Dysregulated apoptosis in primary varicose veins.

OBJECTIVE: Programmed cell death plays a critical role in various physiological processes. To investigate its possible pathogenic role in primary varicose veins we studied histological changes in surgical specimens from human varicose veins. In varicose and healthy veins, we also determined the number of cells in apoptosis, and investigated mediators regulating the intrinsic apoptotic mitochondrial pathway (Bax and caspase 9). METHODS: A total 23 varicose veins were obtained from 18 patients undergoing lower-extremity varicose vein surgery for primary varicose disorders. We used nine healthy veins obtained from nine patients undergoing distal arterial bypass grafting surgery as controls. The venous segment analysed was the distal part of the greater saphenous vein. Specimens for histological examination were stained with hematoxylin and eosin, trichromic and Victoria blue. Cell apoptoses and mediators of the mitochondrial pathway were detected in the media by immunohistochemistry using antibodies to peroxidase in situ apoptosis, Bax and caspase 9. Results were expressed as indexes for the three antibodies tested. The Mann-Whitney test was used to compare the results obtained in the two groups. RESULTS: Varicose vein specimens exhibited a more disorganised architecture than healthy veins and showed an increased number of collagen fibres and a decrease in the density and size of elastic fibres. All anti-apoptotic antibodies tested detected significantly fewer immunoreactive cells in tissue sections from the media of varicose veins than of healthy veins (peroxidase in situ, varicose veins (VV) median 2.4% (inter-quartile range 1.6-3.9) versus control (C) 14% (IQR 8.8-19); Bax, VV 1.4% (IQR 0.36-2.4) versus C 11% (IQR 7.6-15); and caspase 9, VV 1.7% (IQR 0.06-3.4) versus C 10% (IQR 9.1-12), P=0.0001 (Mann-Whitney test). CONCLUSION: Apoptosis is down regulated in the medial layer of varicose veins. This dysregulation of the cellular mechanism that maintains normal tissue integrity is mediated through the intrinsic apoptotic pathway and may be among the causes of primary varicose veins.     

Can phlebectomy be deferred in the treatment of varicose veins?

OBJECTIVE: This study was designed to observe the clinical sequelae of varicose veins after great saphenous vein (GSV) ablation and to assess possible predictability of spontaneous varicose vein regression. METHODS: Patients with symptomatic varicose veins secondary to GSV insufficiency treated with radiofrequency ablation (RFA) were enrolled in the study. Up to five of the largest varicose veins in each limb were mapped, sized, and documented before RFA. No varicose vein was treated either at the time of RFA or within 6 months postoperatively. Varicose vein status was recorded at follow-up visits. RESULTS: Fifty-four limbs in 45 patients were included. A total of 222 varicose veins were documented before RFA (4.1 +/- 1.1 varicose veins per limb) with an average size of 11.4 +/- 3.7 mm. During the follow-up period, complete resolution of visible varicose veins was seen in 13% of limbs after RFA alone, and 63 (28.4%) varicose veins spontaneously resolved. A further 88.7% (141/159) of varicose veins decreased in size an average of 34.6% (4.3 +/- 3.4 mm). Preoperatively, 19.4% of varicose veins were above the knee and 75.7% were below the knee. Complete varicose vein resolution was 41.9% (18/43) above the knee and 25.6% (43/168) below the knee. For the above-knee varicose veins, 88.4% (38/43) were located medially, and all the resolved ones (47.4%, 18/38) were medial varicose veins. Resolution rates of the 168 below-knee varicose veins were 30.6% (33/108) of medial, 23.1% (6/26) of anterior, 20.0% (3/15) of lateral, and 5.3% (1/19) of posterior. CONCLUSIONS: Great saphenous vein ablation resulted in subsequent resolution or regression of many lower-limb visible varicose veins. With further study, the predictability of varicose vein regression may perhaps be increased, which can then direct the treatment strategy to further leverage the advantages of minimally invasive endovenous procedures.     

Association of primary varicose veins with dysregulated vein wall apoptosis.

