Functions of melanin.
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Biomedical subjects
Publications and source records attributed to R B Armstrong.
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Adjacent punch biopsy wounds in 20 subjects were treated with a collagen matrix or Monsel's solution. Both techniques were easy to use and were hemostatically effective. The collagen matrix produced less inflammation, had a lower incidence of wound infection, was associated with a faster reepithelialization rate, and healed with a modestly better appearance at four weeks than did Monsel's solution.
The primary objective of this study was to determine if a measurable degree of protective cardiovascular adaptation to hypovolemic shock is developed in response to aerobic training. Twelve rats were trained (T) by running on a rodent treadmill 60 min/day, 5 days/wk at 30 m/min on a 5 degree incline for a period of 13-17 weeks. Elevated levels of SDH activity in the vastus intermedius muscles of the trained group (T) verified physiological training. Each T rat was weight matched with a sedentary untrained (UT) control, anesthetized with sodium pentobarbital, and subjected to a modified Wiggers hemorrhagic shock protocol. The parameters monitored were the maximum reduction in vascular capacitance (ie, maximum blood shed) when MAP was lowered to 30 mm Hg by hemorrhage; the time necessary to achieve maximum blood loss at 30 mm Hg (compensation time); and the time between maximum and 20% uptake of the shed volume from the reservoir (decompensation time). The data show that the initial MAPs for the UT group were significantly higher than the T group (133 +/- 3 mm Hg vs 121 +/- 4 mm Hg). The maximum blood loss normalized to body weight and pressure drop was .268 +/- .012 ml/kg/mm Hg for UT and .343 +/- .02 ml/kg/mm Hg for T (P less than .001), suggesting that T had a better ability to reduce total vascular capacitance. Also, both the compensation and decompensation times were greater in the T than UT groups. These data suggest that treadmill exercise-conditioned rats have a greater inherent cardiovascular compensatory ability than untrained rats.
Solar urticaria is a rare disorder in which patients develop urticarial lesions after exposure to light from the sun or other sources. The etiology is unknown: some cases appear to be mediated by IgE, but other mechanisms may ultimately be found to be more significant. This disease typically persists for years, but may resolve spontaneously. Although fatalities have not yet been reported, episodes of solar urticaria have produced near-fatal accidents. At best, treatment is difficult, but some techniques have afforded some patients substantial or total relief, even if only temporarily.
Phototherapy using 290-320 nm ultraviolet radiation (ultraviolet B) is an effective form of treatment for several skin diseases and is especially useful for psoriasis. Technical advances have made it more economical and convenient to quantify ultraviolet radiation. Ten volunteers received a series of exposures from three ultraviolet B sources to illustrate how variation in the spectral properties of phototherapy devices can lead to unanticipated and potentially severe sunburn reactions. The corresponding minimal erythema dose was then calculated with the use of irradiance data measured with two commercially available photometers. Variation in minimal erythema dose among the three sources tested indicates the need to characterize the emission spectrum of sources and the spectral sensitivity of the photometer used to measure its output.
The most frequently used source of indoor lighting is the fluorescent tube. Although there are major variations in phosphors, the majority of these lamps are safe, efficient, and economical illuminators. These fluorescent light sources are currently our primary source of visible light; however, they emit small amounts of ultraviolet A light (UVA) as well as a somewhat larger percentage of infrared radiation. Photosensitivity diseases have been reported in each of these three broad wavelength bands. Specific examples include heat urticaria from infrared exposure, contact photosensitivity of the phototoxic type following exposure to dyes and visible light, and two relatively rare but disabling conditions from ultraviolet A exposure--solar urticaria and contact photosensitivity of the photoallergic type (persistent light reaction). During the past five years, eight patients with photosensitivity induced by musk ambrette and UVA have been treated at Columbia-Presbyterian Medical Center; six of these have been severely disabled and satisfy the criteria for persistent light reactors. Fifteen patients with solar urticaria have also been observed. Ten of these had reactions in the UVA range. The clinical and laboratory findings of these two groups of patients were presented.
