Subclavian arterial injury associated with blunt trauma.

Blunt subclavian artery trauma is an uncommon but challenging surgical problem. The purpose of this study was to retrospectively review the management of blunt subclavian artery injuries treated by the Trauma and Vascular Surgery Services at the East Tennessee State University-affiliated hospitals between 1992 and 1998. Six patients with seven blunt subclavian artery injuries were identified. Physical signs indicating blunt subclavian artery injury were pain or contusion around the shoulder joint; fractures of the clavicle, scapula, or ribs; periclavicular hematomas; and ipsilateral pulse or neurologic deficits. Seven subclavian artery injuries were treated-two arterial transections, two pseudoaneurysms, and three intimal dissections. Associated injuries included four clavicle fractures, one humerus fracture, one combined rib and scapular fractures, and two pneumothoraxes. Vascular surgical treatment included three primary arterial repairs, two saphenous vein interposition grafts, and one polytetrafluoroethylene (PTFE) graft. One patient was treated nonoperatively with anticoagulation. No deaths occurred. Morbidity occurred in two patients with chronic upper extremity neuropathy producing prolonged disability from pain and weakness; one patient had reflex sympathetic dystrophy, and the other had a brachial plexus injury. In conclusion, blunt subclavian artery trauma can be successfully managed with early use of arteriography and prompt surgical correction by a variety of vascular techniques. Vascular morbidity is usually low, but long-term disability because of chronic neuropathy may result from associated brachial plexus nerve injury despite a successful arterial repair.

Durability of eversion carotid endarterectomy: comparison with primary closure and carotid patch angioplasty.

OBJECTIVES: Despite numerous studies in which various methods for arteriotomy closure after carotid endarterectomy (CEA) have been addressed, the optimum surgical technique to reduce complications and late carotid restenosis has yet to be firmly established. The purpose of this study was to prospectively compare the results of the eversion CEA technique with those of conventional CEA with either primary closure or carotid patch angioplasty, and to determine under clinical conditions whether eversion CEA influences the results and restenosis rate. PATIENTS AND METHODS: Over a 3-year period, 322 CEAs performed on 296 consecutive patients were concurrently evaluated. This study included 118 eversion CEAs, 97 CEAs with primary closure, and 107 CEAs with patch angioplasty. There were no differences in demographics, in surgical indications, or in the severity of carotid disease (not significant [NS]). The choice of CEA technique was not randomized because of technical considerations and surgeon preference. After entry into the protocol, no patients were excluded or withdrawn. Carotid restenosis was defined as a > 60% lumen reduction at the CEA site with established duplex ultrasonography criteria. RESULTS: The mean operative time for eversion CEA was 31 minutes, for CEA-primary closure it was 39 minutes, and for CEA-patch angioplasty it was 46 minutes (P <.01). The operative mortality rate for eversion CEA was 0.8% (1 patient), for CEA-primary closure it was 1.0% (1 patient), and for CEA-patch angioplasty it was 2.8% (3 patients) (NS). The postoperative stroke rate was 0.8% after eversion CEA, 1.0% after CEA-primary closure, and 2.8% after CEA-patch angioplasty (NS). The combined stroke and death rate in each group was thus 0.8% for eversion CEA (1 stroke-death), 1% for CEA with primary closure (1 stroke-death), and 5% for CEA with patch angioplasty (1 stroke-death, 2 fatal myocardial infarctions, and 2 nonfatal strokes) (NS). Transient ischemic attacks occurred in 2.5% after eversion CEA, in 5.2% after CEA-primary closure, and in 2.9% with CEA-patch angioplasty (NS). The mean clinical follow-up for all three groups was 23 months (range, 6-42 months) (NS). The restenosis rate was 1.7% after eversion CEA, 9.3% after CEA-primary closure, and 6.5% after CEA-patch angioplasty (P <.05). CONCLUSIONS: This prospective, nonrandomized clinical study indicates that eversion CEA is an effective surgical option comparable to conventional CEA with either primary arteriotomy closure or carotid patch angioplasty. No differences were found between eversion CEA and these more widely accepted CEA closure techniques with respect to operative morbidity and mortality. These data indicate, however, that eversion CEA has a lower restenosis rate than conventional CEA closure techniques and thus superior long-term durability.

h-Caldesmon, a novel smooth muscle-specific antibody, distinguishes between cellular leiomyoma and endometrial stromal sarcoma.

