. These findings provide further evidence that nitric oxide (NO) functions as a neuronal transmitter to mediate vasodilation in primates and indicate a role for adventitial NO in the pathogenesis of cerebral vasospasm after SAH in humans.

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