Biomedical subjects
Publications and source records attributed to B M O'Brien.
A case is reported of the immediate transfer of a free flap to the lateral pelvic wall utilising radial wrist vessels as a temporary vascular supply as no recipient pelvic vessels were available for anastomosis.
Microvascular blood flow was measured by a laser Doppler flowmeter in rabbit epigastric island flaps made ischemic at 37 degrees C for either 6.5 hr (Group 1; n = 13) or 17.5 hr (Group 2; n = 4). Contralateral flaps raised without ischemia were used as controls. The survival of ischemic flaps in these groups at 7 days was 69 and 0%, respectively. After 6.5 hr of ischemia, microvascular blood flow in the ischemic flap was approximately 20% below that in the control flap for the first 3-4 days postoperatively, presumably reflecting ischemic damage to parts of the cutaneous microcirculation; thereafter, flow was not significantly different from controls up to 7 days postoperatively. Failed 6.5-hr ischemic flaps had initial sluggish blood flow which slowed to zero usually within 4 days postoperatively. After 17.5 hr ischemia, negligible microvascular flow was detectable postoperatively. Failure in the microcirculation as detected by the flowmeter occurred well in advance of any noticeable physical changes in the flap. It is concluded that the percentage ischemic flap flow of control flap flow for each animal (at any selected time up to 24 hr after revascularization) reliably predicts the viability of the flap after 7 days.
The levels of the stable degradation products of prostacyclin (PGI2) and thromboxane A2 (TXA2): 6-oxo-prostaglandin E1 alpha (6-oxo-PGE1 alpha) and thromboxane B2 (TXB2) respectively were determined in the effluent of the rabbit epigastric skin flap after infusion of exogenous arachidonic acid. The blood to the flap passes through the microcirculation and thus the changes in eicosanoid biosynthesis in this part of the vasculature were recorded. The aim was to use inhibitors of arachidonic acid metabolism to increase the PGI2/TXA2 ratio. This may be potentially beneficial to ischaemic skin flaps by reducing platelet aggregation associated with damaged microvascular endothelium, overcoming vasospasm and increasing microvascular blood flow. Increased PGI2/TXA2 ratios (up to 5-fold) were best achieved using TXA2 synthetase inhibitors such as dazoxiben hydrochloride. These were significantly more potent than the phosphodiesterase inhibitor dipyridamole, and the lipoxygenase inhibitor Bay g6575. No increase in blood flow was achieved. The cyclooxygenase inhibitor indomethacin did slow the blood flow at high concentrations (above 10(-5) M), and inhibited both PGI2 and TXA2 synthesis. Approximately 2-fold higher concentrations of dazoxiben hydrochloride and dipyridamole were required to produce the same TXA2 synthetase inhibition in the flap microvasculature in vivo compared with platelets in vitro.
An evaluation of the effect of ischaemia upon the intraluminal pH of microvascular free jejunal autografts was undertaken with a view to developing a monitoring system to be used clinically. Employing a canine model, the intraluminal pH of isolated jejunal segments was measured during normal perfusion and under conditions of arterial and venous occlusion. Ischaemia induced a rapid, easily measured fall in intraluminal pH reversible after 1 h of normothermic ischaemia. The most rapid pH change occurred within the first 10 min. It is felt that continuous intraluminal pH measurement may form a reliable method of monitoring the postoperative vascular perfusion of clinical free jejunal transfers.
Five centimetres long segments of 3 mm internal diameter synthetic expanded polytetrafluorethylene (E-PTFE) vascular graft (Gore-Tex) were implanted into the femoral arteries, proximal to the origin of the saphenous artery, of 10 mongrel dogs. In five cases saphenous island flaps were raised and the femoral artery was ligated distal to the saphenous origin so that a low flow system was created through the graft. In 10 femoral vessels the Gore-Tex graft was inserted without raising a flap and the distal femoral artery not ligated so that the graft acted purely as a conduit for blood flow to the distal limb. This created a high flow rate model compared to the reduced flow in the former group. In the first group flap survival was evaluated daily by direct observation of the flaps and graft patency was assessed every 48 h by means of Doppler ultrasound. None of these flaps survived longer then 48 h. In the second group, graft patency was monitored every 48 h with Doppler ultrasound and exploration of Gore-Tex grafts at 3 weeks showed that all had thrombosed.