We studied the distribution of blood flow within and among muscles of partially curarized (40-100 micrograms/kg body wt) rats during preexercise and at 1 min of low-speed treadmill exercise (15 m/min). Glycogen loss in the deep red muscles and parts of muscles was significantly reduced in the curarized animals during exercise, indicating the fibers in these muscles were recruited to a lesser extent and/or had lower metabolisms than fibers in the same muscles of control rats. However, elevations in blood flow in the red muscles of the curarized rats were as great or greater than those in the control rats. Thus reduced recruitment and/or metabolism of the deep red muscle fibers of the curarized animals was not accompanied by reduced blood flow. These findings suggest a dissociation between red fiber metabolism and blood flow in the curarized rats during the 1st min of slow treadmill exercise and indicate that release of vasodilator substances or local physical factors associated with muscle fiber activity are not solely responsible for the initial hyperemia during exercise.
We previously studied blood flow distribution within and among rat muscles as a function of speed from walking (15 m/min) through galloping (75 m/min) on a motor-driven treadmill. The results showed that muscle blood flows continued to increase as a function of speed through 75 m/min. The purpose of the present study was to have rats run up to maximal treadmill speeds to determine if blood flows in the muscles reach a plateau as a function of running speed over the animals' normal range of locomotory speeds. Muscle blood flows were measured with radiolabeled microspheres at 1 min of running at 75, 90, and 105 m/min in male Sprague-Dawley rats. The data indicate that even at these relatively high treadmill speeds there was still no clear evidence of a plateau in blood flow in most of the hindlimb muscles. Flows in most muscles continued to increase as a function of speed. These observed patterns of blood flow vs. running speed may have resulted from the rigorous selection of rats that were capable of performing the high-intensity exercise and thus only be representative of a highly specific population of animals. On the other hand, the data could be interpreted to indicate that the cardiovascular potential during exercise is considerably higher in laboratory rats than has normally been assumed and that inadequate blood flow delivery to the muscles does not serve as a major limitation to their locomotory performance.
Fast-twitch-oxidative-glycolytic (FOG), fast-twitch-glycolytic (FG) and slow-twitch-oxidative (SO) fibres are distributed within and among physiological extensor muscles in mammals in predictable patterns. Deep muscles and the deep portions of extensor muscles are primarily composed of SO and FOG fibres, and the more peripheral portions of the muscles have higher concentrations of FG fibres. During terrestrial locomotion, the fibres are recruited in this same general order from postural standing through high speed running to jumping (i.e. during standing deep SO fibres are active and during locomotion there is a progressive peripheral recruitment of fibres from SO to FOG to FG). Several metabolic indicators may be used to map these fibre recruitment patterns, including glycogen loss in fibres, metabolic enzyme changes during training at different speeds, and distribution of blood flow within and among the muscles. Concerning the latter, during standing in rats blood flows in the hindlimb muscles are directly proportional to the SO fibre populations in the muscles. However, during locomotion the elevations in blood flow over pre-exercise are a function of the populations of FOG fibres in the muscles. Blood flows in the peripheral white portions (FG fibres) of extensor muscles are not significantly elevated until the rats run at high speeds, when the FG fibres presumably are recruited. During swimming, when flexor muscles are relatively more active than extensor muscles (as compared with terrestrial locomotion), blood flows in the flexors are correspondingly higher. Thus, there exists a clear 'biological economy' in the matching of blood flow to the specific fibres that are active within and among muscles during exercise.
