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Altered Vascular Reactivity Induced By Malaria Parasites
ISSN
0043-3144
Date Issued
2011-01
Author(s)
Olutayo Ajayi
University of Global Health Equity
Chukwuemeka R Nwokocha
Anthony Benjamin Ebeigbe
Abstract
Objective:
In this study, we have examined the possibility that there is altered vascular reactivity due to
the direct interaction between parasitized erythrocytes and vascular endothelial cells.
Method:
Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were
mounted in 20 ml organ baths containing PSS under an initial load of 1g, maintained at 37°C at pH 7.4
and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate
before the commencement of the various protocols:
* Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+)
* Acetylcholine (Ach) – induced relaxation in phenylephrine-contracted rings (pre-contraction was
induced by EC70 concentration of phenylephrine)
* Ach-induced relaxation in PE-precontracted, endothelium-denuded rings
* Also, relaxation responses to acetylcholine was investigated through application of a single
(EC70) concentration of acetylcholine in rings exposed to blood with varying concentrations and
dilutions of parasitized blood and varying durations of exposure.
Results:
Incubation with parasitized blood resulted in a significant increase in maximum contractile
response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of
the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the
addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10-7 to 5 x 10-6M. Following
exposure to parasitized blood, the magnitude of Ach-induced relaxation responses reduced significantly
from 73 ± 3.6 to 24.75 ± 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly
enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable
and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the
relaxation response. Following endothelium removal, there was a marked impairment in endotheliumdependent
relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized
blood did not significantly alter contractile responses induced by potassium depolarization.
Conclusions:
This gives evidence in support of an endothelium-dependent action of malaria parasites
as vascular effects of malaria parasites are mediated, at least in part, via endothelium-dependent
mechanism(s).
In this study, we have examined the possibility that there is altered vascular reactivity due to
the direct interaction between parasitized erythrocytes and vascular endothelial cells.
Method:
Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were
mounted in 20 ml organ baths containing PSS under an initial load of 1g, maintained at 37°C at pH 7.4
and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate
before the commencement of the various protocols:
* Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+)
* Acetylcholine (Ach) – induced relaxation in phenylephrine-contracted rings (pre-contraction was
induced by EC70 concentration of phenylephrine)
* Ach-induced relaxation in PE-precontracted, endothelium-denuded rings
* Also, relaxation responses to acetylcholine was investigated through application of a single
(EC70) concentration of acetylcholine in rings exposed to blood with varying concentrations and
dilutions of parasitized blood and varying durations of exposure.
Results:
Incubation with parasitized blood resulted in a significant increase in maximum contractile
response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of
the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the
addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10-7 to 5 x 10-6M. Following
exposure to parasitized blood, the magnitude of Ach-induced relaxation responses reduced significantly
from 73 ± 3.6 to 24.75 ± 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly
enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable
and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the
relaxation response. Following endothelium removal, there was a marked impairment in endotheliumdependent
relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized
blood did not significantly alter contractile responses induced by potassium depolarization.
Conclusions:
This gives evidence in support of an endothelium-dependent action of malaria parasites
as vascular effects of malaria parasites are mediated, at least in part, via endothelium-dependent
mechanism(s).
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