Injured Veins Research Articles

Major venous injuries and bullet wounds

A review of the reported incidence, management and results of treatment of major vein injuries is presented and a brief account given of the mechanism of vascular damage by high-velocity bullet wounds. This paper reports 3 cases of isolated major venous injury caused by high-velocity bullets. Repair was performed in each case. Two patients survived with a good shortterm clinical result. The third patient died during operation. The advantages of repairing injured veins are discussed.

Effects of heparin and epsilon-aminocaproic acid in dogs on plasmin-125-I generation in response to urokinase injections and venous injury.

The isotopic method described previously for quantification of plasmin- (125)I by disc gel electrophoresis was modified by inclusion of euglobulin precipitation to expand its applicability to plasmas containing low radioactivity of plasmin- (125)I and plasminogen- (125)I. It was found that the euglobulin precipitation method precipitates 72.4+/-2.1 (sd)% of both plasmin- (125)I and plasminogen- (125)I. Using this method and plasminogen- (125)I as a tracer, studies were first made of the effects of heparin and epsilon-aminocaproic acid in dogs on plasmin- (125)I generation in responese to a single injection of urokinase and to venous injury; second, of the effects of venous occlusion and thrombosis on plasmin- (125)I generation; and third, in vitro studies of plasminogen- (125)I affinity to fibrin and its activation in blood clots. The venous injury was produced by the damage of venous endothelium by an injection of 90% phenol and the thrombosis by a thrombin injection into an occluded vein. Heparin and epsilon-aminocaproic acid under the present experimental conditions inhibited about 78 and 100%, respectively of plasmin- (125)I generation by the urokinase injection. Similar inhibitory effects of heparin and epsilon-aminocaproic acid were observed on plasmin- (125)I generation in response to venous injury. The venous occlusion caused a small degree of plasmin- (125)I generation, but thrombin thrombosis did not seem to stimulate the generation of plasmin- (125)I. The in vitro studies showed that plasminogen- (125)I does not have a specific affinity to fibrin and is incorporated into blood clots in approximately equal concentrations as those in serum during clotting processes, and that blood clots per se do not stimulate plasmin- (125)I generation. These results suggest that injured veins release considerable amounts of vascular plasminogen activators into circulation and that these play an important role in thrombus dissolution in vivo.

A study on the ground substance of arteries, veins and grafted veins in dogs

The ground substance of autogenous vein grafts used as arterial replacements in dogs showed an intense metachromatic reaction with toluidine blue. This was not found in normal veins but appeared identical with that present in normal artery at varying pH values and after methylation and “demethylation”. The staining was not simply related to trauma as it was not seen in injured veins left in the venous circulation. Metachromasia was again demonstrated in fascia used to patch the aortic wall but not in control specimens grafted into the abdominal wall. These observations suggest that there is considerable accumulation of acidic mucopolysaccharide in autogenous vein and fascia grafts placed in arteries due to the pressure, and/or tension exerted on them by the arterial blood.

Effect of antiheparin agents on venous thrombosis following vascular injury.

The effect of the antiheparin agents hexadimethrine bromide and protamine sulfate on venous thrombosis have been studied in the rat, rabbit, and dog. Untreated traumatized veins were not thrombosed. Traumatized veins treated with these agents topically, or in some species intravenously, thrombosed. The thrombi so produced consisted of an occluding mass of platelet trabeculae at the site of vascular injury, a red and white proximal tail, and a distal stasis clot. The hexadimethrine bromide-induced thrombus in the rat is prevented by pretreatment with Dicumarol or heparin. It is suggested that the antiheparin agents bring about thrombosis of the injured veins by neutralizing an anticoagulant liberated locally.

THE MECHANISM OF CAPILLARY CONTRACTION

(1) From this series of experiments carried out under good optical conditions, in one case as good as present lenses allow, we conclude that capillary contraction occurs in the rabbit's ear‐chamber, that this contraction is under the control of the sympathetic nervous system, and that endothelial swelling causes the obliteration of the vessels. No positive evidence was obtained of the participation of Rouget cells in this contraction.(2) “Spikes” on the endothelium of slightly injured veins have been noted. Red corpuscles hang on these, often for several seconds.The chambers have been made in the laboratory by Mr. S. W. Bush, to whose skill we are greatly indebted. Mr. J. Kent has had charge of the animals. The drawing is by Mr. H. Axtell.