The difficulty in distinguishing between smooth muscle and endometrial stromal-derived neoplasms of the uterine corpus is a notorious and clinically relevant problem in pathology of the female genital tract. Immunohistochemistry offers some aid in resolving this difficulty, because the expression of smooth muscle markers is reputed to indicate smooth muscle derivation. This expression, however, is not entirely specific, and difficult cases may still present in which immunohistochemistry is of little help. To explore this problem, the authors evaluated the expression of traditional muscle markers and high-molecular-weight caldesmon (h-cal), an actin and tropomyosin binding protein that has recently been described as a useful muscle marker, in uterine leiomyosarcoma (LMS), cellular leiomyomata (CL), and endometrial stromal sarcoma (ESS). Formalin-fixed and paraffin-embedded tissue sections from nine LMSs, 11 CLs, and 12 ESSs were evaluated with commercially available monoclonal antibodies against smooth muscle actin (SMA), desmin, and h-cal. Established morphologic criteria were used to classify the neoplasms. We found that there was, as expected, a significant difference in the expression of traditional smooth muscle markers (SMA and desmin) between tumors derived from smooth muscle and those derived from endometrial stroma (p = 0.005 for LMS and 0.013 for CL). We further found that h-cal was most useful in distinguishing between CL and ESS (p = 0.01). A significant difference between h-cal expression in LMS versus ESS was not found. Of note, one ESS expressed both SMA and desmin but lacked h-cal expression. Our findings confirm the most useful immunohistochemical data to date; smooth muscle neoplasms are generally distinguishable from endometrial stromal tumors by the expression of conventional muscle markers. We also report here that h-cal is useful more specifically in the differentiation of CL from ESS.

Symmetrical peripheral gangrene: a new presentation of an old disease.

This report concerns two cases and a review of the literature on the subject of symmetrical peripheral gangrene. Symmetrical peripheral gangrene is defined as symmetrical distal ischemic damage in two or more sites in the absence of major vascular occlusive disease. It occurs in patients who are septic and have disseminated intravascular coagulation and in nonseptic patients who have cardiogenic or hypovolemic shock. The syndrome is devastating and rare, and controlled studies of its etiology and management are lacking. Recommendations are presented for its prevention and treatment. Cooperative multicenter studies may be necessary to obtain valid data about its prevention and management.

A prospective evaluation of atherosclerotic risk factors and hypercoagulability in young adults with premature lower extremity atherosclerosis.

PURPOSE: Fifty-one consecutive patients with premature lower extremity atherosclerosis were prospectively evaluated for atherogenic risk factors and primary or acquired hypercoagulability, which might contribute to early ischemia and revascularization failure. METHODS: Laboratory tests included plasma assays of (1) natural anticoagulants (NAC), lipoprotein (a) (Lp[a]), and anticardiolipin antibodies, and (2) fibrinolytic activators and inhibitors at baseline and stimulated after 20 minutes of upper extremity venous occlusion. RESULTS: Forty-six (90%) of these 51 patients had laboratory abnormalities. One or more NAC deficiencies were found in 15 (30%) patients and included antithrombin III (n = 5), protein C (n = 8), protein S (n = 4), and heparin cofactor II (n = 2). Hypofibrinolysis was identified as a deficiency of stimulated tissue plasminogen activator in 22 (45%) patients and elevated plasminogen activator inhibitor-1 (PAI-1) in 29 (59%). Elevated Lp(a) was found in 43 (86%) patients. Five (10%) patients had anticardiolipin antibodies. Ten patients had combined NAC deficiency and hypofibrinolysis. Five (10%) patients had no abnormality. NAC deficiencies, especially protein C deficiency, were associated with acute ischemia (p < 0.01), prior vascular intervention (p < 0.01), an increasing number of total vascular procedures (p < 0.01), and major amputation (p < 0.01). PAI-1 was associated with a history of heart disease (p < 0.05) and prior vascular procedures (p < 0.05). Elevated Lp(a) was associated with elevated PAI-1 (p < 0.05). Retesting in 20 patients suggested that 80% of NAC deficiencies were acquired, but abnormalities persisted in 66% of patients with elevated PAI-1 and in 93% of those with elevated Lp(a). CONCLUSIONS: These data strongly support the hypothesis that the convergence of atherogenic risk factors and hypercoagulability play an important role in early ischemia and poor results reported for lower extremity vascular procedures in young adults.