BACKGROUND: Disordered programmed cell death may play a role in the development of superficial venous incompetence. We have determined the number of cells in apoptosis, and the mediators regulating the intrinsic and extrinsic pathways in specimens of varicose vein. METHODS: Venous segments were obtained from 46 patients undergoing surgical treatment for primary varicose veins. Controls samples were obtained from 20 patients undergoing distal arterial bypass grafting surgery. Segments of the distal and proximal saphenous trunk as well as tributaries were studied. Cell apoptoses and mediators of the mitochondrial and trans membrane pathway were evaluated with peroxidase in situ apoptosis detection, Bax and Fas detection, caspase-9 and 8 detection in the medial layer. RESULTS: Disorganised histological architecture was observed in varicose veins. Primary varicose veins also contained fewer peroxidase in situ-positive cells than control veins (2.6% S.D. 0.2% versus 12% S.D. 0.93%, P=.0001, Mann-Whitney u test), fewer Bax positive cells (2.1.% S.D. 0.3% versus 13% S.D. 0.9%, P=.0001) and fewer Caspase 9 positive cells (3.2% S.D. 1% versus 12% S.D. 1.3%, P=.0001). Similar findings were observed in saphenous trunk, main tributaries and accessory veins. In patients with recurrent varicose veins in whom the saphenous trunk had been preserved showed similar findings to primary varicose veins. Residual varicose veins contained fewer peroxidase in situ-positive cells than healthy veins (3.2% S.D. 0.6% versus 11% S.D. 2%, P=.0001), fewer Bax positive cells (2.2% S.D. 0.3% versus 12% S.D. 0.7%, P=.0001) and fewer Caspase 9 positive cells (2.6% S.D. 0.6% versus 12% S.D. 1%, P=.0001). Immunohistochemical detection for Fas and caspase 8 remained equal was the same in the varicose vein and control groups. CONCLUSION: Apoptosis is down regulated in the medial layer of varicose veins. This dysregulation is attributable to a disorder of the intrinsic pathway and involves the great saphenous vein trunk, major tributaries and accessory veins. This process may be among the causes of primary varicose veins.     

Progesterone differentially regulates pro- and anti-apoptotic gene expression in cerebral cortex following traumatic brain injury in rats

Although the administration of progesterone has been shown to be neuroprotective in experimental models of traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. The present study examined the effects of progesterone on mRNA and protein levels of the Bcl-2 apoptosis regulatory genes, bax, bad, bcl-2, and bcl-x(L), in cerebral cortex after TBI. Male Sprague-Dawley rats were subjected to either sham surgery or lateral fluid percussion brain injury of moderate severity (2.4-2.6 atm). Within 1 h post-surgery, progesterone (4 mg/kg) or vehicle (corn oil) administration was initiated for 1-7 days postoperatively. Our results indicate that bax and bad mRNA levels and Bax and Bad protein expression in the ipsilateral, injured cerebral cortex were significantly elevated post-TBI, while mRNA levels of bcl-2 and bcl-x(L) or Bcl-2 and Bcl-x(L) protein expression were not changed. Under the sham-treated condition, progesterone significantly increased mRNA levels of the anti-apoptotic gene, bcl-2, but down-regulated pro-apoptotic gene expression (bax and bad) in cerebral cortex. After TBI, progesterone treatment reduced bax and bad mRNA levels in the ipsilateral cerebral cortex of TBI rats, and decreased Bax and Bad protein levels. In addition, bcl-2 and bcl-x(L) mRNA levels, as well as Bcl-2 and Bcl-x(L) protein expression, were increased by progesterone in TBI injured cortex. These data indicate that one of the neuroprotective mechanisms of progesterone may be related to its differential regulation of apoptotic signals.     

Diameter-reflux relationship in perforating veins of patients with varicose veins.