Mammalian skeletal muscles are composed of three primary muscle fiber types, FOG, FG, and SO. These fiber types are distributed within and among muscles in predictable patterns. Current data indicate that blood flows to inactive muscles composed of the various fiber types are approximately equal. Total muscle blood flow increases when the animal stands up. When maintaining posture (standing), the muscular force is provided by the SO fibers. These fibers receive the highest blood flows under these conditions. When the animal walks the SO fibers remain active and the additional muscular force is provided by FOG fibers. The increased muscle blood flow during exercise is primarily directed to the active FOG fibers. At fast running speeds, FG fibers are additionally recruited and blood flow increases in muscle areas composed of FG fibers. However, the FG blood flows per gram of tissue are much less than in the oxidative muscles. Thus, muscle blood flow is primarily directed to the active high oxidative muscle fibers within and among the muscles during normal activities. Much is known about factors believed to link blood flow to metabolism in skeletal muscle and about the reflex control of skeletal muscle vascular beds. However, the mechanisms responsible for blood flow control during locomotory exercise are yet to be established. It appears that the different muscle fiber types may have qualitatively similar blood flow control mechanisms with quantitative differences in relation to each fiber type. The capacity for blood flow in skeletal muscle is related to the oxidative potential of the muscles. Blood flows in high-oxidative muscles may reach 400-600 ml/min/100 g, which is considerably higher than the commonly accepted values for maximal muscle blood flow. Also, muscle blood flows are higher during locomotory exercise in conscious animals than in in situ electrical stimulation experiments. Chronic exercise training does not appear to change total muscle blood flow during locomotory exercise. However, the distribution of blood flow within and among muscles changes so that the deep red muscle fibers have higher flows during exercise. While data exist suggesting that blood flow capacity is increased with exercise training, this remains controversial.
A 55-year-old woman developed a dermatitis confined to light-exposed areas while taking quinidine gluconate, warfarin sodium, furosemide, spironolactone, and digoxin after cardiac surgery. Phototesting indicated a normal erythematous response to 290- to 320-nm ultraviolet radiation, but she developed erythema from 6 joules/sq cm of 320- to 400-nm radiation (ultraviolet A [UV-A]), a much lower dose than needed to produce a reaction in normal individuals. Two days after she discontinued quinidine and warfarin, phototesting showed no reaction to as much as 20 joules/sq cm of UV-A. One week after resuming quinidine (but not warfarin), she again reacted to 8 joules/sq cm of UV-A. No reactivity was elicited when the preparation was applied to the skin or injected into the dermis either with or without subsequent UV-A irradiation.
A 35-year-old woman would develop urticarial lesions over one to four hours after irradiation with sunlight or artificial ultraviolet radiation. Lesions could persist for days before resolving. Although lesions were morphologically typical of solar urticaria, their evolution and resolution were both much slower than expected. Histologically, the lesions showed leukocytoclastic vasculitis. This unexpected finding suggests the possibility that there may be novel mechanisms involved in the pathogenesis of some cases of solar urticaria.
Two groups totaling 162 patients hospitalized for modified Goeckerman treatment of severe psoriasis were matched for sex, age, and season of admission and followed up for two years after discharge. One group remained hospitalized throughout their average 20.8-day course; the other half was hospitalized 14 days, then transferred to an ambulatory center for the remainder of a course averaging 20.8 days. No difference was detected between the groups in the duration that improvement equaled or exceeded progress achieved at discharge. The percentage of patients remaining continuously improved after discharge was 80% at one month, 55% at six months, 40% at 12 months, and 20% at 24 months. rates of relapse requiring readmission or alternate therapy were also similar: 75% had not relapsed by 12 months and 60% had not relapsed by 24 months.
The purpose of this study was to estimate the absolute and relative masses of the three types of skeletal muscle fibers in the total hindlimb of the male Sprague-Dawley rat (Rattus norvegicus). For six rats, total body mass was recorded and the following weights taken from dissection of one hindlimb: 32 individual major muscles or muscle parts, remaining skeletal musculature (small hip muscles and intrinsic foot muscles), bone, inguinal fat pad, and skin. The fibers from the 32 muscles or muscle parts (which constituted 98% of the hindlimb skeletal muscle mass) were classified from histochemistry as fast-twitch oxidative glycolytic (FOG), fast-twitch glycolytic (FG), or slow-twitch oxidative (SO), and their populations were determined. Fiber cross-sectional areas from the same muscles were measured with a digitizer. Mass of each of the fiber types within muscles and in the total hindlimb was then calculated from fiber-type population, fiber-type area, and muscle-mass data. Skeletal muscle made up 71% of the total hindlimb mass. Of this, 76% was occupied by FG fibers, 19% by FOG fibers, and 5% by SO fibers. Thus, the FG fiber type is clearly the predominant fiber type in the rat hindlimb in terms of muscle mass. Fiber-type mass data are compared with physiological (blood flow) and biochemical (succinate dehydrogenase activities) data for the muscles taken from previous studies, and it is demonstrated that these functional properties are closely related to the proportions of muscle mass composed of the various fiber types.
