In Vitro Therapy with Dobutamine, Isoprenaline and Sodium Nitroprusside Protects Vascular Smooth Muscle Metabolism from Subarachnoid Haemorrhage Induced Cerebral Vasospasm

2001 ◽  
Vol 143 (7) ◽  
pp. 721-728 ◽  
Author(s):  
J. F. Clark ◽  
G. J. Pyne ◽  
O. J. Choutka ◽  
J. A. Carrozzella ◽  
J. Khoury ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Subarachnoid Haemorrhage ◽  
Sodium Nitroprusside ◽  
Cerebral Vasospasm ◽  
Muscle Metabolism

High-Throughput Microtissue Contractility Assay for In Vitro Analysis of Vascular Mechanics

2013 ◽  
Author(s):  
Eric S. Hald ◽  
Zaw Win ◽  
Marianne R. Scheitel ◽  
Patrick W. Alford
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cerebral Vasospasm ◽  
High Throughput ◽  
Vascular Dysfunction ◽  
Vascular Mechanics ◽  
Vitro Analysis ◽  
In Vitro Analysis

Vascular smooth muscle (VSM) plays a key role in regulation of vascular mechanics through modulation of contractile tone. Studies suggest that mechanical or biochemical perturbation can lead to dysfunctional VSM behavior [1, 2]. This aberrant contractility may play a role in vascular dysfunction ranging from cerebral vasospasm to aneurysm genesis.

scholarly journals Magnesium Therapy for Subarachnoid Hemorrhage Induced Cerebral Vasospasm as Assessed by In Vitro Studies on the Porcine Carotid Artery

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 330-330
Author(s):  
Gail J Pyne ◽  
Shinsuke Nakayama ◽  
Ondrej J Choutka ◽  
Thomas Ad Cadoux-Hudson ◽  
Joseph F Clark
Keyword(s):  
Smooth Muscle ◽  
Oxygen Consumption ◽  
Subarachnoid Hemorrhage ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Cerebral Vasospasm ◽  
Isometric Force ◽  
Intracellular Magnesium ◽  
Porcine Carotid Artery

82 Background: Mg 2+ has been used therapeutically in the treatment of eclampsia and it has recently become a novel avenue in the treatment of stroke because it can relax vascular smooth muscle. Currently there is a clinical trial, on going in England, involving Mg 2+ administration to stroke patients. But relatively little is known regarding the function or mechanism of Mg2+ treatment following subarachnoid hemorrhage (SAH). We therefore set out to determine if Mg 2+ could be used to prevent or reverse the in vitro vasospasm caused by the CSF from vasospastic (SAH) patients. Methods: Oxygen consumption and isometric force measurements of the isolated porcine carotid artery were used to assess the functional and metabolic responses of the vascular smooth muscle following stimulation by CSF from SAH patients with cerebral vasospasm. We used a method of exposing the vascular smooth muscle to 12 mM MgCl 2 for 1 hour to increase intracellular magnesium. This method has been shown to increase intracellular Mg 2+ to levels reached with two to three days of Mg 2+ therapy. Results: CSF from SAH patients with vasospasm will cause vasospasm when applied to vessels in vitro . Following this in vitro vasospasm, Mg 2+ caused a dose dependant decrease in tension (relaxation) following exposure to CSF from vasospasm patients. Exposure of vessels to 12 mM Mg 2+ normalized the rate of relaxation in the presence of CSF from SAH patients was normalized (2.70±0.71 Nm -2 s -1 in the presence of CSF; 15.8±4.20 Nm -2 s -1 with CSF and Mg 2+ ; and 16.1±4.85 Nm -2 s -1 without CSF). Mg 2. significantly (P≤0.05) decreased the rate of oxygen consumption observed when stimulated by CSF (0.70±0.03 μmol O 2 min -1 g -1 with CSF alone and 0.46±0.08 μmol O 2 min -1 g 1 with CSF and Mg 2+ ). Conclusion: These results suggest that Mg 2+ is a potent vasodilator that helps to normalize contractile behavior and metabolism of the porcine carotid artery exposed to the CSF of SAH patients with vasospasm. Therefore, Mg 2+ therapy is a possible avenue for treating patients with cerebral vasospasm by causing a relaxation of vascular smooth muscle.

scholarly journals Effects of Hyperglycemia on Vascular Smooth Muscle Ca2+Signaling

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Nahed El-Najjar ◽  
Rashmi P. Kulkarni ◽  
Nancy Nader ◽  
Rawad Hodeify ◽  
Khaled Machaca
Keyword(s):  
Insulin Resistance ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Vascular Smooth Muscle ◽  
Complex Disease ◽  
Prolonged Exposure ◽  
In Vitro System ◽  
A7r5 Cells

Diabetes is a complex disease that is characterized with hyperglycemia, dyslipidemia, and insulin resistance. These pathologies are associated with significant cardiovascular implications that affect both the macro- and microvasculature. It is therefore important to understand the effects of various pathologies associated with diabetes on the vasculature. Here we directly test the effects of hyperglycemia on vascular smooth muscle (VSM) Ca2+signaling in an isolated in vitro system using the A7r5 rat aortic cell line as a model. We find that prolonged exposure of A7r5 cells to hyperglycemia (weeks) is associated with changes to Ca2+signaling, including most prominently an inhibition of the passive ER Ca2+leak and the sarcoplasmic reticulum Ca2+-ATPase (SERCA). To translate these findings to the in vivo condition, we used primary VSM cells from normal and diabetic subjects and find that only the inhibition of the ER Ca2+leaks replicates in cells from diabetic donors. These results show that prolonged hyperglycemia in isolation alters the Ca2+signaling machinery in VSM cells. However, these alterations are not readily translatable to the whole organism situation where alterations to the Ca2+signaling machinery are different.

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