scholarly journals Role of Red Blood Cell Lysis and Iron in Hydrocephalus after Intraventricular Hemorrhage

2014 ◽  
Vol 34 (6) ◽  
pp. 1070-1075 ◽  
Author(s):  
Chao Gao ◽  
Hanjian Du ◽  
Ya Hua ◽  
Richard F Keep ◽  
Jennifer Strahle ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Intraventricular Hemorrhage ◽  
Intraventricular Injection ◽  
Heme Oxygenase 1 ◽  
Ventricular Enlargement ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
The Right

Thrombin and iron are two major players in intracerebral hemorrhage-induced brain injury and our recent study found that thrombin contributes to hydrocephalus development in a rat model of intraventricular hemorrhage (IVH). This study investigated the role of red blood cell (RBC) lysis and iron in hydrocephalus after IVH. There were three parts to this study. First, male Sprague-Dawley rats received an injection of saline, packed, or lysed RBCs into the right lateral ventricle. Second, rats had an intraventricular injection of iron or saline. Third, the rats received intraventricular injection of lysed RBCs mixed with deferoxamine (0.5 mg in 5 μL saline) or saline. All rats underwent magnetic resonance imaging at 24 hours and were then euthanized for brain edema measurement, western blot analysis, or brain histology. We found that intraventricular injection of lysed RBCs, but not packed RBCs, resulted in ventricular enlargement and marked increases in brain heme oxygenase-1 and ferritin at 24 hours. Intraventricular injection of iron also resulted in ventricular enlargement and ventricular wall damage 24 hours later. Coinjection of deferoxamine reduced lysed RBC-induced ventricular enlargement ( P<0.01). These results suggest that iron, a degradation product of hemoglobin, has an important role in hydrocephalus development after IVH.

scholarly journals Hydrocephalus after Intraventricular Hemorrhage: The Role of Thrombin

2013 ◽  
Vol 34 (3) ◽  
pp. 489-494 ◽  
Author(s):  
Feng Gao ◽  
Fuyi Liu ◽  
Zhi Chen ◽  
Ya Hua ◽  
Richard F Keep ◽  
...  
Keyword(s):  
Lateral Ventricle ◽  
Intraventricular Hemorrhage ◽  
Autologous Blood ◽  
Intraventricular Injection ◽  
Sprague Dawley ◽  
Blood Brain Barrier Disruption ◽  
Sprague Dawley Rats ◽  
Blood Injection ◽  
Brain Barrier Disruption ◽  
The Right

Previous studies demonstrated that thrombin is an important factor in brain injury after intracerebral hemorrhage. This study investigated the effect of thrombin on hydrocephalus development in a rat intraventricular hemorrhage (IVH) model. There were three parts in this study. First, male Sprague–Dawley rats had an injection of 200  μL saline, autologous blood or heparinized blood, into the right lateral ventricle. Second, rats had an injection of 50  μL saline or 3U thrombin into the right lateral ventricle. Third, rats had an injection of thrombin (3U) with a protease-activated receptor-1 (PAR-1) antagonist, SCH79797 (0.15 nmol), or vehicle into the right lateral ventricle. Lateral ventricle volumes were measured by magnetic resonance imaging and the brains were used for immunohistochemistry and western blot analyses. Intraventricular injection of autologous blood induced hydrocephalus from day 1 to 28. Heparinized blood injection resulted in less hydrocephalus at all time points compared with blood injection alone ( P<0.05). Intraventricular injection of thrombin caused significant hydrocephalus, ventricular wall damage, and periventricular blood–brain barrier disruption. Thrombin-induced hydrocephalus was reduced by co-injection of the PAR-1 antagonist SCH79797 ( P<0.05). In conclusion, thrombin contributes to hydrocephalus development after IVH and thrombin-induced hydrocephalus is through PAR-1.

Measurement of subscellular calcium distribution in cardiac muscle in the presence of caffeine and elevated extracellular calcium

1990 ◽  
Vol 48 (2) ◽  
pp. 170-171
Author(s):  
B. J. Hurley ◽  
M. E. Cantino
Keyword(s):  
Cardiac Muscle ◽  
Papillary Muscle ◽  
Myocardial Contraction ◽  
Extracellular Calcium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tension Transducer ◽  
The Right ◽  
Rat Papillary Muscle

Calcium is thought to play a major role in the activation of mammalian cardiac muscle. Several investigators have utilized Electron Probe X-ray Microanalysis (EPMA) to study the role of calcium in myocardial contraction. The purpose of this study is to measure subcellular elemental concentrations in rat papillary muscle under the influence of caffeine or elevated extracellular calcium. Of particular interest is the concentration of calcium in the junctional sarcoplasmic reticulum (jSR) under these conditions.Male Sprague-Dawley rats weighing approximately 300 g were anesthetized using I.P. Na-pentabarbitol injection. The hearts were carefully removed and back-perfused with a modified Tyrodes solution via cannulation of the aorta. The wall of the right ventricle was cut away revealing the papillary muscles. The tendon and wall ends of the papillary muscle were then sutured and the muscle was carefully cut out of the heart. The papillary muscle was then placed on the freezing device holder and the suture tied to a fixed post and tension transducer post, as shown in Figure 1.