PURPOSE: Treatment of chronic venous valvular insufficiency requires understanding of the hemodynamics of perforating veins. To preserve normal veins or veins that can function normally once primary sources of valvular insufficiency are removed, a better understanding of the diameter-reflux relationship is desirable. We measured reflux and diameters in 500 perforating veins of patients with varicose veins (C(2)E(P)A(SP)P(R)). METHODS: Color flow duplex ultrasonography scanning was performed with the patient standing. Perforating veins were mapped medially in the thigh and medially, laterally, and posteriorly in the calf. Reflux was defined as reverse flow that lasted longer than 0.5 seconds. Diameters were measured on B-mode transverse projections at the crossing of the fascia. Competent versus incompetent vein diameters were compared by means of Student t test, one-way analysis of variance, and Bonferroni t test. RESULTS: Diameters of competent and incompetent perforators averaged 2.5 +/- 0.9 mm (n = 17) and 4.7 +/- 1.9 mm (n = 17) at the medial thigh (P <.0002), 2.2 +/- 0.8 mm (n = 179) and 3.7 +/- 1.0 mm (n = 210) at the medial calf (P <.0001), 2.2 +/- 0.6 mm (n = 13) and 3.5 +/- 0.8 mm (n = 37) at the posterior calf (P <. 0001), and 2.1 +/- 0.8 mm (n = 9) and 3.3 +/- 0.7 mm (n = 18) at the lateral calf (P <.003), respectively. Perforating vein diameters of 3.5 mm or larger in the calf and thigh were associated with reflux in more than 90% of the cases. CONCLUSION: An enlargement in the diameter of the perforating veins of 1 to 1.5 mm in the calf or 2 mm in the thigh of patients with varicose veins could be the difference between normal flow and reflux. Further studies are needed to confirm if elimination of reflux in patients with primary varicosity will transform incompetent perforators to competent ones.     

Preoperative and intraoperative evaluation of diameter-reflux relationship of calf perforating veins in patients with primary varicose vein

OBJECTIVE: Interruption of incompetent perforating veins (PVs) is important for varicose vein surgery. The purpose of this study was to evaluate the preoperative and intraoperative diameter-reflux relationship of PVs and to evaluate the accuracy of preoperative duplex scanning in patients with varicose vein. METHODS: Patients with primary varicose veins were retrospectively investigated. Diameters and reflux of PVs were evaluated before surgery with color flow duplex ultrasound scan (US). During operation, the incompetent PVs were defined as those that showed an outward spurt of blood flow from the stump of the PVs. The sensitivity and specificity of US in the detection of reflux of PVs were calculated. Competent versus incompetent vein diameters were compared with the Student t test and one-way analysis of variance. RESULTS: Three hundred twenty-four calf PVs were detected in 304 legs of 175 patients with varicose vein. Diameters of competent and incompetent PVs confirmed with intraoperative finding averaged 2.67 +/- 1.10 mm (n = 28) and 3.28 +/- 1.01 mm (n = 58), respectively, at the upper calf (P =.012), 2.85 +/- 0.85 mm (n = 53) and 3.68 +/- 0.94 mm (n = 137), respectively, at the lower calf (p <.001), and 2.67 +/- 0.99 mm (n = 14) and 3.27 +/- 0.66 mm (n = 22), respectively, at the posterior calf (P =.036). The overall sensitivity of detection of reflux with US was 87.7%, and the specificity was 75.3%. Diameters of true-incompetent PVs and false-incompetent PVs were 3.59 +/- 0.94 mm (n = 199) and 3.31 +/- 0.84 mm (n = 24), respectively (P =.157). Diameters of true-competent PVs and false-competent PVs were 2.61 +/- 0.91 mm (n = 73) and 2.89 +/- 0.82 mm (n = 28), respectively (P =.158). CONCLUSION: Although the diameter of incompetent PVs was larger than that of competent PVs in both US and intraoperative findings, diameter measurement alone can not completely distinguish competent and incompetent PVs. The sensitivity and specificity of reflux obtained with US showed that the accuracy of preoperative duplex scanning to evaluate PV competency was not sufficient.     

Pulmonary embolism after endovenous thermal ablation of the saphenous vein

Pulmonary embolism (PE) after venous procedures is fortunately rare. Our goal was to analyze the data of patients who developed PE after endovenous thermal ablation and phlebectomy for varicose veins and to review the literature on this subject. We report on three patients who developed PE after radiofrequency ablation of the great saphenous vein and mini phlebectomy for symptomatic primary lower-extremity varicose veins. Early postoperative duplex scans confirmed successful closure of the great saphenous vein in all. One patient presented with chest pain and dyspnea, one with blood-tinged sputum, and the third with symptoms of saphenous thrombophlebitis. Two patients had PE from the saphenous vein thrombus and the third had gastrocnemius vein thrombosis extending into the popliteal vein. One had previous deep vein thrombosis. Computed tomography of the chest confirmed PE in all. Two patients were treated with anticoagulation, but the third patient with small PE declined such treatment. One patient underwent temporary inferior vena cava filter placement because of recurrent PE. In conclusion, PE is very rare but it can occur after endovenous thermal ablation of lower-extremity varicose veins. Selective thrombosis prophylaxis and preoperative counseling of the patients about signs and symptoms of deep vein thrombosis and PE are warranted for early recognition and rapid treatment.     

