Impact of age on cardiovascular function, inflammation, and oxidative stress in experimental asphyxial cardiac arrest

Secher, Niels; Østergaard, Leif; Tønnesen, Else; Hansen, Frederik B; Granfeldt, Asger

doi:10.1111/aas.13014

Cited by 6 publications

(4 citation statements)

References 51 publications

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“…We studied healthy young male rats only. More pronounced systemic cytokine response was observed in aged rats subjected to asphyxial CA (41). A significant difference in plasma cytokine response to CA between sexes have been observed by others (30).…”

Section: Discussionsupporting

confidence: 65%

Targeting TNFα‑mediated cytotoxicity using thalidomide after experimental cardiac arrest in rats: An exploratory study

et al. 2022

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Cardiac arrest (CA) results in a central and systemic cytokine and inflammatory response. Thalidomide has been reported to be neuroprotective by selectively decreasing TNFα synthesis. We hypothesized that thalidomide would decrease the systemic and organ-specific TNFα/cytokine response and biomarkers of injury in rats subjected to 10 min CA. Naïves, CA treated with vehicle (CA) and CA treated with thalidomide (50 mg/kg; CA+T) were studied (n=6 per group). TNFα and key cytokines were assessed at 3 h after resuscitation in the cortex, hippocampus, striatum, cerebellum, plasma, heart and lung. Neuron specific enolase (NSE), S100b, cardiac troponin T (cTnT) and intestinal fatty acid binding protein (IFABP) were used to assess neuronal, glial, cardiac and intestinal damage, respectively. CA increased TNFα and multiple pro-inflammatory cytokines in plasma and selected tissues with no differences between the CA and CA+T groups in any region. NSE, S100b, cTnT and IFABP were increased after CA or CA+T vs. in the naïve group (all P<0.05) without significant differences between the CA and CA+T groups. In conclusion, CA resulted in a TNFα and cytokine response, with increased biomarkers of organ injury. Notably, thalidomide at a dose reported to improve the outcome in in vivo models of brain ischemia did not decrease TNFα or cytokine levels in plasma, brain or extracerebral organs, or biomarkers of injury. Although CA at 3 h post resuscitation produces a robust TNFα response, it cannot be ruled out that an alternative dosing regimen or assessment at other time-points might yield different results.The marked systemic and regional cytokine response to CA remains a potential therapeutic target.

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Section: Discussionsupporting

confidence: 65%

Targeting TNFα‑mediated cytotoxicity using thalidomide after experimental cardiac arrest in rats: An exploratory study

et al. 2022

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“…Some differences in risk factors were reported between PAD and CAD [ 24 , 25 ]. Although the mechanism of low plasma HO-1 levels in patients with PAD remains unclear, HO-1 defensive response to oxidative stress was reported to be attenuated at an advanced age [ 26 ] and the late stage of DM [ 27 ]. The HO-1 induction in plasma and tissues was decreased in aged rats after cardiac arrest [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…Although the mechanism of low plasma HO-1 levels in patients with PAD remains unclear, HO-1 defensive response to oxidative stress was reported to be attenuated at an advanced age [ 26 ] and the late stage of DM [ 27 ]. The HO-1 induction in plasma and tissues was decreased in aged rats after cardiac arrest [ 26 ]. In diabetic mice, HO-1 activity and mRNA expression were increased in the early stage of DM while decreased in the late stage of DM [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Plasma Heme Oxygenase-1 Levels in Patients with Coronary and Peripheral Artery Diseases

