Hydrogen sulfide improves neural function in rats following cardiopulmonary resuscitation

Abstract

Abstract. The alleviation of brain injury is a key issue following cardiopulmonary resuscitation (CPR). Hydrogen sulfide (H 2 S) is hypothesized to be involved in the pathophysiological process of ischemia-reperfusion injury, and exerts a protective effect on neurons. The aim of the present study was to investigate the effects of H 2 S on neural functions following cardiac arrest (CA) in rats. A total of 60 rats were allocated at random into three groups. CA was induced to establish the model and CPR was performed after 6 min. Subsequently, sodium hydrosulfide (NaHS), hydroxylamine or saline was administered to the rats. Serum levels of H 2 S, neuron-specific enolase (NSE) and S100β were determined following CPR. In addition, neurological deficit scoring (NDS), the beam walking test (BWT), prehensile traction test and Morris water maze experiment were conducted. Neuronal apoptosis rates were detected in the hippocampal region following sacrifice. After CPR, as the H 2 S levels increased or decreased, the serum NSE and S100β concentrations decreased or increased, respectively (P<0.0w. The NDS results of the NaHS group were improved compared with those of the hydroxylamine group at 24 h after CPR (P<0.05). In the Morris water maze experiment, BWT and prehensile traction test the animals in the NaHS group performed best and rats in the hydroxylamine group performed worst. At day 7, the apoptotic index and the expression of caspase-3 were reduced in the hippocampal CA1 region, while the expression of Bcl-2 increased in the NaHS group; and results of the hydroxylamine group were in contrast. Therefore, the results of the present study indicate that H 2 S is able to improve neural function in rats following CPR.

Hypothermic properties of dexmedetomidine provide neuroprotection in rats following cerebral ischemia‑reperfusion injury

“…Although CA can lead to ischemia/reperfusion (I/R) injury in every organ in the body, it is especially detrimental to the brain and the heart. The principal pathological cause of organ damage is excessive apoptosis and autophagy (4,5), the extent of which has been found to correlate with poor neurological prognosis (6)(7)(8). A number of studies have demonstrated that hypothermia can attenuate neurological damage following I/R injury by reducing neural apoptosis and preventing autophagy overactivation (4,9,10).…”

NaHS Protects against the Impairments Induced by Oxygen-Glucose Deprivation in Different Ages of Primary Hippocampal Neurons

“…Furthermore, the levels of MDA, NO, and hydrogen peroxide were significantly elevated by OGD insults, and subsequently inhibited by NaHS treatment as well. Recent studies have shown that ROS have multiple biological functions other than directly damaging brain cells during I/R injury, such as activating the HIF-1 pathway which is critical to the IPC ( Wang et al, 2015 ; Lin et al, 2016 ). In aged brain cells, these ROS-induced protective signaling pathway can be activated transcriptionally, but are eventually inhibited ( Signorini et al, 2014 ).…”

“…Stroke is commonly caused by either interrupted or reduced blood supply to the brain such as ischemia, thereby leaving brain cells in a oxygen-glucose deprivation (OGD) condition. Even a short term of OGD can cause irreversibe damages to brain cells, while subsequent reperfusion, restoring blood supply to the brain, may aggravate the damage even further ( Lin et al, 2016 ). Ischemia/reperfusion (I/R) induced oxidative stress, caused by impaired metabolism in the brain cells, is believed to be the one of the major contributors to brain I/R injury ( Zeiger et al, 2009 ; Ma et al, 2015 ).…”

Effects of NaHS and hydroxylamine on the expressions of brain-derived neurotrophic factor and its receptors in rats after cardiac arrest and cardiopulmonary resuscitation

“…The rats in Inhibition group were intravenously injected with 1 mL sterile diluted hydroxylamine (an inhibitor for H2S, CAS 7803-49-8, Sigma) at a dose of 40 μmoL/kg·d at 1 h after ROSC. The doses of NaHS and hydroxylamine were chosen based on our previous study and other references [19] [20] [21]. The rats in Control group received 1 mL sterile saline at 1 h after ROSC.…”