Morphologic characteristics of varicose veins: possible role of metalloproteinases

BACKGROUND: Although varicose veins are a common cause of morbidity, etiologic factors predisposing to dilatation, elongation, and tortuosity of the saphenous vein and its tributaries are poorly understood. We compared histologic features of normal and varicose saphenous veins and investigated the role of enzyme or inhibitor imbalance in development of varicosities. METHODS: Eight normal and 10 varicose (C(2,3)E(P,S)A(S)P(R,O)) vein segments were used for this analysis. Matrix metalloproteinase (MMP) expression and activity were analyzed with Western blotting and zymography. Venous architecture and protein localization were determined with histology and immunohistochemistry. RESULTS: Western blot analysis demonstrated the presence of MMP- 1, MMP-2, MMP-9, and MMP-12, as well as small quantities of tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 in protein isolates from normal and varicose veins. Both vein types demonstrated MMP-2, MMP-9, and MMP-12 activity by gelatin zymography, although varicose vein expressed less MMP-9 activity than normal vein did. Compared with normal veins, changes in varicose veins were not uniformly distributed along the circumference; areas of intimal thickening were often interspersed with focal areas of dilatation. Fragmentation of elastic lamellae and loss of circular and longitudinal muscle fibers were evident in the varicosities. Focal aggregates of macrophages were detected within the media and adventitia of both normal and varicose veins. MMP-1 and MMP-9 were expressed in both types of vein segments; however, their immunohistochemical localization was distinctly different. In normal vein, endothelial cells, occasional smooth muscle cells (SMC), and adventitial microvessels expressed MMP-1, whereas its expression was localized to fibroblasts, SMC, and endothelial cells throughout involved portions of varicose veins. MMP-9 was localized to endothelial cells, medial SMC, and adventitial microvessels in both normal and varicose veins, although varicose veins demonstrated increased medial smooth muscle cell staining. MMP-12 was found in SMC and fibroblasts in both normal and varicose veins. Neither TIMP-1 nor TIMP-2 were detected with immunohistochemistry in any specimens examined. CONCLUSIONS: There are distinct differences in the structural architecture and localization of MMP expression in normal and varicose veins. Although the changes observed are not sufficiently definitive to enable a causal relationship, they do suggest a possible mechanism for the alterations in matrix composition observed between normal and varicose veins.     

Venous reflux and venous distensibility in varicose and healthy veins.

OBJECTIVES: The aim of this study was to analyse venous diameter changes and venous reflux parameters, assessed during a standardised Valsalva manoeuvre in healthy subjects and in patients with varicose veins. METHODS: Measurements were carried out in 444 vein segments, (96 legs of 48 healthy volunteers, 52 legs of 35 patients with varicose veins). The common femoral vein (CVF), the femoral vein (FV) and the great saphenous vein (GSV) were investigated. The parameters of reflux and the relative venous diameter change (VD diff %) were measured simultaneously during a standardised Valsalva manoeuvre. RESULTS: Venous diameter changes during Valsalva manoeuvre (VD diff) were significantly greater in the GSV and in the deep veins of varicose patients compared to healthy subjects. The median (Interquartile range) of VD max in the CFV was: 13.1 (3.5) mm and 11.2 (3.4) mm (p=0.0002, Mann-Whitney - U test), in the FV 7.8 (2.7) mm and 6.9 (2.0) mm (p=0.01, Mann-Whitney), in the GSV: 7.3 (3.7) mm and 4.2 (1.1) mm (p<0.0001, Mann-Whitney) for the varicose and healthy veins respectively. Good correlation was seen for the retrograde peak reflux velocity (PRV) and VD diff % in varicose veins (r=0.71 (0.57 - 0.81) p<0.0001, Mann-Whitney). CONCLUSION: Relative venous diameter--changes during a standardised Valsalva manoeuvre are significantly larger in the deep and superficial veins of varicose vein patients compared with healthy veins, the increased distensibility correlates with venous reflux parameters in varicose vein patients.     

