Abstract
Background. Protamine administration may lead to systemic hypotension, perhaps because of vasodilatation produced by endothelial nitric oxide. This study compared release of vasoactive substances from canine coronary microvessels with that from paired conductance arteries. Methods. Microvessels were mounted in a videoscopic no-flow system, and circumflex arteries were studied in organ chambers; both were induced to contract by endothelin-1. Results. Protamine (10 to 160 μg/mL) produced concentration- dependent relaxation in both microvessel and conductance arteries (46% ± 14% maximal relaxations in microvessel and 82% ± 15% in conductance arteries, n = 10 each). Removal of the endothelium abolished this relaxation (P < .05, n = 6). Indomethacin (10-5 mol/L) did not alter the relaxation in either group (51% ± 10% in microvessel and 103% ± 7% in conductance arteries, n = 6 each). N(G)-monomethyl-L-arginine (L-NMMA, 10-4 mol/L) attenuated relaxation in conductance arteries (38% ± 12%, p = .04, n = 6) but had no effect on microvessel arteries (58% ± 10%, n = 6). Tetraethylammonium chloride (10-3 mol/L), an inhibitor of voltage-dependent potassium channels, had no effect on conductance arteries (103% ± 9%, n = 6) but abolished relaxation in microvessels (-25% ± 11%, P =.03, n = 6). Conclusions. Protamine sulfate causes endothelium-dependent relaxation in microvessel and conductance arteries in the heart by different mechanisms - that is, by nitric oxide release in conductance arteries and by endothelium- derived hyperpolarizing factor (EDHF) release in microvessels. This is the first description of the release of EDHF in response to protamine administration.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 835-841 |
| Number of pages | 7 |
| Journal | Surgery |
| Volume | 126 |
| Issue number | 5 |
| DOIs | |
| State | Published - 1999 |
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Different effects of protamine on canine coronary microvessel and conductance arteries : Evidence of hyperpolarizing factor release. / Cable, David G.; Sorajja, Paul; Oeltjen, Marilyn R.; Schaff, Hartzell V.
In: Surgery, Vol. 126, No. 5, 1999, p. 835-841.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Different effects of protamine on canine coronary microvessel and conductance arteries
T2 - Evidence of hyperpolarizing factor release
AU - Cable, David G.
AU - Sorajja, Paul
AU - Oeltjen, Marilyn R.
AU - Schaff, Hartzell V
PY - 1999
Y1 - 1999
N2 - Background. Protamine administration may lead to systemic hypotension, perhaps because of vasodilatation produced by endothelial nitric oxide. This study compared release of vasoactive substances from canine coronary microvessels with that from paired conductance arteries. Methods. Microvessels were mounted in a videoscopic no-flow system, and circumflex arteries were studied in organ chambers; both were induced to contract by endothelin-1. Results. Protamine (10 to 160 μg/mL) produced concentration- dependent relaxation in both microvessel and conductance arteries (46% ± 14% maximal relaxations in microvessel and 82% ± 15% in conductance arteries, n = 10 each). Removal of the endothelium abolished this relaxation (P < .05, n = 6). Indomethacin (10-5 mol/L) did not alter the relaxation in either group (51% ± 10% in microvessel and 103% ± 7% in conductance arteries, n = 6 each). N(G)-monomethyl-L-arginine (L-NMMA, 10-4 mol/L) attenuated relaxation in conductance arteries (38% ± 12%, p = .04, n = 6) but had no effect on microvessel arteries (58% ± 10%, n = 6). Tetraethylammonium chloride (10-3 mol/L), an inhibitor of voltage-dependent potassium channels, had no effect on conductance arteries (103% ± 9%, n = 6) but abolished relaxation in microvessels (-25% ± 11%, P =.03, n = 6). Conclusions. Protamine sulfate causes endothelium-dependent relaxation in microvessel and conductance arteries in the heart by different mechanisms - that is, by nitric oxide release in conductance arteries and by endothelium- derived hyperpolarizing factor (EDHF) release in microvessels. This is the first description of the release of EDHF in response to protamine administration.
AB - Background. Protamine administration may lead to systemic hypotension, perhaps because of vasodilatation produced by endothelial nitric oxide. This study compared release of vasoactive substances from canine coronary microvessels with that from paired conductance arteries. Methods. Microvessels were mounted in a videoscopic no-flow system, and circumflex arteries were studied in organ chambers; both were induced to contract by endothelin-1. Results. Protamine (10 to 160 μg/mL) produced concentration- dependent relaxation in both microvessel and conductance arteries (46% ± 14% maximal relaxations in microvessel and 82% ± 15% in conductance arteries, n = 10 each). Removal of the endothelium abolished this relaxation (P < .05, n = 6). Indomethacin (10-5 mol/L) did not alter the relaxation in either group (51% ± 10% in microvessel and 103% ± 7% in conductance arteries, n = 6 each). N(G)-monomethyl-L-arginine (L-NMMA, 10-4 mol/L) attenuated relaxation in conductance arteries (38% ± 12%, p = .04, n = 6) but had no effect on microvessel arteries (58% ± 10%, n = 6). Tetraethylammonium chloride (10-3 mol/L), an inhibitor of voltage-dependent potassium channels, had no effect on conductance arteries (103% ± 9%, n = 6) but abolished relaxation in microvessels (-25% ± 11%, P =.03, n = 6). Conclusions. Protamine sulfate causes endothelium-dependent relaxation in microvessel and conductance arteries in the heart by different mechanisms - that is, by nitric oxide release in conductance arteries and by endothelium- derived hyperpolarizing factor (EDHF) release in microvessels. This is the first description of the release of EDHF in response to protamine administration.
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UR - http://www.scopus.com/inward/citedby.url?scp=0032740455&partnerID=8YFLogxK
U2 - 10.1016/S0039-6060(99)70023-1
DO - 10.1016/S0039-6060(99)70023-1
M3 - Article
C2 - 10568182
AN - SCOPUS:0032740455
VL - 126
SP - 835
EP - 841
JO - Surgery (United States)
JF - Surgery (United States)
SN - 0039-6060
IS - 5
ER -