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Biomedical subjects

G R Phillips

Publications and source records attributed to G R Phillips.

24 records · Page 2Linked to original sources

Late complications of revascularization for radiation-induced arterial disease.

During a 14-year period 23 patients underwent 25 revascularizations for radiation-induced arterial obstructive disease. An average of 5000 rads was delivered, 3 to 24 (mean 9) years before arterial insufficiency, for malignancies of the following origin: gynecologic (n = 9), lymphoma (n = 7), head and neck (n = 5), testicular (n = 1), and lower extremity sarcoma (n = 1). Arterial occlusive disease occurred in the aortic arch vessels (n = 8), visceral aortic vessels (n = 1), and aortofemoral vessels (n = 16). Presenting symptoms were claudication (n = 8), rest pain or nonhealing ulcers (n = 7), transient ischemic attacks (n = 6), asymptomatic bruit (n = 1), and renal insufficiency (n = 1). Reconstructive operations included anatomic bypass (n = 10), extra-anatomic bypass (n = 4), patch angioplasty (n = 5), endarterectomy (n = 3), and resection with interposition graft (n = 1). In this group of patients there were no major perioperative wound complications or other major radiation-associated morbidity. Five patients had late graft infections that manifested from 2 to 5 years after surgery. All occurred in anatomic regions where the bypass graft passed through previously irradiated tissues. Presenting symptoms of infection included a draining groin sinus (n = 3) or soft tissue abscess (n = 2). In all cases the graft had not incorporated into the surrounding tissues when passing through the irradiated area. Treatment included graft excision and extra-anatomic bypass through nonirradiated tissue. One patient died of systemic sepsis. Vascular reconstructive surgery can safely be performed for radiation-induced arterial disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial Occlusive Diseases↗

Potentiation of the protective effects of a converting enzyme inhibitor and a thromboxane synthetase inhibitor in hemorrhagic shock.

The effect of a specific inhibitor of thromboxane (Tx) A2 synthesis, CGS-13080, a new angiotensin converting enzyme inhibitor, CGS-16617, and a combination of both drugs was studied in hemorrhagic shock in rats. Treatment with CGS-16617 (1 microgram/kg) or CGS-13080 (200 micrograms/kg) alone did not alter significantly postoligemic hypotension or the increase in plasma cathepsin D activity in shocked rats, compared with hemorrhaged rats receiving only their vehicle. Combined treatment with both drugs maintained postreinfusion mean arterial blood pressure and attenuated the increase in plasma cathepsin D activity in hemorrhaged rats. Treatment of shocked rats with each drug alone attenuated the accumulation of a myocardial depressant factor activity in the plasma, but the lowest myocardial depressant factor activities were observed in rats treated with the drug combination. Additionally, animals treated with the drug combination exhibited significantly longer postreinfusion survival times than rats receiving either the vehicle (P less than .01), CGS-16617 (P less than .05) or CGS-13080 (P less than .02). CGS-16617 (1 microgram/kg) attenuated significantly the pressor response to angiotensin I throughout the shock period. CGS-13080 attenuated the increase in TxB2 plasma concentrations in shock when compared with hemorrhaged rats receiving the vehicle (P less than .05). Greater attenuation of TxB2 was found after treatment with the drug combination (P less than .01 from vehicle, P less than .05 from CGS-13080 alone). CGS-16617, but not CGS-13080, was also found to have a direct antiproteolytic action in pancreatic homogenates. However, the drug combination (CGS-16617 and CGS-13080) decreased proteolytic activity even further (P less than .001) from CGS-16617 alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗

Protective action of a thromboxane synthetase inhibitor in preventing extension of infarct size in acute myocardial infarction.

U-63,557A, a new selective thromboxane synthetase inhibitor, was evaluated for its ability to prevent the extension of myocardial infarct size. Left coronary arteries of male Sprague-Dawley rats (230 - 270 g) were acutely ligated, producing a consistent model of myocardial infarction (MI) in rats analyzed 48 hours later. Left ventricular free wall (LVFW), creatine kinase (CK) activity, and amino-nitrogen concentrations were assayed as indices of infarct size. U-63,557A was administered intravenously in two doses (4 and 8 mg/kg) with a split schedule (2 min post-ischemia and either 4 or 24 hrs later). Administration of the thromboxane synthetase inhibitor significantly reduced both myocardial CK and amino-nitrogen loss at a dose of 8 mg/kg, but it was only slightly effective at 4 mg/kg. Drug treatment significantly increased the percent LVFW spared; 27 +/- 3% (vehicle) vs 43 +/- 7% and 52 +/- 7% (8 mg/kg). U-63,557A is an effective agent in myocardial ischemia for limiting the extension of infarct size after acute coronary artery ligation. Previous studies of other thromboxane synthetase inhibitors showed effectiveness in the early stages of MI. This study shows an effect on true infarct size 48 hours post-ligation, and suggests that inhibition of thromboxane A2 plays an important role in the pathogenesis of ischemic damage in the myocardium.

Animals↗

Mercury accumulation in and growth rate of rainbow trout, Salmo gairdneri, stocked in an eastern Oregon reservoir.

Mercury concentrations in lateral muscle tissue from rainbow trout (Salmo gairdneri) stocked in a mercury contaminated eastern Oregon reservoir increased linearly during the first five months that the fish were in the reservoir, followed by a leveling off period during which the mercury uptake curve became nearly asymptotic after eight months. In addition, the mean mercury concentrations present in three year classes of trout which had lived in the reservior for 7, 19, and 31 months, respectively, were not significantly different, indicating that the uptake curve remains nearly asymptotic indefinitely. The shape of the curve is believed to be a result of exchange equilibria between water and tissue and factors that influence fish metabolism. It is estimated that 0.05 microgram Hg/L of methylmercury in water would have accounted for all of the methylmercury accumulated by trout in the reservoir. Growth rates (mg/g per day) of trout in the reservoir ranged from 0.7 in December to 39.7 in April, resulting in food consumption rate estimates ranging from 25 to 140 mg/g per day.

Animals↗