Obstructive lymphedema is a pathologic condition resulting in the accumulation and stagnation of serum proteins in the lymphatics and interstitial spaces. In a canine model of obstructive lymphedema, one limb was rendered lymphedematous, and various biochemical parameters were determined in this and an unaffected control limb. Both lymph and interstitial fluid had significantly decreased acid proteinase activity (comprising mostly cathepsin D-like enzymes) and neutral proteinase activity (comprising metallo, sulfhydryl, and serine proteinases, and collagenase). Possible reasons for these decreases could be: (1) saturation of macrophages and their surrounding environment with whole or partially digested proteins, or (2) elevation in the levels of circulating inhibitors like alpha 2-macroglobulin. The lymphedematous skin was significantly thicker than control skin and had elevated levels of collagen. However, unlike some fibrotic conditions, the relative proportions of types I, III, and V collagen, as determined by pepsin solubilization and neutral salt fractionation of the collagen fibrils, were similar to those found in normal skin. It is speculated that a decrease in the breakdown of collagen by collagenase and a continuing synthesis of collagen by fibroblasts led to an imbalance in favor of collagen deposition in the skin.
It has been shown that during expansion there is a component of migration of surrounding tissue that probably contributes to the available tissue in local reconstructive procedures. Although there is a 63 per cent increase through expansion of a given flap with a particular expander, this results in only a 30 per cent increase after elevation and inset. This increase is basically maintained for a 3- or 4-month period. The 56 per cent decrease in area probably results from contraction of the extensible skin. The 30 per cent that remains probably results from a combination of stretch evidenced by reorientation, along with an increase in the cellular and extracellular components of expanded tissue. Therefore, there are components of both loan and dividend in tissue expansion. This further understanding should be helpful in the planning of tissue expansion. (Editors' note: Although there may be some element of "loan" initially, from peripheral regions, no thinning of the periphery has been observed. To the contrary, the periphery appears normal. It is likely that transient thinning of the periphery causes increased mitotic activity, and that this area is also made to produce a "dividend" ultimately. Unless permanent thinning can be documented, the "dividend hypothesis" remains valid.
The cutaneous microvascular flow of the rabbit epigastric island flap under the influence of various prostanoid modifiers has been determined semiquantitatively with a Laser Doppler flowmeter. Infused prostacyclin, diluted with arterial blood to an estimated concentration of 2.5 ng/ml in the microvasculature, increased the microvascular blood flow to approximately 130% of the buffer control. The three thromboxane synthetase inhibitors tested--dazoxiben hydrochloride, UK-38,485, and 7-(1-imidazolyl) heptanoic acid--at concentrations up to 3 X 10(-5) M in the microvasculature, failed to induce any change in blood flow compared to a control neutral-buffered saline infusion. Preliminary results also found that the lipoxygenase inhibitor Bay g6575 did not alter microvascular flow up to 7 X 10(-6) M, but the prostacyclin analog carbacyclin at 30 ng/ml in the microvasculature induced a similar response to 2.5 ng/ml prostacyclin. While such responses are well known for the major vessels, this is one of the few reports with semiquantitative data on the influence of prostanoid synthesis modifiers on blood flow for the microcirculation.
Twenty toe-to-hand transfers in 17 patients with an average follow-up of 54 months have been reviewed to quantify hand function and donor morbidity. Eleven toe-to-thumb and nine toe-to-finger procedures were performed. Surgical and follow-up data were available for all patients. Twelve patients (14 procedures) were reviewed in detail, with particular attention given to foot and hand function. Total active motion after toe-to-thumb transfer was 48 degrees and 106 degrees after toe-to-finger transfer. Two-point discrimination was less than or equal to 15 mm in 13 digits (65%). Grip and pinch power were related to the number of digits present on the reconstructed hand and to the presence or absence of functioning thenar muscles. Eleven of 12 patients can walk and run normally (mean of 5 years after surgery). Six (50%) cannot wear thongs or heavy boots, but all can wear normal shoes. The transferred great toe decreased in volume by an average of 10% over the years since the operation. Transferred toes became useful digits in the hand, and foot morbidity was minor and not progressive.
To determine the end point of histopathologic damage in avulsed arteries, the forearm arteries of five monkeys being sacrificed were avulsed longitudinally and samples of proximal and distal arteries prepared for light microscopy and transmission and scanning electron microscopy. A severe and consistent circumferential skip lesion was found on the luminal surface involving the intima and media. In 30 percent of vessels, histopathologic damage extended more than 3.0 cm from the rupture point. Similar circumferential tears occurred on the luminal surface of resected human avulsed arteries collected at the time of replantation surgery. No consistent lesions were noted in resected veins from human avulsed amputations. It is possible that in the human artery (as in the monkey) circumferential lesions frequently extend many centimeters from the rupture point and therefore beyond resection distances. Lesions present in the vessel after resection and microsurgical repair might be the site of thrombosis and subsequent occlusion.
