Abstract
Methods Adult male Sprague Dawley rats were studied in 4 groups: (1) sham; (2) stroke; (3) stroke treated with pharmacological hypothermia before reperfusion (interischemia hypothermia); and (4) stroke treated with pharmacological hypothermia after reperfusion is initiated (inter-reperfusion hypothermia). The combination of chlorpromazine and promethazine with dihydrocapsaicin (DHC) was used to induce hypothermia. To compare the neuroprotective effects of drug-induced hypothermia between the interischemia and inter-reperfusion groups, brain damage was evaluated using infarct volume and neurological deficits at 24 h reperfusion. In addition, mRNA expressions of NADPH oxidase (NOX) subunits (gp91phox, p67phox, p47phox, and p22phox) and glucose transporter subtypes (GLUT1 and GLUT3) were determined by real-time PCR at 6 and 24 h reperfusion. ROS production was measured by flow cytometry assay at the same time points. Results In both hypothermia groups, the cerebral infarct volumes and neurological deficits were reduced in the ischemic rats. At 6 and 24 h reperfusion, ROS production and the expressions of NOX subunits and glucose transporter subtypes were also significantly reduced in both hypothermia groups as compared to the ischemic group. While there were no statistically significant differences between the two hypothermia groups at 6 h reperfusion, brain damage was significantly further decreased by interischemia hypothermia at 24 h. Conclusion Both interischemia and inter-reperfusion pharmacological hypothermia treatments play a role in neuroprotection after stroke. Interischemia hypothermia treatment may be better able to induce stronger neuroprotection after ischemic stroke. This study provides a new avenue and reference for stronger neuroprotective hypothermia before vascular recanalization in stroke patients.
Highlights
Stroke is a leading cause of severe disability and a serious threat to human health worldwide
All adult male Sprague Dawley rats (280–320 g, Vital River Laboratory Animal Technology Co., Ltd., Beijing, China) were randomly divided into 4 groups (Figure 1(a)): (1) sham-operated group without middle cerebral artery occlusion (MCAO); (2) stroke group without pharmacological hypothermia (MCAO 2 h); (3) stroke group treated with pharmacological hypothermia 1 h before reperfusion (MCAO 2 h/1 h); and (4) stroke group treated with pharmacological hypothermia after reperfusion is initiated (MCAO 2 h/2 h)
In the interischemia hypothermia group, a 2.23°C drop was seen in the temperature within 30 minutes of drug administration at 1 h after stroke (1 h before reperfusion) and continued to fall to the lowest of 3.68°C below the initial temperature at 1.5 h reperfusion (Figure 1)
Summary
Stroke is a leading cause of severe disability and a serious threat to human health worldwide. Because of the narrow “time window,” high bleeding risk, inadequate national health consciousness, poor medical resource distribution, and problematic traffic congestion in our country, the actual thrombolysis rate is less than 30% [3] Because of these limitations, a majority of patients cannot get timely and effective treatment [4]. To compare the neuroprotective effects of drug-induced hypothermia between the interischemia and inter-reperfusion groups, brain damage was evaluated using infarct volume and neurological deficits at 24 h reperfusion. In both hypothermia groups, the cerebral infarct volumes and neurological deficits were reduced in the ischemic rats. Both interischemia and inter-reperfusion pharmacological hypothermia treatments play a role in neuroprotection after stroke. Interischemia hypothermia treatment may be better able to induce stronger neuroprotection after ischemic stroke. Interischemia hypothermia treatment may be better able to induce stronger neuroprotection after ischemic stroke. is study provides a new avenue and reference for stronger neuroprotective hypothermia before vascular recanalization in stroke patients
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