scholarly journals A novel DDAH-1 inhibitor improved cardiovascular function in a short-term anesthetized rat model of sepsis

Critical Care ◽  
2011 ◽  
Vol 15 (S3) ◽  
Author(s):  
Z Wang ◽  
V Taylor ◽  
R Stidwill ◽  
J Leiper ◽  
M Singer
2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Klaske Oberman ◽  
Iris Hovens ◽  
Jacco de Haan ◽  
Joana Falcao-Salles ◽  
Barbara van Leeuwen ◽  
...  

Abstract Background Inflammation is considered a key factor in the development of postoperative cognitive dysfunction (POCD). Therefore, we hypothesized that pre-operative anti-inflammatory treatment with ibuprofen would inhibit POCD in our rat-model. Methods Male Wistar rats of 3 or 23 months old received a single injection of ibuprofen (15 mg/kg i.p.) or were control handled before abdominal surgery. Timed blood and fecal samples were collected for analyses of inflammation markers and gut microbiome changes. Behavioral testing was performed from 9 to 14 days after surgery, in the open field, novel object- and novel location-recognition tests and Morris water maze. Neuroinflammation and neurogenesis were assessed by immune histochemistry after sacrifice on postoperative day 14. Results Ibuprofen improved short-term spatial memory in the novel location recognition test, and increased hippocampal neurogenesis. However, these effects were associated with increased hippocampal microglia activity. Whereas plasma cytokine levels (IL1-β, IL6, IL10, and TNFα) were not significantly affected, VEGF levels increased and IFABP levels decreased after ibuprofen. Long-term memory in the Morris water maze was not significantly improved by ibuprofen. The gut microbiome was neither significantly affected by surgery nor by ibuprofen treatment. In general, effects in aged rats appeared similar to those in young rats, though less pronounced. Conclusion A single injection of ibuprofen before surgery improved hippocampus-associated short-term memory after surgery and increased neurogenesis. However, this favorable outcome seemed not attributable to inhibition of (neuro)inflammation. Potential contributions of intestinal and blood-brain barrier integrity need further investigation. Although less pronounced compared to young rats, effects in aged rats indicate that even elderly individuals could benefit from ibuprofen treatment.


2008 ◽  
Vol 29 (6) ◽  
pp. 1062-1068 ◽  
Author(s):  
Daiana Silva Ávila ◽  
Priscila Gubert ◽  
Roselei Fachinetto ◽  
Caroline Wagner ◽  
Michael Aschner ◽  
...  

2018 ◽  
Vol 134 ◽  
pp. 332-342 ◽  
Author(s):  
Mais M. Aljunaidy ◽  
Jude S. Morton ◽  
Raven Kirschenman ◽  
Tom Phillips ◽  
C. Patrick Case ◽  
...  

2020 ◽  
pp. 147451512094458
Author(s):  
Zhongyou Li ◽  
Wentao Jiang ◽  
Yu Chen ◽  
Guanshi Wang ◽  
Fei Yan ◽  
...  

Objective: The role of sauna bathing in cardiovascular function treatment has been increasingly explored, but insufficient attention has been paid to its efficacy. We performed a meta-analysis to provide more evidence for the efficacy of sauna treatment in cardiovascular nursing. Methods: Sixteen peer-reviewed journal articles were screened to summarize the efficacy of the sauna on cardiovascular function. Both acute (0–30 min after the sauna) and short-term (2–4 weeks following the sauna treatment) efficacies were investigated. Results: For pooled acute efficacy, body temperature and heart rate significantly ( p<0.001) grew by 0.94℃ and 17.86 beats/min, respectively; reductions of 5.55 mmHg ( p<0.001) and 6.50 mmHg ( p<0.001) were also observed in systolic blood pressure and diastole blood pressure, respectively. For combined short-term efficacy, left ventricular ejection fraction (LVEF), 6-min walk distance, and flow-mediated dilation ( p<0.001) increased by 3.27%, 48.11 m, and 1.71%, respectively; greater amelioration in LVEF was observed in participants with lower LVEF. The proportion of patients with New York Heart Association class III and IV decreased by 10.9% and 12.2%, respectively. Systolic blood pressure, diastolic blood pressure, brain natriuretic peptide concentration, left ventricular end-diastolic dimension, cardiothoracic ratio, and left atrial dimension reduced by 5.26 mmHg ( p<0.001), 4.14 mmHg ( p<0.001), 116.66 pg/mL ( p<0.001), 2.79 mm ( p<0.001), 2.628% ( p<0.05), and 1.88 mm ( p<0.05), respectively, while the concentration of norepinephrine in the plasma remained unchanged. Conclusion: Sauna treatment was found to play a positive role in improving cardiovascular function and physical activity levels, especially in patients with low cardiovascular function. These findings reveal that thermal intervention may be a promising means for cardiovascular nursing.