Percutaneous transluminal angioplasty in adults less than 45 years of age with premature lower extremity atherosclerosis.

Despite poor results reported with conventional vascular bypasses in young adults with ischemia from premature lower extremity atherosclerosis (PLEA), little attention has been given to alternative revascularization techniques. This study evaluated 32 patients (21 males and 11 females) < 45 years of age with PLEA who underwent 53 primary percutaneous transluminal angioplasty (PTA) procedures for treatment of 46 ischemic limbs. A residual arterial stenosis < 30% was achieved in 83% of PTA sites. Mean degree of stenosis decreased from 79.9% to 24.1% (p < 0.0001). Clinical improvement in ischemic symptoms was obtained in 39 (85%) limbs. Hemodynamic improvement was achieved in 31 (70%) of 40 limbs as documented by ankle/brachial indices. All criteria for early clinical success were met in 70%. Another 13% met all criteria except that the residual stenosis was < 50%. Hematoma and early restenosis were reported in two patients each. Mean follow-up was 27.3 months (range 1 to 84 months). Cumulative patency by life-table analysis was 81% at 1 year, 77% at 2 years, and 71% at 3 years. Thirteen (41%) patients required secondary PTA or bypass; 85% were performed within 1 year. Two patients had adjunctive bypasses; six (19%) were performed after PTA failure. Only one (3%) patient required major amputation. Neither cardiovascular risk factors, treatment indication, location of the diseased arterial segment, nor quality of distal runoff vessels predicted the need for secondary PTA or surgical procedures. PTA of the proximal arteries in young patients with PLEA is an effective primary revascularization technique with results comparable to those of conventional operative revascularization procedures.

Fasciotomy in vascular trauma: is it too much, too often?

Fasciotomy has been used as a prophylactic measure against development of compartment syndrome and as a treatment modality when the syndrome has developed in patients suffering vascular trauma. The hospital records of 36 patients who underwent surgical repair of their traumatic vascular injuries were reviewed. All 36 patients had at least one indication for fasciotomy at the time of repair; i.e., ischemic time of more than 6 hours or combined arterial and venous injury. Prophylactic fasciotomies were performed in 18 of the patients at the time of vascular repair; 18 did not have fasciotomies performed at the time of initial repair. The decision to perform a fasciotomy was made by the operating surgeon based on well-defined criteria. Hospital stay was significantly longer for the fasciotomy group. Four of the fasciotomy-related complications were infective in nature. Only one patient who did not undergo fasciotomy at the time of original repair developed a compartment syndrome during the postoperative period. Selective fasciotomy based on well-defined criteria instead of serial physical examinations or measurement of compartment pressures will effectively save limbs; there is an increased hospital stay.

Lower extremity ischemia in adults younger than forty years of age: a community-wide survey of premature atherosclerotic arterial disease.