Reappraisal of the oxygenation of blood in varicose veins

Raised oxygen tension in the blood of varicose veins has led to arteriovenous communications being implicated in the pathogenesis of varicose veins. The aim of this study was to compare the oxygen tension of blood from varicose veins with that from normal legs, and to observe the effect of posture on these measurements. Twenty-six subjects (13 normal controls and 13 with uncomplicated varicose veins) had blood sampled from the long saphenous vein or a varicose vein near the ankle. Samples were taken after 30 min in the supine position and repeated after 30 min standing. Samples were also taken simultaneously from the arm. Transcutaneous oxygen measurements of the gaiter skin were performed continuously throughout the experiment. In the supine position, blood from varicose veins had a significantly higher oxygen tension (median = 6.09 kPa) than that from normal veins (median = 4.54 kPa) (P = 0.022). In all subjects, there was a higher oxygen tension in leg vein blood when lying (varicose vein median value = 6.09 kPa, control median value = 4.54 kPa) than while standing (varicose vein median value = 3.93 kPa, control median value = 3.74 kPa) (P less than 0.002, varicose vein group; P = 0.005, normal group). Changes in transcutaneous oxygen tension correlate poorly with changes in venous blood. It is concluded that the theory of arteriovenous anastomoses is only one among a number of possible explanations for the pathogenesis of varicose veins.     

Selective loss of extracellular matrix proteins is linked to biophysical properties of varicose veins assessed by ultrasonography

BACKGROUND: Dilatation and enhanced distensibility are specific biophysical properties of varicose veins. Both can be assessed by ultrasonography. The aim of this study was to analyse correlations between the vein wall protein content and these two biophysical properties of varicose veins. METHODS: Twenty-seven patients having surgery for varicose veins and six control patients with normal veins undergoing arterial bypass surgery were examined clinically and with ultrasonography the day before surgery. Fifty-two varicose and six control vein rings were harvested and analysed histopathologically and morphometrically; vascular tissue microarrays incorporated 116 vein wall sectors. RESULTS: Elastin loss in the adventitia (P = 0.010) and reduction of type III collagen in the intima and media (P = 0.004) were observed in varicose veins. Elastin loss correlated negatively with vein diameter at rest (P = 0.005), whereas loss of type III collagen in the intima correlated negatively with the increase in vein diameter at the Valsalva manoeuvre (P < 0.001). CONCLUSION: Loss of elastin and type III collagen occurs in varicose veins and can be assessed with ultrasonography in vivo by measuring vein diameter and distensibility.     

Viscoelastic properties and collagen content of the long saphenous vein in normal and varicose veins

Veins taken from patients undergoing surgery for varicose veins were compared with those obtained from patients undergoing other surgical procedures ('normals'). Varicose veins had a lower breaking strength and breaking energy than normal veins. Elastic stiffness was less in normals (tan theta = 41 (24] than in varicose veins (tan theta = 55 (18); P less than 0.01). There was no difference in viscoelastic behaviour between samples taken above, at, or below the valve leaflet insertion. In normals, perivalvular vein wall exhibited a 50 per cent lower breaking strength and elastic stiffness than vein from other sites. Collagen content was significantly higher in normal vein specimens in all sites examined (mean collagen content = 70 (21) micrograms/mg, versus 51 (20) micrograms/mg for varicose veins; P less than 0.001). We conclude that significant structural changes are seen in varicose veins. In normal veins, the perivalvular vein wall has distinct viscoelastic features when compared with vein wall from other sites. This difference was not found in veins which became varicose.     

32 P局部照射对移植静脉内膜平滑肌细胞增殖与凋亡的影响

目的 研究β射线局部照射对自体移植静脉内膜平滑肌细胞（VSMC）增生与凋亡的影响及可能机制。方法 建立80只大鼠自体静脉移植模型,随机分成^32P局部照射组、对照组,每组按3、7、14、28d随机分成4个亚组、每亚组10只。取材固定,弹力纤维染色,增殖细胞核抗原、p53、bcl-2、bax免疫组化测定,TUNEL法检测静脉平滑肌细胞的凋亡,计算机图象分析仪测量移植血管内膜厚度,计算细胞增殖及凋亡百分化。结果 术后2组移植静脉段的内膜平均厚度：7、14、28d,照射组明显 于对照组（t＝15．694,P＜0．05）;7、14d照射组VSMC增殖较对照组受到明显抑制（t＝60．157,P＜0．01）。凋亡指数14d照射组高于对照组（t＝56．176,P＜0．01）。p53的表达,2组间差异无显著性意义（t＝0．473,P＞0．05）,bax与bcl－2的表达,14d照射组高于对照组（t＝9．783,P＜0．05）。结论 ^32P局部照射可以抑制自体移植静脉的内膜增生及VSMC的增殖,促进VSMC的凋亡,可能是通过bax、bcl－2基因的表达实现的。     