2006 ◽  
Vol 101 (3) ◽  
pp. 809-816 ◽  
Author(s):  
Alastair J. Thomson ◽  
Gordon B. Drummond ◽  
W. Stephen Waring ◽  
David J. Webb ◽  
Simon R. J. Maxwell

Both hypoxia and hyperoxia have major effects on cardiovascular function. However, both states affect ventilation and many previous studies have not controlled CO2 tension. We investigated whether hemodynamic effects previously attributed to modified O2 tension were still apparent under isocapnic conditions. In eight healthy men, we studied blood pressure (BP), heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI) and arterial stiffness (augmentation index, AI) during 1 h of hyperoxia (mean end-tidal O2 79.6 ± 2.0%) or hypoxia (pulse oximeter oxygen saturation 82.6 ± 0.3%). Hyperoxia increased SVRI (18.9 ± 1.9%; P < 0.001) and reduced HR (−10.3 ± 1.0%; P < 0.001), CI (−10.3 ± 1.7%; P < 0.001), and stroke index (SI) (−7.3 ± 1.3%; P < 0.001) but had no effect on AI, whereas hypoxia reduced SVRI (−15.2 ± 1.2%; P < 0.001) and AI (−10.7 ± 1.1%; P < 0.001) and increased HR (18.2 ± 1.2%; P < 0.001), CI (20.2 ± 1.8%; P < 0.001), and pulse pressure (13.2 ± 2.3%; P = 0.02). The effects of hyperoxia on CI and SVRI, but not the other hemodynamic effects, persisted for up to 1 h after restoration of air breathing. Although increased oxidative stress has been proposed as a cause of the cardiovascular response to altered oxygenation, we found no significant changes in venous antioxidant or 8-iso-prostaglandin F2α levels. We conclude that both hyperoxia and hypoxia, when present during isocapnia, cause similar changes in cardiovascular function to those described with poikilocapnic conditions.


2000 ◽  
Vol 93 (5) ◽  
pp. 1279-1284 ◽  
Author(s):  
Matthew D. Thompson ◽  
William J. Gallagher ◽  
Paul A. Iaizzo ◽  
William L. Lanier

Background In the rat model of forebrain ischemia, long-term dexamethasone treatment is reported to cause hyperglycemia and worsen postischemic functional and histologic injury. This effect was assumed to result from glucose enhancement of intraischemic lactic acidosis within the brain. Short-term insulin therapy restored normoglycemia but did not return histologic injury completely to baseline values. Using a nonischemic rat model, the current study attempted to identify a metabolic basis for such outcome data. Methods Fifty-eight halothane-anesthetized (1.3% inspired) Sprague-Dawley rats were assigned randomly to be administered either no treatment (N = 18) or 2 mg/kg intraperitoneal dexamethasone (N = 40). The latter were administered dexamethasone 3 h before the study only (N = 8) or for 3 h before the study plus daily for 1 day (N = 8), 2 days (N = 8), or 4 days (N = 16). Of the rats treated with dexamethasone for 4 days, one half (N = 8) were administered an insulin-containing saline infusion subsequently to restore normoglycemia short-term. All other rats (N = 50) were administered an infusion of saline without insulin. Plasma glucose was quantified, and brains were excised after in situ freezing. Brain glucose and glycogen concentrations were measured using enzymatic fluorometric analyses. Results After 4 days of dexamethasone treatment, plasma glucose was 159% greater than in rats administered placebo (i.e., 22.01 +/- 4.66 vs. 8.51 +/- 1.65 micromol/ml; mean +/- SD; P &lt; 0.0001). Brain glucose concentrations increased parallel to plasma glucose. An insulin infusion for 27 +/- 5 min restored normoglycemia but resulted in a brain-to-plasma glucose ratio that was 32% greater than baseline values (P &lt; 0.01). Neither dexamethasone nor the combination of dexamethasone plus insulin affected brain glycogen concentrations. Conclusions In a nonischemic rat model, dexamethasone alone had no independent effect on the brain-to-plasma glucose ratio. However, short-term insulin therapy caused a dysequilibrium between plasma and brain glucose, resulting in an underestimation of brain glucose concentrations when normoglycemia was restored. The dysequilibrium likely was caused by the rapid rate of glucose reduction. The magnitude of the effect may account for the failure of insulin to reverse dexamethasone enhancement of neurologic injury completely in a previous report that used the rat model of forebrain ischemia.


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