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Abnormal venous valvular function may produce venous reflux and venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency. While valvular agenesis is a known, but rare cause of venous insufficiency, little work has been done on the relative number of greater saphenous vein (GSV) valves in patients with venous insufficiency. This study investigates whether the GSV in patients with symptomatic venous insufficiency has fewer valves than the GSV of patients without venous insufficiency. The number of GSV valves in patients (n = 51) with symptomatic venous insufficiency undergoing saphenectomy (VI) were compared with the number of GSV valves in patients (n = 26) without venous insufficiency undergoing in situ GSV bypass under angioscopic surveillance who served as a control group. The two groups differed, as expected, in age and sex distribution. The VI group had a mean of 25.7 +/- 11.0 centimeters of GSV between valves, while the control group had 19.0 +/- 9.7 centimeters of GSV between valves (F = 6.99; p = 0.01). The mean number of valves in the saphenous veins of the two groups also differed significantly: VI = 2.3 +/- 0.83 versus control (CTRL) = 4.8 +/- 2.01 (F = 61.86; p < 0.0001). That properly functioning valve leaflets help maintain physiologic antegrade venous flow is indisputable. This study, however, suggests that the relative lack of valves may be related to the development of venous insufficiency. This report documents that patients with symptomatic reflux in the GSV have significantly fewer valves than patients with apparently normal functioning saphenous veins.

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Chronic venous insufficiency which produces lipodermatosclerosis, varicosities, or ulceration, is frequently caused by superficial venous reflux and deep venous incompetence. The anatomy of venous insufficiency has been clarified with duplex ultrasound, thus allowing appropriately directed therapy. However, postoperative venous physiology in patients undergoing superficial venous ablation has been infrequently reported. This study was undertaken to document the effect of superficial venous ablation on deep venous reflux. Between April 1994 and May 1995, 45 patients were examined preoperatively with duplex ultrasound. All patients had symptomatic venous insufficiency and were found to have greater saphenous vein reflux. Clinical classification of venous insufficiency (according to the criteria of the joint councils of the vascular societies) included class I in 30 patients, class II in 12, and class III in 3. Seventeen patients (38%) had reflux in the femoral venous system in addition to superficial reflux. All patients underwent removal of the proximal greater saphenous vein in concert with multiple stab avulsions of identified varicosities. Postoperative interrogation of the venous system revealed that in 16 (94%) of 17 patients, coexistent femoral venous insufficiency completely resolved. Thus ablation of superficial venous reflux eliminated incompetence in the deep venous system in patients with combined disease. These preliminary results suggest that superficial venous incompetence may be a cause of deep venous insufficiency. Whereas alternative methods to correct deep venous insufficiency have met with limited success, it appears that saphenectomy (when combined disease is present) may be effective in correction of deep venous reflux.

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A new method for arresting uncontrollable intercostal hemorrhage is presented. It consists of selective transcatheter embolization of the bleeding artery, either by pieces of gel foam or autologous blood clots. In the patient presented in this paper, the hemorrhage was identified and successfully controlled by embolizing the bleeding artery. Thoracotomy was unnecessary, and there were no complications related to the procedure.

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Trained dogs with chronically implanted catheters and left ventricular (LV) pressure transducers were anesthetized with 2.3 per cent (1 + MAC) and 3.6 per cent enflurane. Left ventricular function and metabolism were studied while the dogs were awake and during exposure to the two anesthetic concentrations. Enflurane depressed LV function in a dose-dependent fashion. Myocardial blood flow and oxygenation mirrored the functional changes. Myocardial oxygen extraction decreased and lactate extraction increased to the myocardium. Low concentrations of halothane in the same dogs on different days had similar effects. However, 2 MAC halothane resembled 1.6 MAC enflurane, suggesting that the cardiovascular dose-effect curve for enflurane is steeper than that for halothane. Both anesthetics produce dose-dependent negative inotropic effects in the intact dog, accompanied by equivalent decreases in cardiac oxygen demand. Contrary to previous suggestions, enflurane appears to be at least at depressant to the dog heart as halothane.

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Halothane, methoxyflurane, and enflurane produce dose-dependent depression in ventricular function in the dog. Myocardial blood flow and oxygen consumption are decreased accordingly without evidence of myocardial tissue hypoxia. Low-dose fluoxene does not depress the heart, while there is less depression with high-dose fluroxene than with the other anesthetics. In spite of this depression, myocardial blood flow was unchanged, and the decreased oxygen consumption during high-dose fluroxene was a result of decreased oxygen extraction by the heart. Sympathetic nervous system stimulation produced by fluroxene anesthesia is probably responsible for these effects, but further work is necessary for confirmation of this hypothesis.

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Chronically catheterized dogs were studied awake and during anesthesia with high and low concentrations of halothane to assess the relationship between cardiac function and metabolism. Low concentrations of halothane (0.79 per cent endtidal) increased heart rate and decreased left ventricular stroke volume, stroke work, and dP/dt without producing other hemodynamic changes. However, similar heart rate increases produced by atrial pacing in awake animals increased aortic pressure and cardiac output and decreased left atrial pressure. Consequently, the halothane-induced tachycardia partially compensated for the negative inotropic effect of the halothane. High concentrations of halothane (1.74 per cent endtidal) further increased heart rate and elevated left atrial pressures. Cardiac output, stroke volume, stroke work, aortic pressure, LV dP/dt, myocardial blood flow and oxygen consumption were markedly decreased. Myocardial glucose extraction was also decreased. Myocardial oxygen extraction was unchanged, and lactate extraction rose with both concentrations of halothane. Consequently, the dose-dependent negative inotropic effect of halothane resulted in a decrease in cardiac oxygen demand which was equal to or greater than the decrease in oxygen delivery. Whether the same relationship would be seen in the ischemic heart is yet to be demonstrated.

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