A retrospective community-wide survey identified 109 patients younger than 40 years of age with lower extremity ischemia: 72 men and 37 women, mean age 36 years (range 25 to 40 years), black-to-white ratio-1:1. Initially, 66 patients had claudication and 43 had severe ischemia. Cardiovascular risk factors were smoking (85%), hypertension (47%), coronary artery disease (30%), hyperlipidemia (27%), diabetes (25%), and visceral arteriopathy (17%). Unique risk factors included hypercoagulability (15%) and clinical arterial hypoplasia (15%). Twenty-three (21%) patients were treated medically; 74 (68%) underwent primary revascularization and 12 (11%) primary major limb amputation. Forty-six (53%) patients required secondary procedures, of which 34 (74%) were performed within 1 year of primary intervention. A total of 29 (27%) patients ultimately required amputation (10 bilateral). Women had higher prevalence of diabetes (p < 0.01), arterial hypoplasia (p < 0.05), and tendency for more severe ischemia (p = 0.11). No racial differences in severity of symptoms or outcome of treatment were found. By multiple logistic regression analysis, typical cardiovascular risk factors did not predict severity of symptoms, need for surgical treatment, or outcome. However, diabetes was associated with tissue loss (p < 0.05) and primary amputation (p < 0.001). Further, adjusted odds ratios indicate that arterial hypoplasia had a protective effect on distal vasculature (p < 0.05) and predicting need for revascularization (p < 0.05), but not on treatment failure. Hypercoagulability had the highest predictive value for presence of severe ischemia (p < 0.05), need for primary amputation (p < 0.01), and early failure of surgical treatment (p < 0.05).

Hypercoagulable states as an evolving risk for spontaneous venous and arterial thrombosis.

This study of 49 patients with spontaneous venous and arterial thrombosis identified 27 with hypercoagulable states: 13 had only venous thrombosis (VT), six had episodes of VT followed by arterial thrombosis (AT) and eight had AT only. All 27 patients were less than 42 years of age; 22 had specific natural anticoagulant or fibrinolytic deficiencies: antithrombin III (nine patients), protein C (eight patients), protein S (three patients), heparin cofactor II (two patients), tissue plasminogen activator release (one patient) and mixed antithrombin III and protein S (one patient). The remaining five patients had recurrent thrombotic events associated with resistance to heparin anticoagulation, but no established laboratory diagnosis. Clotting complications included recurrent VT, pulmonary embolism, multiple failed arterial procedures and lower extremity amputation. The remaining 22 patients (mean age of 53 years, range of 46 to 63 years), 12 with VT and ten with AT, did not have laboratory evidence of hypercoagulability and none had recurrent vascular occlusions. All these patients were successfully treated by conventional therapy without any additional thrombotic events during the follow-up period. Young adults with spontaneous thrombotic events should be screened for possible hypercoagulable states. Additionally, these young patients need further evaluation and treatment of cardiovascular risk factors. Those with premature atherosclerosis have an especially poor prognosis despite surgical intervention and anticoagulant therapy.

Rare presentation of anastomotic iliac artery false aneurysm: rupture with formation of ilio-iliac arteriovenous fistula.

A rare complication of aortoiliac bypass procedure resulting in the formation of an acute ilio-iliac arteriovenous fistula was presented. The latter was a first manifestation of anastomotic iliac pseudoaneurysm. This is only the second such case reported in the English literature. Iliac anastomotic pseudoaneurysm although rarely detected, is a potentially lethal complication that has to be repaired close to the time of its detection.

The safety, efficacy, and durability of external carotid endarterectomy.

Results of 21 external carotid endarterectomies (ECEAs) in 19 patients with symptoms were reviewed retrospectively. No patients died or had new strokes referable to ECEA within 30 days of surgery. Overall, six (32%) patients died during an average 41 months of follow-up (range 1 to 134 months). Persistent symptoms followed five (71%) of seven ECEAs performed for cerebrovascular insufficiency or transient ischemic attacks. One patient treated urgently for an evolving stroke failed to improve and died after hospital discharge. Another patient with crescendo transient ischemic attacks had a preoperative deficit that did not resolve for 6 months and had a second stroke 2 years later. Another patient had a stroke after a contralateral carotid reconstruction but recovered. In contrast, only two (14%) of 14 ECEAs performed for monocular amaurosis fugax had persistent symptoms after surgery. Durability of 16 ECEAs was evaluated by arteriography or duplex scanning. Of six ECEAs closed primarily, three (50%) occluded, one has 60% restenosis, and only two (33%) had no restenosis (mean follow-up 36 months). Of 10 ECEAs closed by patch angioplasty, none occluded, 2 had 20% restenosis, and eight (80%) had no restenosis (mean follow-up 47 months). Life-table analysis indicated improvement in ECEA patency and durability with patch angioplasty (p = 0.011). From these data, ECEA can be performed with relative safety but is more effective for treatment of monocular amaurosis fugax in patients with a microembolic source at the external carotid origin. Patients with any other indications for ECEA did not benefit consistently from this operation.