Delayed myocardial preconditioning by alpha1-adrenoceptors involves inhibition of apoptosis

OBJECTIVE: Previous studies have demonstrated that alpha1-adrenoceptor activation increases myocardial resistance to ischemic injury 24 hours later. Here we tested the hypothesis that delayed protection is associated with limited infarction and involves altered expression of pro-apoptotic and/or anti-apoptotic proteins. METHODS: Rabbits were treated with phenylephrine or an equivalent volume of vehicle (n = 6 per group). Twenty-four hours after pretreatment, isolated hearts were perfused with a bovine erythrocyte suspension in modified Krebs solution, subjected to 45 minutes of global ischemia (37 C), and reperfused for 120 minutes. Infarct size was determined by triphenyltetrazolium chloride staining. Apoptosis was quantified by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling. Left ventricular tissue from separate groups of animals (n = 5 per group), 24 hours after pretreatment with phenylephrine or vehicle but without ischemia and reperfusion, was analyzed by Western blotting for content of the anti-apoptotic protein, bclx, and pro-apoptotic protein, bax. RESULTS: Isolated hearts after phenylephrine pretreatment had increased end-reperfusion developed pressures (56.8 +/- 4.9 vs 36.2 +/- 3.9 mm Hg for vehicle, P =.008) and decreased elevated end-diastolic pressures (26.7 +/- 4.5 vs 42.3 +/- 5.0 mm Hg for vehicle, P =.04). Phenylephrine pretreatment abrogated infarction (9.9 +/- 2.4% vs 42.6 +/- 6.3% for vehicle, P =.002) and reduced the number of apoptotic nuclei (24 +/- 4.8 vs 51 +/- 4.6 for vehicle, P = .038). Analysis by Western blotting showed that the ratio of bclx to bax protein increased in phenylephrine-pretreated hearts (2.65 +/- 0.5 vs 1.0 +/- 0.1 for vehicle, P =.008). CONCLUSION: Delayed myocardial protection to infarction mediated by alpha1-adrenoceptor activation involves an increased bclx/bax ratio, thereby limiting apoptotic cell death.     

Increased prostacyclin and thromboxane A2 formation in human varicose veins

Increased urinary metabolites of the antiaggregatory vasodilator prostacyclin (PGI2) and the proaggregatory vasoconstrictor thromboxane A2 (TXA2) have been reported in deep vein thrombosis; however, the tissue(s) of origin is uncertain. Because little is known about the formation of PGI2 or TXA2 from its common precursor, prostaglandin (PG) endoperoxide H2 (PGH2), by varicose veins, we determined the formation of 6-keto-PGF1 alpha (the stable metabolite of PGI2), TXB2 (the stable metabolite of TXA2), and PGE2. Segments of normal saphenous vein and varicose vein (nine and six patients, respectively) were incubated with 10 microM [14C]PGH2 for 2 min at 37 degrees C; products were separated by thin-layer chromatography. Surface area and mass of normal and varicose vascular segments were 19.5 +/- 0.8 versus 18.8 +/- 0.6 mm2 and 11.6 +/- 1.4 versus 10.7 +/- 0.7 mg, respectively. Formation of 6-keto-PGF1 alpha and TXB2 by the segments of varicose vein was significantly increased over that of normal vein: 157 +/- 14 versus 243 +/- 17 pmole of 6-keto-PGF1 alpha (P less than 0.005) and 22 +/- 3 versus 35 +/- 5 pmole of TXB2 (P less than 0.01). The formation of PGE2 by segments of varicose vein was not significantly different from that of normal vein (201 +/- 9 vs 219 +/- 11, respectively). Deoxyribonucleic acid (DNA) content of normal and varicose vein was 1.69 +/- 0.12 and 1.51 +/- 0.13 mg per gram of tissue, respectively. The data suggest that the increased PGI2 formation may reflect increased activity or content of PGI2 synthase. The increase in TXA2 formation may reflect increased productivity or an increased presence of residual platelets or microemboli.