Functional and morphologic endothelial damage in rabbit external jugular veins stored in heparinized normal saline.

Department of Surgery, Duke University Medical Center, Durham, N.C.
Blood vessels 02/1991; 28(6):511-9. DOI: 10.1159/000158897
Source: PubMed

ABSTRACT Previous studies have demonstrated that vein storage in normal saline leads to significant mechanical morphological, and biochemical aberrations. However, little information is available regarding the functional damage that occurs. The purpose of this study was to evaluate the effect of saline storage on venous smooth muscle and endothelial function. Segments of ten external jugular veins from male New Zealand White rabbits were placed nondistended in either modified Krebs solution at 37 degrees C (Krebs-stored, KS) or heparinized normal saline at room temperature (saline-stored, SS) for 1 h. Segments 4 mm in length were then simultaneously studied in vitro under isometric tension. There was no difference in maximum tension or sensitivity to either bradykinin or histamine. Acetylcholine-induced relaxation in KS segments was not significantly different from relaxation in a historical cohort of nonstored segments (nonstored 87.4 +/- 1.0% vs. KS 84.5 +/- 2.0%; p = NS). However, there were significant attenuations in SS segment endothelium-dependent relaxation in response to both acetylcholine (KS 84.5 +/- 2.0% vs. SS 76.4 +/- 2.7%, p less than 0.02) and adenosine diphosphate (KS 47.9 +/- 2.9% vs. SS 40.6 +/- 3.7%, p less than 0.002). Relaxant responses to sodium nitroprusside (endothelium-independent) were not significantly different in the two groups (KS 94.6 +/- 1.6% vs. SS 95.7 +/- 2.2%; p = NS). Electron microscopic evaluation of SS segments revealed endothelial cell disruption with cellular edema and loss of intact junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

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    ABSTRACT: It has been shown that suboptimal preparation of a vein graft prior to its insertion results in immediate morphologic and functional damage to the endothelial cells but not to the underlying smooth muscle cells. However, little is known about whether such perioperative injury to the vein grafts influences the subsequent development of intimal hyperplasia and smooth muscle cell contractility. This study examines the influence of storage in saline solution or Ringer's lactate on the development of intimal hyperplasia and vasomotor function in experimental vein grafts. Twenty-six New Zealand white rabbits had a carotid vein bypass graft performed after the veins had been immersed (15 minutes) in either heparinized saline solution (Sal; n = 13) or Ringer's lactate (RL; n = 13), and each group was harvested after 28 days for either histologic (n = 8) or functional studies (n = 5; four 5 mm rings/graft). Saline storage of the vein graft resulted in a 38% increase in the thickness of the intimal hyperplasia (113 +/- 2 vs. 83 +/- 2 microns, Sal vs. RL; mean +/- SEM; p < 0.05) without a change in medial thickness (87 +/- 5 vs. 86 +/- 8 microns, Sal vs. RL; p > 0.05). The two sets of vein grafts showed no difference in sensitivity to norepinephrine, serotonin, and bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)
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    ABSTRACT: Vasoreactivity of 11 coronary artery vein bypass grafts and 13 human saphenous veins was examined. Isometric tension studies were performed in response to potassium chloride (110 mmol/l), noradrenaline (10(-9)-10(-4) mol/l), serotonin (10(-9)-10(-4) mol/l) and histamine (10(-8)-10(-2) mol/l). After precontraction with noradrenaline (10(-5) mol/l), the response to acetylcholine (10(-8)-10(-4) mol/l) and the calcium ionophore A23187 (10(-8)-10(-4) mol/l) was also assessed. Results are given as mean(s.e.m.). Compared with saphenous veins, vein grafts showed decreased sensitivity to noradrenaline (1.7(0.5) versus 0.4(0.1) mumol/l, P = 0.01), no change in sensitivity to serotonin (55(18) versus 37(15) mumol/l, P > 0.05) and supersensitivity to histamine (3.2(0.9) versus 30.1(13.2) mumol/l, P = 0.01). Vein grafts had a decreased maximal contraction to potassium chloride (1.1(0.3) versus 5.5(0.8) g, P = 0.0001), noradrenaline (1.2(0.3) versus 4.1(0.8) g, P = 0.005), histamine (1.2(0.3) versus 4.5(0.8) g, P = 0.003) and serotonin (0.7(0.2) versus 5.7(0.6) g, P = 0.0002) compared with saphenous vein. Precontracted vein grafts did not relax in response to acetylcholine; in contrast, saphenous vein relaxed in a dose-dependent manner to a maximal relaxation of 22(3) per cent. Both saphenous vein and vein graft relaxed in response to A23187. Vein graft intimal thickness was approximately fourfold greater than that of saphenous vein (540(110) versus 136(30) microns). Scanning electron microscopy of vein and vein graft revealed an intact endothelium. Coronary artery vein grafts are capable of responding to various contractile agonists; these response are notably different from those of saphenous vein and there is a loss of endothelium-dependent relaxation. Even at a late stage vein grafts are not inert but are functional conduits with an abnormally responsive endothelium and a less potent, but significantly altered, smooth muscle contractile profile.
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    ABSTRACT: The development of intimal hyperplasia in reversed vein grafts is associated with altered endothelial and vasomotor function. This study examines the effect of surgery on the morphology and vasomotor function of experimental arterial and venous vein bypass grafts. Twelve reversed vein grafts, 12 in situ vein grafts and 12 venovenous grafts were placed in 24 New Zealand White rabbits. All grafts remained patent and were harvested after 28 days. Isometric contraction to norepinephrine, histamine, bradykinin, serotonin and relaxation to acetylcholine and sodium nitroprusside following pre-contraction with prostaglandin F(2 alpha) were determined on the grafts and on contralateral jugular veins. Compared to the contralateral jugular veins, norepinephrine supersensitivity was induced in the reversed vein grafts, and venovenous vein grafts but not in the in situ vein grafts. Decrease in histamine sensitivity occurred in all grafted vessels. Bradykinin responses were significantly reduced in the in situ vein grafts and reversed vein grafts. Contractile responses to serotonin developed in the in situ vein grafts and reversed vein grafts only. Acetylcholine-induced endothelium-derived relaxing factor-mediated relaxation of the contralateral jugular veins was preserved in both venovenous grafts and in situ vein grafts but was lost in reversed vein grafts. All tissues relaxed to sodium nitroprusside in dose-dependent manner. The data suggest that norepinephrine supersensitivity in reversed vein grafts results from excision of the vessel. Attenuation of bradykinin responses and the enhanced contractile responses to serotonin appear predominantly to result from arterialization. Decreases in histamine sensitivity appear related both to excision and to arterialization. Neither the excision of the vein nor arterialization individually influences the alterations in endothelium-derived relaxing factor-mediated relaxation. However, a combination of excision and arterialization results in the altered endothelium-derived relaxing factor-mediated relaxation. This study suggests that the surgical preparation of the vein and the surgical procedure used have significantly different effects on endothelium-derived relaxing factor-mediated relaxation and smooth muscle contractility in vein grafts.
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