Noninvasive diagnosis of vascular trauma by duplex ultrasonography.

Duplex ultrasonography was used prospectively in the initial evaluation of 198 patients with 319 potential vascular injuries of the neck and extremities. Patients who were unstable or who had obvious arterial trauma were excluded. Injury was caused by gunshot in 104 (53%), blunt trauma in 42 (21%), stab wound in 34 (17%), and shotgun in 18 (9%). Duplex ultrasonography correctly characterized and localized vascular injuries in 23 patients: arterial disruptions (13), intimal flaps (4), acute pseudoaneurysms (3), arteriovenous fistulas (2), and shotgun pellet arteriopuncture (1). Nineteen other patients had vasospasm (13) or external compression (6) without evidence of intrinsic vessel injury, these 42 studies had true-positive results. Twenty patients underwent arterial repair (13 on the basis of duplex ultrasonography alone), one had primary amputation, three required fasciotomy, and 18 were observed. Two patients with false-negative results had minor shotgun pellet arteriopunctures that were missed by duplex ultrasonography, but neither needed repair. One hundred fifty-three patients had true-negative results on duplex ultrasonography: all clinically had only proximity injuries and easily palpable distal pulses. The result of one duplex ultrasonography study was found to be false-positive on arteriography. The sensitivity of duplex ultrasonography was 95%, the specificity was 99%, and the overall accuracy was 98%. These results closely approximate those reported with the use of exclusion arteriography in the evaluation of similar vascular trauma patients. Furthermore, duplex ultrasonography has no interventional risks and is more cost-effective for screening such injuries than arteriography or exploration. Duplex ultrasonography is a reliable method of diagnosis in patients with potential peripheral vascular injuries.

Penetrating injuries of the abdominal aorta.

The charts of 56 consecutive patients with penetrating injuries to the abdominal aorta were reviewed in an attempt to identify prognostic factors. Mechanism of injury was gunshot wound (GSW), 82 per cent (.22 cal: 15.2%; greater than .38 cal: 84.8%); shotgun wound (SGW), 5 per cent; and stab wound (SW), 13 per cent. Overall mortality was 73 per cent, with GSW 78 per cent (.22 cal: 0%; greater than .38 cal: 92%), 67 per cent with SGW, and 43 per cent with SW. Average initial systolic blood pressure (ISBP) was 53 (0-130); 87 (0-120) in survivors; and 40 (0-130) in nonsurvivors (NS). Eighteen patients (32%) had no ISBP, with one survivor. Thirty (54%) patients had ISBP less than 70, with three survivors. Six Emergency Department (ED) thoracotomies were performed, with five patients surviving to reach the operating room (OR), and none surviving long-term. Ten patients died in the ED, 18 during surgical intervention, six within 24 hr, and seven greater than 24 hr postop. Average time from injury to OR was 75 minutes, with 122 minutes in survivors, and 53 minutes in nonsurvivors (P less than 0.05); 49 minutes in those dying in the OR; and 58 minutes in those surviving the OR but dying postop (NS). At surgery, six patients had thoracotomy before celiotomy for control of the thoracic aorta, with three surviving the OR and two surviving long-term. Survivors had 2.53 associated injuries; nonsurvivors had 2.89 (NS). No significant difference was noted in number or location of associated injuries between survivors and nonsurvivors.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Does open fasciotomy contribute to morbidity and mortality after acute lower extremity ischemia and revascularization?

