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Experimental malaria: the in vitro and in vivo blood pressure paradox
Date Issued
2012-03
Author(s)
CR NWOKOCHA,
MI NWOKOCHA,
DU OWU,
IO AJAYI
University of Global Health Equity
AB EBEIGBE
Abstract
Objective:
Malaria causes more deaths worldwide than anyother parasitic disease. Many aspects of the biology that governs the pathogenesis of this parasite are still unclear. Therefore insight into the complexity of the pathogenesis of malaria is vital to understand the disease, particularly as it relates to blood pressure.
Methods:
In vivo and in vitro experimental models were used for this study. In the in vivo study, mean arterial pressure, pulse rates and heart rates were recorded by cannulation of the carotid artery of rats. In the in vitro study, ring preparations of blood vessels from the rat aorta were studied using standard organ bath techniques. Dose–response curves for phenylepherine (PE)- and acetylcholine (Ach)-induced relaxation were constructed for rings pre-contracted with PE.
Results:
Our results showed a significant (p < 0.05) reduction in the mean arterial pressure and pulse rates, while the heart rates remained unaltered in rats with malaria parasites, compared with the controls. Incubation of rat aortic rings with parasitised blood resulted in a significant (p < 0.05) increase in maximum contractile response to phenylephrine in the rat aortic rings but there was no effect on the baseline. The dose–response curve showed a significant (p < 0.05) leftward shift following the addition of parasitised blood and the EC70 (M) values increased from 7 × 10-7 to 5 × 10-6 M. Following exposure to parasitised blood, the magnitude of Ach-induced relaxation responses reduced significantly (p < 0.05) from 73 ± 3.6 to 24.75 ± 7.25% in the rat aortic rings.
Conclusions:
The results suggest that malaria parasitaemia caused in vivo reduction in blood pressure, and enhanced the responses to contractile agents and reduced relaxation responses to acetylcholine in vitro. This appears to be a paradox but is explainable by the complex cardiovascular control mechanisms in vivo. This may be independent of direct action on vascular smooth muscle.
Malaria causes more deaths worldwide than anyother parasitic disease. Many aspects of the biology that governs the pathogenesis of this parasite are still unclear. Therefore insight into the complexity of the pathogenesis of malaria is vital to understand the disease, particularly as it relates to blood pressure.
Methods:
In vivo and in vitro experimental models were used for this study. In the in vivo study, mean arterial pressure, pulse rates and heart rates were recorded by cannulation of the carotid artery of rats. In the in vitro study, ring preparations of blood vessels from the rat aorta were studied using standard organ bath techniques. Dose–response curves for phenylepherine (PE)- and acetylcholine (Ach)-induced relaxation were constructed for rings pre-contracted with PE.
Results:
Our results showed a significant (p < 0.05) reduction in the mean arterial pressure and pulse rates, while the heart rates remained unaltered in rats with malaria parasites, compared with the controls. Incubation of rat aortic rings with parasitised blood resulted in a significant (p < 0.05) increase in maximum contractile response to phenylephrine in the rat aortic rings but there was no effect on the baseline. The dose–response curve showed a significant (p < 0.05) leftward shift following the addition of parasitised blood and the EC70 (M) values increased from 7 × 10-7 to 5 × 10-6 M. Following exposure to parasitised blood, the magnitude of Ach-induced relaxation responses reduced significantly (p < 0.05) from 73 ± 3.6 to 24.75 ± 7.25% in the rat aortic rings.
Conclusions:
The results suggest that malaria parasitaemia caused in vivo reduction in blood pressure, and enhanced the responses to contractile agents and reduced relaxation responses to acetylcholine in vitro. This appears to be a paradox but is explainable by the complex cardiovascular control mechanisms in vivo. This may be independent of direct action on vascular smooth muscle.
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