scholarly journals Prx2 (Peroxiredoxin 2) as a Cause of Hydrocephalus After Intraventricular Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
Xiaoxiao Tan ◽  
Jingyin Chen ◽  
Richard F. Keep ◽  
Guohua Xi ◽  
Ya Hua
Keyword(s):  
Choroid Plexus ◽  
Intraventricular Hemorrhage ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Intraventricular Injection ◽  
Ventricular Wall ◽  
Sprague Dawley ◽  
Peroxiredoxin 2 ◽  
Sprague Dawley Rats ◽  
Epiplexus Cells

Background and Purpose— Our recent study demonstrated that release of Prx2 (peroxiredoxin 2) from red blood cells (RBCs) is involved in the inflammatory response and brain injury after intracerebral hemorrhage. The current study investigated the role of extracellular Prx2 in hydrocephalus development after experimental intraventricular hemorrhage. Methods— There were 4 parts in this study. First, Sprague-Dawley rats received an intraventricular injection of lysed RBC or saline and were euthanized at 1 hour for Prx2 measurements. Second, rats received an intraventricular injection of Prx2, deactivated Prx2, or saline. Third, lysed RBC was coinjected with conoidin A, a Prx2 inhibitor, or vehicle. Fourth, rats received Prx2 injection and were treated with minocycline or saline (i.p.). The effects of Prx2 and the inhibitors were examined using magnetic resonance imaging assessing ventriculomegaly, histology assessing ventricular wall damage, and immunohistochemistry to assess inflammation, particularly at the choroid plexus. Results— Intraventricular injection of lysed RBC resulted in increased brain Prx2 and hydrocephalus. Intraventricular injection of Prx2 alone caused hydrocephalus, ventricular wall damage, activation of choroid plexus epiplexus cells (macrophages), and an accumulation of neutrophils. Conoidin A attenuated lysed RBC-induced injury. Systemic minocycline treatment reduced the epiplexus cell activation and hydrocephalus induced by Prx2. Conclusions— Prx2 contributed to the intraventricular hemorrhage-induced hydrocephalus, probably by inducing inflammatory responses in choroid plexus and ventricular wall damage.

Resorption of Residual Ridges (RRR) in Rats

1987 ◽  
Vol 66 (12) ◽  
pp. 1753-1757 ◽  
Author(s):  
I. Nishimura ◽  
P.J. Damiani ◽  
D.A. Atwood
Keyword(s):  
Bone Resorption ◽  
Alveolar Bone ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Minimal Trauma ◽  
Specific Factors ◽  
Maxilla And Mandible ◽  
The Right ◽  
Mandibular First Molar

The post-extraction resorption of residual ridges (RRR) is a major and largely unsolved health problem, probably of multifactorial etiology. In order for one to study the role of specific factors in the pathophysiology of RRR, the use of animal models is desirable. The purpose of this study was to establish a reliable animal model and a standardized assay system to measure RRR for future experiments. A new oblique cephalometric device was designed to take pairs of xeroradiographs on the right and left sides of the rat skull and mandible at a 45-degree angle to the horizontal plane. Preliminary studies confirmed the reproducibility of the technique. All molars were extracted with minimal trauma from the right maxilla and mandible in five male Sprague-Dawley rats (40 days old). Longitudinal cephalographic examinations were performed before and immediately after extraction and at two, four, eight, and 12 weeks after extraction. Alveolar bone resorption was measured on enlarged cephalographs (5. 7X) at a point mesial to the mandibular first molar. Sequential mean bone resorption was 0.8 ± 0.2 mm (S.D.), 1.0 ± 0.3, 1.3 ± 0.3, and 1.5 ± 0.4, respectively. Graphically, these findings produced bone loss curves similar to those observed in man. These results indicate that the rat model may be utilized in longitudinal studies of the resorption of the residual ridge.