A retrospective review was undertaken of 127 lower extremity fasciotomies performed for compartment syndrome after acute ischemia and revascularization in 73 patients with vascular trauma and 49 patients with arterial occlusive disease. One hundred twelve (88%) fasciotomies were performed early (at the time revascularization); 15 (12%) were delayed because of late compartment syndrome diagnosis. Ninety-four (77%) patients had more than one accepted indication for fasciotomy. Double-incision fasciotomy was used in 98 (77%) extremities, single-incision fasciotomy was used in 19 (15%), and fasciotomy-fibulectomy was used in 10 (8%). Fasciotomies were closed in 88 (69%) patients an average of 14 days after surgery. Seven patients needed multiple skin grafting procedures or myocutaneous flaps to close the wound; none compromised limb salvage. Five other patients had minor wound infections that resolved. Functional status returned to preoperative levels by the time of discharge from the hospital in 59 (48%) patients. Thirty-one (24%) patients had residual lower extremity disability related to delayed union of the fracture (five), chronic neuropathy (20), leg swelling (one), or ischemic nonhealing fasciotomy wounds (three); two patients had unrelated disabilities. Fourteen (11%) amputations were required for refractory limb ischemia; two (1.6%) were required for wet gangrene of the foot, which infected the fasciotomy site; the others had open noninfected incisions. Eighteen (15%) patients died of cardiopulmonary failure or multisystem failure or both, without fasciotomy-related problems. Open fasciotomy for compartment syndrome after acute lower extremity ischemia and revascularization was associated with an increased risk of minor wound morbidity. However, limb loss and death resulted from persistent ischemia and underlying systemic disease processes or injuries, but not from open fasciotomy wound complications.

Penetrating injury to the carotid artery. A reappraisal of management.

Penetrating trauma remains the most common cause of cervical carotid artery injury. Controversy persists regarding proper management of these injuries, especially in the presence of a neurologic deficit. Recent experience with 24 patients over a 5-year period is reviewed. In patients with preoperative neurologic deficits, neither repair nor ligation of the injured vessel altered outcome. Outcome correlated only with preoperative neurologic status. All patients without preoperative neurologic deficits should have repair attempted when technically feasible. Although controversial, this study supports carotid artery repair except in comatose patients who have profound neurologic deficits.

Prostacyclin and thromboxane A2 formation by atherosclerotic carotid artery: comparison with normal aorta, saphenous vein, and platelets.

Prostacyclin (PGI2) and thromboxane A2 (TxA2) formation by whole-tissue segments of nine carotid endarterectomy specimens (CES), five normal aortic specimens (NAS), six saphenous vein specimens (SVS), and four platelet samples were determined by incubation with 10 mumol/L 1-14C-radiolabeled prostaglandin endoperoxide H2 (PGH2), and in other experiments with and without 10 mumol/L of CGS 13080, a TxA2 synthase inhibitor. PGI2 formation (expressed as picomoles 6-keto-PGF1 alpha/2-min incubation per sample) by nonatheromatous proximal intima of CES (307 +/- 23, mean +/- standard error) and distal intima of CES (260 +/- 22) was not statistically different; however, it was greater than atheromatous transitional plaque (159 +/- 13 pmol) (p less than 0.01) and ulceration regions (140 +/- 15 pmol) (p less than 0.01) of CES, NAS (204 +/- 16 pmol) (p less than 0.01), and SVS (165 +/- 9 pmol) (p less than 0.01). TxA2 formation (expressed as picomoles TxB2/2-min incubation per sample) by CES ulceration (51 +/- 2 pmol) was low but greater than proximal (17 +/- 2 pmol) (p less than 0.01), distal (19 +/- 3 pmol) (p less than 0.01), and transitional (23 +/- 3 pmol) (p less than 0.01) regions. TxA2 formation by NAS and SVS was not detected (less than 10 pmol). CGS 13080 inhibited TxA2 formation by CES below the limits of detection. Incubation of 1.9 x 10(5) intact platelets with 10 mumol/L of PGH2 formed a quantity of TxA2 equal to that of CES ulceration.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostacyclin, thromboxane A2, and prostaglandin E2 formation in atherosclerotic human carotid artery.

