Effect of tromethamine (THAM) on infarct volume following permanent middle cerebral artery occlusion in rats
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K L Kiening1, G H Schneider, A W Unterberg
1Department of Neurosurgery, Virchow Medical Center, Humboldt University of Berlin, Federal Republic of Germany.
Abstract:
This study investigates the influence on tromethamine (THAM) on ischemic volume induced by permanent middle cerebral artery occlusion (MCAO) in rats. 14 male Sprague Dawley rats underwent left sided permanent MCAO by electro coagulation. Animals were treated either by 3-M THAM given intravenously in a single dosage of 0.6 mmol/kg body weight (THAM group: n = 7) 10 min following MCAO and again 1, 2, 3, 4 and 5 hours later or by NaCl 0.9% (placebo group: n = 7) in the same mode. Mean arterial blood pressure (MABP) was monitored for 30 min post MCAO and arterial blood gases were taken 10 min after the first injection. The extent of ischemia volume was assessed by planimetry of coronal sections stained with triphenyl-tetrazolium chloride (TTC) and with hematoxilin/eosin (HE). Tests for significance were accomplished by ANOVA on ranks. A difference of p < 0.05 was considered significant. The THAM group showed an insignificant decrease in MABP 1 min after injection (THAM: 75 +/- 11 mmHg, placebo: 86 +/- 10 mmHg). Arterial pH was significantly different (THAM: 7.46 +/- 0.04; placebo: 7.32 +/- 0.03). In TTC staining, the ischemia volume--given in absolute values and percentage of the total left volume--was significantly reduced in the THAM group (THAM: 43.9 +/- 8.3 mm3/7.0 +/- 1.3%; placebo: 95.2 +/- 13.8 mm3/14.2 +/- 2.0%). In HE staining, the reduction of ischemia, volume did not reach statistical significance (THAM: 49.1 +/- 9.9 mm3/9.6 +/- 1.8%; placebo: 66.3 +/- 14.5 mm3/13.1 +/- 2.8%). Based on these results, a moderate neuroprotective effect of THAM in experimental cerebral infarction could be demonstrated.
Insights
Tromethamine (THAM) significantly reduced ischemic brain volume in rats after middle cerebral artery occlusion (MCAO). This neuroprotective effect suggests THAM
Area of Science:
- Neuroscience
- Pharmacology
- Cerebrovascular Research
Background:
- Ischemic stroke, particularly middle cerebral artery occlusion (MCAO), causes significant brain damage.
- Identifying effective neuroprotective agents is crucial for stroke treatment.
- Tromethamine (THAM) is a buffer with potential therapeutic applications.
Purpose of the Study:
- To investigate the neuroprotective effects of tromethamine (THAM) on ischemic volume.
- To assess the influence of THAM on brain tissue damage following experimental MCAO in rats.
Main Methods:
- Permanent middle cerebral artery occlusion (MCAO) was induced in 14 male Sprague Dawley rats.
- Rats were treated with either THAM (0.6 mmol/kg) or saline placebo intravenously at multiple time points post-MCAO.
- Ischemic volume was quantified using triphenyl-tetrazolium chloride (TTC) and hematoxylin/eosin (HE) staining.
Main Results:
- THAM treatment resulted in a significantly reduced ischemic volume (43.9 mm3) compared to placebo (95.2 mm3) as assessed by TTC staining.
- Arterial pH was significantly higher in the THAM group (7.46) versus the placebo group (7.32).
- While HE staining showed a trend towards reduced ischemia in the THAM group, it did not reach statistical significance.
Conclusions:
- Tromethamine (THAM) demonstrates a moderate neuroprotective effect in a rat model of experimental cerebral infarction.
- THAM may be a potential therapeutic agent for reducing brain damage in ischemic stroke.
- Further research is warranted to explore THAM's efficacy and mechanisms in stroke treatment.