Effects of in vivo treatment with interleukins 1β and 6 on rat mesenteric vascular bed reactivity
Summary 1 Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has been shown that an abnormal microcirculatory system is implicated. 2 Therefore, the effects of in vivo treatment for three days with interleu...
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| Published in | Autonomic & autacoid pharmacology Vol. 23; no. 2; pp. 125 - 131 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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Oxford, UK
Blackwell Science Ltd
01.04.2003
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| Abstract | Summary
1 Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has been shown that an abnormal microcirculatory system is implicated.
2 Therefore, the effects of in vivo treatment for three days with interleukins 1β and 6 were investigated on rat isolated mesenteric vascular bed (MVB).
3 A significant concentration‐dependent increase in vascular response to noradrenaline (NA) was found, with a significant difference in Emax between control (93.01 ± 16.78 mmHg) and treated preparations (137.91 ± 5.20 mmHg). Endothelin‐1(ET‐1) induced a significantly greater increase of perfusion pressure in treated rats in comparison with control rats at the highest concentration used (0.1 μm).
4 The concentration‐dependent decrease of perfusion pressure induced by acetylcholine (ACh) in MVB precontracted with NA was significantly reduced in specimens from treated rats in comparison with control rats, with a significant difference in Emax between control and treated preparations.
5 Perivascular nerve stimulation (PNS) evoked contractions with no difference between treatments. Similarly, no difference in relaxant effect was found after PNS in specimens precontracted with NA, in the presence of guanethidine.
6 These findings indicate that the precocious inflammation acts only at postsynaptic level, facilitating vascular contraction. These data seem to support the hypothesis that vascular dysfunction caused by overproduction of ILs may contribute, among other immunological factors, to vasculitis in IBD that leads to intestinal ischaemia through vasoconstriction. |
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| AbstractList | Summary
1
Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has been shown that an abnormal microcirculatory system is implicated.
2
Therefore, the effects of
in vivo
treatment for three days with interleukins 1
β
and 6 were investigated on rat isolated mesenteric vascular bed (MVB).
3
A significant concentration‐dependent increase in vascular response to noradrenaline (NA) was found, with a significant difference in E
max
between control (93.01 ± 16.78 mmHg) and treated preparations (137.91 ± 5.20 mmHg). Endothelin‐1(ET‐1) induced a significantly greater increase of perfusion pressure in treated rats in comparison with control rats at the highest concentration used (0.1
μ
m
).
4
The concentration‐dependent decrease of perfusion pressure induced by acetylcholine (ACh) in MVB precontracted with NA was significantly reduced in specimens from treated rats in comparison with control rats, with a significant difference in E
max
between control and treated preparations.
5
Perivascular nerve stimulation (PNS) evoked contractions with no difference between treatments. Similarly, no difference in relaxant effect was found after PNS in specimens precontracted with NA, in the presence of guanethidine.
6
These findings indicate that the precocious inflammation acts only at postsynaptic level, facilitating vascular contraction. These data seem to support the hypothesis that vascular dysfunction caused by overproduction of ILs may contribute, among other immunological factors, to vasculitis in IBD that leads to intestinal ischaemia through vasoconstriction. Summary 1 Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has been shown that an abnormal microcirculatory system is implicated. 2 Therefore, the effects of in vivo treatment for three days with interleukins 1β and 6 were investigated on rat isolated mesenteric vascular bed (MVB). 3 A significant concentration‐dependent increase in vascular response to noradrenaline (NA) was found, with a significant difference in Emax between control (93.01 ± 16.78 mmHg) and treated preparations (137.91 ± 5.20 mmHg). Endothelin‐1(ET‐1) induced a significantly greater increase of perfusion pressure in treated rats in comparison with control rats at the highest concentration used (0.1 μm). 4 The concentration‐dependent decrease of perfusion pressure induced by acetylcholine (ACh) in MVB precontracted with NA was significantly reduced in specimens from treated rats in comparison with control rats, with a significant difference in Emax between control and treated preparations. 5 Perivascular nerve stimulation (PNS) evoked contractions with no difference between treatments. Similarly, no difference in relaxant effect was found after PNS in specimens precontracted with NA, in the presence of guanethidine. 6 These findings indicate that the precocious inflammation acts only at postsynaptic level, facilitating vascular contraction. These data seem to support the hypothesis that vascular dysfunction caused by overproduction of ILs may contribute, among other immunological factors, to vasculitis in IBD that leads to intestinal ischaemia through vasoconstriction. |
| Author | Piepoli, A. L. De Salvia, M. A. Nacci, C. Porro, C. Mitolo-Chieppa, D. De Salvatore, G. Natale, L. Mitolo, C. I. |
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| Cites_doi | 10.1016/0014-2999(96)00347-0 10.1016/0014-2999(92)90539-G 10.1023/A:1005519304829 10.1046/j.1365-2680.1998.1820075.x 10.1093/oxfordjournals.epirev.a036296 10.3109/00365529609009132 10.1136/gut.33.7.933 10.1002/ibd.3780050108 10.1007/PL00005358 10.1080/00365529850172070 10.1046/j.1365-2362.2003.01200.x 10.1016/0016-5085(92)91182-4 10.1016/0016-5085(89)90068-1 10.1016/0016-5085(94)90223-2 10.1016/S0002-9610(97)00141-4 10.1136/gut.31.6.686 10.1084/jem.167.4.1341 10.1136/jcp.50.12.1013 10.1016/0140-6736(92)90077-G 10.1038/335164a0 10.1016/0016-5085(93)90834-Y 10.1007/BF02919744 |
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1 Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has... Summary 1 Inflammatory bowel disease (IBD) is a condition that involves proinflammatory cytokines such as interleukins 1β and 6 (ILs). In this disease, it has... |
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| Title | Effects of in vivo treatment with interleukins 1β and 6 on rat mesenteric vascular bed reactivity |
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