PubMed Health⌕ Search

Biomedical subjects

C G Mellow

Publications and source records attributed to C G Mellow.

25 records · Page 2Linked to original sources
PubMed1990

Effect of a thromboxane synthetase inhibitor UK-38,485 on the tolerance of skin flaps of primary ischaemia.

The harmful effects of ischaemia or skin flaps were modified using the thromboxane synthetase inhibitor UK-38,485. The epigastric island flaps of Sprague-Dawley rats (n = 288) were subjected to 10, 12 or 14 h of total pedicle occlusion, or 3, 5 or 7 h of venous occlusion of the sole vascular pedicle. Within each time period, rats received intravenous doses of either physiological saline (controls) or UK-38,485 at the beginning or end of the ischaemic episode. Flaps treated with UK-38,485 overall had a higher survival rate than control ischaemic flaps (P less than 0.001). This applied both to total (arterial) ischaemia (P less than 0.001) and partial (venous) ischaemia (P less than 0.01). There was no significant difference between treatment given at the beginning or at the end of the ischaemic episode. These results may be explained by reduced platelet aggregation and thrombosis in the microvasculature due to the lower thromboxane/prostacyclin ratios for treated flaps. The possible inter-relationship of the prostanoids with free radical mechanisms in the no-reflow phenomenon is also discussed.

Animals↗
PubMed1990

Secondary ischemia time in rodents: contrasting complete pedicle interruption with venous obstruction.

The current study investigated the effect of secondary ischemic insults on ultimate flap survival. Rodent skin flaps subjected to 8 hours of secondary ischemia with total pedicle obstruction had 56 percent survival (7 of 12) compared with primary ischemic flaps of the same time, which all survived. At 10 hours of ischemia, only 42 percent of secondary ischemic flaps survived compared with 67 percent (8 of 12) of primary ischemic flaps. When the secondary ischemia was caused by venous obstruction, the results were even more striking. Ninety-two percent (11 of 12) of primary venous obstruction flaps survived 3 hours of ischemia and 75 percent (9 of 12) survived 5 hours of ischemia, while only 56 percent (7 of 12) and 8 percent (1 of 12) of flaps subjected to secondary venous obstruction survived at the same times, respectively. The explanation of these observations on the basis of tissue pathophysiologic changes will require further study. The results support the need for close monitoring of clinical flaps to ensure optimal survival.

Animals↗
PubMed1989

The effect of deferoxamine on tolerance to secondary ischaemia caused by venous obstruction.

The current study investigated the efficacy of deferoxamine for treating secondary ischaemia due to venous obstruction in a rodent epigastric pedicle flap model. Rats receiving one dose of the free radical scavenger and iron chelator deferoxamine (150 mg/kg) intravenously prior to reperfusion had a mild improvement in flap survival: 46% in controls, 77% in deferoxamine-treated. This was statistically significant at p less than 0.05 (chi 2 = 5.2). This suggests that free radicals are partly involved in the mechanism of ischaemia/reperfusion injury in secondary ischaemia, as has been previously demonstrated for primary ischaemia (Angel et al., 1986b). Supporting biochemical evidence will be necessary to understand better the mechanisms involved in secondary ischaemia.

Animals↗
PubMed1989

Prior elevation of vascular island skin flaps: intolerance to ischemia caused by venous obstruction.

Previous experiments in our laboratory have shown that prior elevated flaps, those elevated 24 hr prior to complete ischemia, are more tolerant of the ischemic insult than acutely ischemic flaps that have had no prior elevation. In the current study, the effect of prior elevation was observed on tolerance to ischemia caused by venous occlusion alone. Under these conditions, limited blood flow may be possible via the unclamped artery, so a state of partial ischemia exists. After seven hours of venous obstruction, acutely elevated flaps had a 50 percent survival rate at postoperative day 7. This was significantly better (p less than 0.005, chi 2 test) than the 0 percent survival rate for prior elevated flaps for the same period of venous obstruction. It is speculated that the more rapid generation of cytotoxic free radicals during the period of partial ischemia is more detrimental to the prior elevated flaps that have greater blood flow, than to the controls.

Animals↗
PubMed1989

The effect of time of vascular island skin flap elevation on tolerance to warm ischemia.

The effect of time of vascular island skin flap elevation on tolerance to a subsequent 12-hour period of warm ischemia was studied. Sixty rats were separated into five equal groups; the rat epigastric island flap was used as the model. In group 1 flaps were elevated and immediately subjected to 12 hours of complete ischemia by application of microvascular clamps to both artery and vein of the pedicle. In group 2 the flap was elevated, and after 12 hours of recovery ischemia was induced for 12 hours. Groups 3 to 5 were similar to group 2 except that the time interval between initial elevation and subsequent ischemia varied: 24 hours for group 3; 72 hours for group 4; 144 hours for group 5. Necrosis was evaluated on postoperative day 7. Those flaps elevated 24 hours before ischemic insult (group 3) had significantly better survival than all other groups (p less than 0.025 at least). There were no significant differences between the other groups. Flap elevation 24 hours before a complete ischemic episode significantly increased tolerance to ischemia. Elevating a flap earlier or later than 24 hours did not have any significant benefit.

Animals↗
PubMed1989

The effect of prior elevation of skin flaps and ischemia on blood thromboxane levels.

The physiological factors that allow for the survival of ischemic skin flaps have not been clearly elucidated. Previous work by others has shown that elevation of a flap 24 hours before an episode of complete ischemia significantly improved survival, presumably by delaying the onset of the no-reflow phenomenon. The current study, using an epigastric flap, investigated the role of thromboxane in these events by observing postischemic plasma levels of thromboxane B2, the stable metabolite of the short-lived thromboxane A2. Acutely ischemic flaps were compared with those elevated 24 hours before ischemia. After the ischemic insult, blood was drawn from the venous effluent of the flaps. Thromboxane levels after 4 hours of ischemia were significantly decreased (p less than 0.001) in the postischemic period in those flaps elevated 24 hours before ischemia compared with flaps that had undergone ischemia acutely. Moreover, acutely ischemic flaps had significantly more thromboxane than nonischemic controls (p less than 0.001). These results confirm the importance of thromboxane metabolism in the no-reflow phenomenon.

Animals↗