Seventy femoral arterial avulsions with interpositional microvenous graft repairs were performed in rabbits and were divided into three groups. In Group A clamps were reapplied for 15 minutes with an overall patency rate of 97% after 3 weeks. The overall patency rate in Group B with 30 minutes reclamping was 93% three weeks later. Group C without clamping served as Controls and a 100% patency rate was achieved. The position of the microclamps, static blood in the region of the anastomoses and in the microvenous grafts as well as the time of reclamping up to 30 minutes did not influence the patency rate in damaged vessels after sufficient resection of injured vessel walls. The results of this experiment suggest that if necessary clamps can be reapplied safely in the clinical situation for up to 30 minutes after microvenous grafts have been completed to enable the microsurgeon to perform further dissection in a bloodless field.
A comparison was made between operating microscope observations and histopathological examination of the ruptured ends of experimentally avulsed rabbit femoral arteries and veins. Under the operating microscope no damage was evident in arteries or veins more than 0.8 cm (on average) from the rupture site, the common lesions being tears, holes, bruising, sleeving and dilatations. In light microscope and electron microscope studies arterial and venous lesions were often noted up to 4 cm from the rupture site both proximally and distally. Severe circumferential skip lesions involving the tunica intima and media in the arteries were noted, and commonly deep clefts also extended through all three tunicae at arterial bifurcations. In avulsed veins complete tears through all tunicae or partial loss of intima and media were observed. The extensive nature of these lesions is the most likely reason for the lower success rate of avulsed digits in replantation surgery.
Prostacyclin was investigated for its ability to overcome surgically induced spasm of the femoral artery and to increase blood flow through the rabbit epigastric free flap. Topical prostacyclin (200 ng/ml) and lignocaine (20 mg/ml or 2%) each produced near-maximal vasodilatation of large conducting vessels. This resulted in a significant increase in blood flow after 5 minutes for each form of topical treatment, compared to a saline control. However the vasodilatation obtained from lignocaine tended to wear off over 30 minutes. Treatment with systemic indomethacin did not prevent surgical spasm nor the action of prostacyclin in relieving it. Topical 6-oxo-prostaglandin F1 alpha, the major breakdown metabolite of prostacyclin, was not responsible for the vasodilatory action of prostacyclin. Topical prostacyclin (200 ng/ml) also caused platelet disaggregation and some rebleeding from the anastomotic site, nevertheless there was no significant difference in flap survival between the use of topical prostacyclin and topical lignocaine.
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The rabbit epigastric free flap was used to investigate the effect of prostacyclin and drugs modifying its synthesis in vivo on microvascular blood flow. Prostacyclin and its analogue carbacyclin caused an increase in flow with a maximal twofold increase at approximately 6.5 and 250 ng/ml, respectively, in the flap. Thromboxane synthetase inhibitors such as dazoxiben hydrochloride, UK-38,485, 7-IHA, and imidazole (up to 7 X 10(-4) M in the flap) as well as the prostaglandins 6-oxo-PGF1 alpha and PGE2 (up to 3.7 and 9.2 ng/ml, respectively, in the flap) all failed to modify the control flow rate in the cutaneous microcirculation. It is concluded that the vasodilatory properties of prostacyclin and carbacyclin, together with their known platelet antiaggregatory properties, warrant further study in problem areas of microsurgery such as flap ischemia. The use of thromboxane synthetase inhibitors had no demonstrable effect on the normal flap, and their effect on the ischemic flap remains to be investigated.
The viability of the rabbit epigastric flap was investigated after a period of cold ischemia of 3, 4, or 5 days. Groups of flaps were either perfused with Ross's solution before ischemia (early perfusion), after ischemia (late perfusion), or not at all (control). Significantly more flap necrosis was formed at exploration 7 days after revascularization in the early perfusion group than in the control group (p less than 0.01). Late perfusion was not significantly detrimental to flap survival as compared with cold storage alone (0.1 less than p less than 0.5). It is concluded that early perfusion is detrimental to the ultimate fate of the cold ischemic flap, whereas late perfusion offers no advantage over cold storage alone.
A cortical bone graft on a muscle pedicle was taken from the ulna and transferred to bridge a complete defect of the radius in 16 dogs. In 14 control dogs a free graft was used, that is, one without a muscle pedicle. Union in the group with pedicle grafts was far superior to that in the group with free grafts, mainly because in those with pedicle grafts there was good subperiosteal new bone formation from active viable periosteum. In six of the pedicle grafts the viability of some osteocytes was retained over a 12-week period and in five the graft was almost completely replaced by new bone.
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