et al. 2018

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Aims Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate CO, biliverdin, and iron. Since these products have antiatherogenic properties, HO-1 may play a protective role against the progression of atherosclerosis. However, plasma HO-1 levels in patients with atherosclerotic diseases, such as coronary artery disease (CAD) and peripheral artery disease (PAD), have not been clarified yet. Methods We investigated plasma HO-1 levels by ELISA in 410 consecutive patients undergoing elective coronary angiography who also had an ankle-brachial index (ABI) test for PAD screening. Results Of the 410 study patients, CAD was present in 225 patients (55%) (1-vessel (1-VD), n = 91; 2-vessel (2-VD), n = 66; 3-vessel disease (3-VD), n = 68). PAD (ABI < 0.9) was found in 36 (9%) patients. Plasma HO-1 levels did not differ between 225 patients with CAD and 185 without CAD (median 0.44 versus 0.35 ng/mL), but they were significantly lower in 36 patients with PAD than in 374 without PAD (0.27 versus 0.41 ng/mL, P < 0.02). After excluding the 36 patients with PAD, HO-1 levels were significantly higher in 192 patients with CAD than in 182 without CAD (0.45 versus 0.35 ng/mL, P < 0.05). HO-1 levels in 4 groups of CAD(−), 1-VD, 2-VD, and 3-VD were 0.35, 0.49, 0.44, and 0.44 ng/mL, respectively, and were highest in 1-VD (P < 0.05). In the multivariate analysis, HO-1 levels were inversely associated with PAD, whereas they were also associated with CAD. The odds ratios for PAD and CAD were 2.12 (95% CI = 1.03–4.37) and 0.65 (95% CI = 0.42–0.99) for the HO-1 level of <0.35 ng/mL, respectively. Conclusions Plasma HO-1 levels were found to be low in patients with PAD, in contrast to high levels in patients with CAD.

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“…This is in line with the results reported by Signorelli et al [24], who noted that the serum HO-1 levels were lower in 27 patients with PAD compared to 27 controls. Although the mechanism of low plasma HO-1 levels in patients with PAD remains unclear, the HO-1 defensive response to oxidative stress was reported to be attenuated at advanced age [98] and at the late stage of diabetes mellitus [99]. A long duration of a severe stress condition may therefore cause some disruption of the HO-1 defense system.…”

Section: Ho-1 Expression In Patients With Atherosclerotic Diseasesmentioning

confidence: 99%

The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

Kishimoto

Kondo

Momiyama

2019

IJMS

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Heme oxygenase-1 (HO-1) is an intracellular enzyme that catalyzes the oxidation of heme to generate ferrous iron, carbon monoxide (CO), and biliverdin, which is subsequently converted to bilirubin. These products have anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-thrombotic properties. Although HO-1 is expressed at low levels in most tissues under basal conditions, it is highly inducible in response to various pathophysiological stresses/stimuli. HO-1 induction is thus thought to be an adaptive defense system that functions to protect cells and tissues against injury in many disease settings. In atherosclerosis, HO-1 may play a protective role against the progression of atherosclerosis, mainly due to the degradation of pro-oxidant heme, the generation of anti-oxidants biliverdin and bilirubin and the production of vasodilator CO. In animal models, a lack of HO-1 was shown to accelerate atherosclerosis, whereas HO-1 induction reduced atherosclerosis. It was also reported that HO-1 induction improved the cardiac function and postinfarction survival in animal models of heart failure or myocardial infarction. Recently, we and others examined blood HO-1 levels in patients with atherosclerotic diseases, e.g., coronary artery disease (CAD) and peripheral artery disease (PAD). Taken together, these findings to date support the notion that HO-1 plays a protective role against the progression of atherosclerotic diseases. This review summarizes the roles of HO-1 in atherosclerosis and focuses on the clinical studies that examined the relationships between HO-1 levels and atherosclerotic diseases.

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Impact of age on cardiovascular function, inflammation, and oxidative stress in experimental asphyxial cardiac arrest

Cited by 6 publications

References 51 publications

Targeting TNFα‑mediated cytotoxicity using thalidomide after experimental cardiac arrest in rats: An exploratory study

Targeting TNFα‑mediated cytotoxicity using thalidomide after experimental cardiac arrest in rats: An exploratory study

Plasma Heme Oxygenase-1 Levels in Patients with Coronary and Peripheral Artery Diseases

The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases

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