Restoration of elbow flexion and arm contour with the latissimus dorsi myocutaneous flap.
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Biomedical subjects
Publications and source records attributed to E S Wheeler.
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Familial lymphedema should be classified in two categories depending on onset. Milroy's disease, or congenital hereditary lymphedema, is present from birth, painless, without tendency to ulcerate, and may have cholestasis or intestinal lymphangiectasia associated with it. Meige's disease, hereditary lymphedema praecox, is lymphedema with onset in the first or second decade, often presenting with inflammation, and may have a number of associated related anomalies including distichiasis, extradural cysts, vertebral anomalies, cerebrovascular malformation, yellow nails, and sensorineural hearing loss. Both types follow an autosomal dominant pattern. This paper presents a family of 39 persons in 5 generations with 13 affected persons having Meige's disease. The importance of recognizing this type of familial lymphedema is discussed.
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Concentrations of prostaglandin E1 (PGE1; 10(-7) M) that do not elicit tension responses in aortic strips potentiate contractions induced by submaximal concentrations (10(-8)-10(-7) M) of norepinephrine (NE) or angiotensin III (Ang III) but not those of high K+ depolarization or maximal NE or Ang III concentrations. Higher concentrations of PGE1 (10(-6) M and above) initiate contractions which are additive with submaximal responses to NE and Ang III but not to K+. These same concentrations of PGE1 also decrease 45Ca retention at high affinity La+++-resistant sites in a manner similar to but not additive with NE and Ang III. Uptake of 45Ca at low affinity La+++-resistant sites (which is increased by high K+-depolarization) is not altered by 10(-6) M PGE1. The effects of PGE1 are not altered by decreased extracellular Ca++ (0.1 mM), decreased temperature, phentolamine or meclofenamate. Thus, PGE1 does not appear to increase uptake of extracellular Ca++ in this smooth muscle tissue. Instead, PGE1 increases mobilization of Ca++ from the same high affinity La+++-resistant sites affected by Ang III and NE and, in this manner, may increase responses to these two stimulatory agents.
Divalent ion chelators (EDTA, EGTA) were found to remove 45Ca from high-affinity binding sites in isolated rabbit aortic smooth muscle in a concentration-dependent manner. Measurement of 14C-labeled EDTA uptake (10 to 60-min incubation periods) yielded tissue/medium ratios equivalent to the extracellular space [14C]-sucrose tissue/medium ratio). Addition of high EDTA concentrations (0.5--1.5 mM) elicits large but reversible increases in 45Ca efflux, rapidly removes virtually all 45Ca from muscles previously incubated with 45Ca for as short a time as 7 min (filling of extracellular and superficial sites) or as long as 180 min (more complete equilibration of 45Ca), and blocks the norepinephrine-induced contractile response (this response is only partially inhibited by 0.05 mM EDTA, a concentration too low to remove most of the 45Ca present). Furthermore, phosphatidyl serine, a compound known to decrease exchangeability of 45Ca in this tissue, inhibits the EDTA-induced increase in 45Ca loss. Thus, those slowly depleted Ca++ stores that are important for the contractile action of norepinephrine are removed by EDTA even though this chelator is confined to the extracellular space. Possibly, release or removal of high-affinity Ca++ is regulated by EDTA-accessible Ca++ bound at relatively superficial membrane sites.
A laboratory model for study of possible reinnervation at the muscle level is presented. The preliminary histochemical results suggest that muscular neurotization occurs following removal of the investing fascia. However, the muscle atrophy (which follows denervation) continues to take place in spite of such reinnervation. The potential clinical relevance of these findings to free muscle grafting is discussed.
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We present a controlled study that indicates faster epithelialization of blister-removed second-degree burn wounds in guinea pigs treated with hyperbaric oxygen (HBO). Assessment of vascularity by india ink perfusion indicated earlier return of capillary patency in the HBO-treated group. An examination of the question of a comparative increase in DNA synthetic activity in the HBO-treated animals showed a slightly higher absolute ratio of labeled to unlabeled cells, but the difference was not statistically significant. It is likely that the mechanisms whereby HBO influenced the above events were mediated not only by increased oxygen delivery, but by increased atmospheric pressure on the wound.
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A reproducible partial-thickness burn was inflicted on 100 albino guinea pigs. With the blister intact, the evaporative water loss from the burn surface was essentially the same as from normal unburned skin. When the blister was removed, the rate of water loss was initially more than 100 times normal, and it remained 20 to 50 times the normal rate throughout the first week. This high rate of water loss was associated with an increasing depth of wound destruction (from dehydration) and a thickening of the overlying crust. Microscopic examination showed that previously viable dermis was incorporated in this crust. The depth of dermal loss was negligible when the blister was left intact, and improved healing resulted. We believe it is important to leave burn blisters intact, whenever possible.
Split thickness tangential excision is a simple means of tattoo removal with very acceptable cosmetic results. The technique has several advantages. (1) The depth of skin removal may accurately be controlled as the tattoo pigment is excised with a dermatome. The major portion, if not all of the remaining pigment, is extruded and sloughs with the crust. (2) Scar formation, if it occurs at all, is negligible. (3) No donor site is created. (4) The procedure may be carried out rapidly without admitting patients to hospital, is inexpensive for patients and conserves time for physicians.
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