Key result
Magnesium sulfate induced vasodilation in both beds, but cerebral arteries in late pregnant and postpartum rats showed significantly diminished responses compared to mesenteric arteries (P<0.01).
Why the study?
Does magnesium sulfate induce vasodilation differently in cerebral versus mesenteric resistance arteries across different gestational states in a rat model?
Does magnesium sulfate induce vasodilation differently in cerebral versus mesenteric resistance arteries across different gestational states in a rat model?
p-value: p=<0.01
Magnesium sulfate is a more potent vasodilator in mesenteric than cerebral arteries, and cerebral vasodilation is blunted during late pregnancy and postpartum, suggesting its efficacy in eclampsia may relate more to systemic blood pressure reduction than direct cerebral effects.
May prioritize systemic over cerebral MgSO4 effects in eclampsia; leaves open human translation from this rat model.
This study compared the vasodilatory responses to magnesium sulfate (MgSO(4)) of cerebral and mesenteric resistance arteries and determined whether the responses varied between different gestational groups. Third-order branches (<200 microm) of the posterior cerebral (PCA) and mesenteric arteries (MA) were dissected from nonpregnant (NP; n = 6), late pregnant (LP; day 19, n = 6), and postpartum (PP; day 3, n = 6) Sprague-Dawley rats. A concentration-response curve was performed by replacing the low-MgSO(4) (1.2 mM) HEPES buffer solution with increasing concentrations of MgSO(4) (4, 6, 8, 16, and 32 mM) and measuring lumen diameter at each concentration. All groups exhibited concentration-dependent dilation to MgSO(4), decreasing the amount of tone in the vessels. However, MA were significantly more sensitive to MgSO(4) than PCA. Whereas there was no difference in the response between different gestational groups in MA, the PCA from the LP and PP groups showed a significantly diminished response to MgSO(4). The percent dilation at 32 mM MgSO(4) for PCA versus MA in NP, LP, and PP animals was 36 +/- 2 vs. 51 +/- 7% (P < 0.05), 19 +/- 9 vs. 54 +/- 6% (P < 0.01 vs. PCA and NP), and 12 +/- 5 vs. 52 +/- 11% (P < 0.01 vs. PCA and NP). These results demonstrate that MgSO(4) is a vasodilator of small resistance arteries in the cerebral and mesenteric vascular beds. The refractory responses of the PCA in LP and PP groups demonstrate changes in the cerebrovascular vasodilatory mechanisms with gestation. The greater sensitivity of the MA to MgSO(4)-induced vasodilation suggests that the prophylactic effect of MgSO(4) on eclamptic seizures may be more closely related to the lowering of systemic blood pressure than to an effect on cerebral blood flow.
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Euser et al. (2004) studied Pregnancy and postpartum state (animal model) (n=18). Magnesium sulfate (MgSO4) vs. Low-MgSO4 (1.2 mM) buffer / Mesenteric arteries was evaluated on Percent dilation at 32 mM MgSO4 for posterior cerebral versus mesenteric arteries (p=<0.01). Magnesium sulfate induced vasodilation in both beds, but cerebral arteries in late pregnant and postpartum rats showed significantly diminished responses compared to mesenteric arteries (P<0.01).
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