Prostaglandin (PG) formation in 16 atherosclerotic human carotid endarterectomy specimens was compared systematically with that of normal carotid artery from seven white pigs and six rhesus monkeys. Prostacyclin (PGI2) formation (picomoles 6-keto-PGF1a/2 min/100 micrograms homogenate protein plus 2 mM glutathione [GSH]) of nonatheromatous intima adjacent proximal (276 +/- 32, mean +/- SEM) or distal (271 +/- 14) to carotid plaque was comparable to that of normal carotid artery from white pig (272 +/- 25, NS) and rhesus monkey (219 +/- 41, NS), and was greater than stenotic intima (156 +/- 17, p less than 0.01), subintimal plaque (168 +/- 14, p less than 0.01), and ulceration (65 +/- 16, p less than 0.01). GSH modulated PGI2 synthesis in all carotid specimens except areas of ulceration (p less than 0.05), but did not restore PGI2 formation in atheromatous fractions to basal level. No detectable arterial thromboxane A2 (TXA2) formation or GSH-dependent PGE2 isomerase activity was observed. The decrement in atherosclerotic carotid artery PGI2 formation was focal (confined to the plaque) and may have been related to loss of effective GSH modulation. These conditions could contribute to a localized imbalance between arterial PGI2 and platelet TXA2 with adverse vascular thromboregulatory consequences.

Risk of infection following penetrating abdominal trauma: a selective review.

Post-operative infectious complications following penetrating abdominal trauma are a major cause of morbidity and contribute significantly to increased length of hospitalization and costs of patient care. Our recent study suggests the individual patient's probability of major infection following traumatic intestinal perforation is high and can be predicted from risk factors identified at the time of surgery. The determinant of primary importance for development of infection confirmed by this study is peritoneal contamination by intestinal contents. Other significant risk factors (p less than 0.05) were number of organs injured, number of units of blood administered, ostomy formation for left colon injury, and the patient's age. Risk of infection can be calculated from these data and could potentially be used to guide post-operative decisions. Areas of trauma care in which alteration of therapy might result in significant savings include choice of antibiotics, duration of antibiotic administration, and wound management. This study supports the use of standardized operative procedures and parenteral antibiotics effective against endogenous aerobic and anaerobic organisms. If such observations continue to be supported by further randomized prospective studies, there is tremendous potential to further tailor surgical management for the individual patient in a more cost-effective manner.

Prostacyclin synthetase activity in human diabetic and nondiabetic vascular tissue.

A decrease in the formation of prostacyclin (PGI2), a potent vasodilating and platelet antiaggregatory substance, has been implicated in the pathogenesis of diabetic vasculopathy. This defect, as well as others, may contribute to imbalances in the thrombo-regulatory system resulting in enhanced platelet aggregability, accelerated atherosclerosis, and subsequent vessel injury. Until recently the major thrust of relevant literature has been directed toward abnormalities in PGI2 quantity or function in vascular tissue from experimentally induced diabetic animal models. For the past 2 years our laboratory has studied prostaglandin metabolism in human diabetic and nondiabetic blood vessels. We determined prostacyclin synthetase (PGI2ase) activity in saphenous veins of diabetic and nondiabetic patients (HSV-D and HSV-ND) undergoing coronary artery bypass grafts and in tibial arteries and tibial veins of diabetic patients (HTA-D and HTV-D) and nondiabetic patients (HTA-ND and HTV-ND) undergoing limb amputation for arterial disease of the lower extremity. Carbon 14-labeled prostaglandin endoperoxide (PGH2) was incubated for 2 minutes with vascular microsomal protein. The products were separated via thin-layer chromatography and quantified by radiochromatographic scan. PGI2ase activity was determined by the formation of 6-keto-PGF1 alpha, the stable breakdown product of PGI2. Results of this study indicate that the microsomal fractions of all vascular tissues studied contain an active PGI2ase capable of forming PGI2; formation is enzymatic, as the amount of product increased with increasing microsomal protein concentration; there is no significant difference in PGI2ase activity between HSV-D and HSV-ND; PGI2ase activity in HTA-D and HTV-D is less than in HSV-D and HSV-ND.(ABSTRACT TRUNCATED AT 250 WORDS)