Effects of remote ischemic preconditioning on the deformability and aggregation of red blood cells in a rat endotoxemia model

2021 ◽  
pp. 1-9
Author(s):  
Yun-Hee Kim ◽  
Sung-Uk Choi ◽  
Jung-Min Youn ◽  
Seung-Ha Cha ◽  
Hyeon-Ju Shin ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Remote Ischemic Preconditioning ◽  
Sprague Dawley ◽  
Aggregation Index ◽  
Sprague Dawley Rats ◽  
Endotoxemia Model ◽  
Elongation Index ◽  
The Right ◽  
Phosphate Buffered Saline ◽  
Severe Ischemia

BACKGROUND: The prevention of rheologic alterations in erythrocytes may be important for reducing sepsis-associated morbidity and mortality. Remote ischemic preconditioning (RIPC) has been shown to prevent tissue damage caused by severe ischemia and mortality resulting from sepsis. However, the effect of RIPC on erythrocytes in sepsis is yet to be determined. OBJECTIVE: To investigate the effect of RIPC on rheologic alterations in erythrocytes in sepsis. METHODS: Thirty male Sprague-Dawley rats were used in this study. An endotoxin-induced sepsis model was established by intraperitoneally injecting 20 mg/kg LPS (LPS group). RIPC was induced in the right hind limb using a tourniquet, with three 10-minute of ischemia and 10 min of reperfusion cycles immediately before the injection of LPS (RIPC/LPS group) or phosphate-buffered saline (RIPC group). The aggregation index (AI), time to half-maximal aggregation (T1/2), and maximal elongation index (EImax) of the erythrocytes were measured 8 h after injection. RESULTS: The AI, T1/2, and EImax values in the LPS and RIPC/LPS groups differed significantly from those in the RIPC group, but there were no differences between the values in the LPS and RIPC/LPS groups. CONCLUSIONS: RIPC did not prevent rheologic alterations in erythrocytes in the rat model of LPS-induced endotoxemia.

scholarly journals Mild DOCA-salt hypertension: sympathetic system and role of renal nerves

2011 ◽  
Vol 300 (5) ◽  
pp. H1781-H1787 ◽  
Author(s):  
Sachin S. Kandlikar ◽  
Gregory D. Fink
Keyword(s):  
Control Period ◽  
Whole Body ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Sympathetic Activation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salt Hypertension ◽  
Hypertension Development

Excess sympathetic nervous system activity (SNA) is linked to human essential and experimental hypertension. To test whether sympathetic activation is associated with a model of deoxycorticosterone acetate (DOCA)-salt hypertension featuring two kidneys and a moderate elevation of blood pressure, we measured whole body norepinephrine (NE) spillover as an index of global SNA. Studies were conducted in chronically catheterized male Sprague-Dawley rats drinking water containing 1% NaCl and 0.2% KCl. After a 7-day surgical recovery and a 3-day control period, a DOCA pellet (50 mg/kg) was implanted subcutaneously in one group of rats (DOCA), while the other group underwent sham implantation (Sham). NE spillover was measured on control day 2 and days 7 and 14 after DOCA administration or sham implantation. During the control period, mean arterial pressure (MAP) was similar in Sham and DOCA rats. MAP was significantly increased in the DOCA group compared with the Sham group after DOCA administration ( day 14: Sham = 109 ± 5.3, DOCA = 128 ± 3.6 mmHg). However, plasma NE concentration, clearance, and spillover were not different in the two groups at any time. To determine whether selective sympathetic activation to the kidneys contributes to hypertension development, additional studies were performed in renal denervated (RDX) and sham-denervated (Sham-DX) rats. MAP, measured by radiotelemetry, was similar in both groups during the control and DOCA treatment periods. In conclusion, global SNA is not increased during the development of mild DOCA-salt hypertension, and fully intact renal nerves are not essential for hypertension development in this model.

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

The Hepatoprotective Role of Warburgia salutaris and Iso-Mukaadial Acetate on Carbon tetrachloride Intoxicated Rats Model

2021 ◽  
Vol 17 ◽  
Author(s):  
Gideon Ayeni ◽  
Mthokozisi Blessing Cedric Simelane ◽  
Shahidul Islam ◽  
Ofentse Jacob Pooe
Keyword(s):  
Carbon Tetrachloride ◽  
Hepatic Injury ◽  
Antioxidant Properties ◽  
Hepatic Necrosis ◽  
Protective Role ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Isolated Compound

Background: Medicinal plants together with their isolated bioactive compounds are known for their antioxidant properties which constitute therapeutic agents that are routinely employed in the treatment of liver diseases. Aims of the Study: The current study sought to explore the protective role of Warburgia salutaris and its isolated compound, iso-mukaadial acetate against carbon tetrachloride (CCl4)-induced hepatic injury. Methods: Thirty-five male Sprague Dawley rats were divided into seven groups of five animals each and injected with CCl4 to induce hepatic injury. Results: Treatment with the crude extract of W. salutaris and of iso-mukaadial acetate significantly reduced the levels of alkaline phosphatase, alanine and aspartate aminotransaminases, total bilirubin and malondialdehyde in a dose dependent manner, when compared to untreated groups. Liver histology revealed a reduction in hepatic necrosis and inflammation. Conclusion: The current investigation has demonstrated that W. salutaris extract and iso-mukaadial acetate could mitigate the acute liver injury inflicted by a hepatotoxic inducer in rats.

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