This study was designed to determine the influence of a long-term, moderate-intensity treadmill training program on the distribution of blood flow within and among muscles of rats during exercise. One group (T) of male Sprague-Dawley rats trained for 1 h/day for 13-17 wk at 30 m/min on a motor-driven treadmill. A second group (UT) of rats was conditioned for 10 min/day for 4 wk at the same speed. Muscle succinate dehydrogenase activities were higher in T than UT rats indicating a significant training effect. Blood flows (BFs) in 32 hindlimb muscles or muscle parts and other selected organs were measured in the two groups with radiolabeled microspheres during preexercise and while the rats ran for 30 s, 5 min, or 15 min at 30 m/min on the treadmill. The data indicate 1) there were no differences in total hindlimb muscle BF between UT and T rats at any time; however, 2) T rats had higher preexercise heart rates and higher muscle BFs in the deep red extensor muscles, suggesting a greater anticipatory response to the impending exercise; 3) T rats demonstrated more rapid elevations in BF in the red extensor muscles at the commencement of exercise; 4) T rats had higher BFs in red extensor muscles during exercise, whereas UT rats had higher BFs in white muscles; and 5) T rats maintained higher BFs in the visceral organs during exercise. These findings demonstrate that exercise training results in changes in the distribution of BF within and among muscles and among organs during exercise. Specifically, data indicate the high-oxidative motor units that are primarily recruited in the muscles during the initial stages of moderate treadmill exercise receive higher blood flows in the trained rats; this presumably contributes to increased resistance to fatigue.
We previously observed that muscle blood flow (MBF) is primarily directed to the active oxidative muscle fibers within muscles of rats during treadmill exercise. Since muscle fiber recruitment patterns and the relative level of activities of muscles are distinctly different in swimming and treadmill exercise, we hypothesized that the distribution of MBF would also be different. The purpose of this study was to measure the distribution of MBF in swimming rats for comparison with the patterns previously observed in treadmill exercise. MBF was measured with labeled microspheres in 25 hindlimb muscles before, during, and after 5 min of swimming. During swimming, MBFs ranged from 10 to 403 ml X min-1 X 100 g-1 in the white vastus lateralis and red tibialis anterior, respectively. MBFs were increased during swimming in most muscles with the flexor muscles generally showing larger increases than the extensor muscles. Comparison of swimming with treadmill exercise indicates that swimming produces greater increases in MBFs in flexor muscles than in extensor muscles, whereas treadmill exercise produces larger increases in extensor muscles. The increased MBF during swimming was directed to the fast-twitch oxidative fibers. Therefore regional hindlimb MBF distribution is different in swimming than in treadmill exercise, and it appears that MBF is matched to the fiber recruitment patterns during both types of locomotory exercise.
Delayed-onset muscular soreness (DOMS), the sensation of pain and stiffness in the muscles that occurs from 1 to 5 d following unaccustomed exercise, can adversely affect muscular performance, both from voluntary reduction of effort and from inherent loss of capacity of the muscles to produce force. This reduction in performance is temporary; permanent impairment does not occur. A number of clinical correlates are associated with DOMS, including elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure; exertional rhabdomyolysis appears to be the extreme form of DOMS. Presently, the best treatment for DOMS appears to be muscular activity, although the sensation again returns following the exercise. Training for the specific contractile activity that causes DOMS reduces the soreness response. The etiology and cellular mechanisms of DOMS are not known, but a number of hypotheses exist to explain the phenomenon. The following model may be proposed: 1) high tensions (particularly those associated with eccentric exercise) in the contractile/elastic system of the muscle result in structural damage; 2) cell membrane damage leads to disruption of Ca++ homeostasis in the injured fibers, resulting in necrosis that peaks about 2 d post-exercise; and 3) products of macrophage activity and intracellular contents accumulate in the interstitium, which in turn stimulate free nerve endings of group-IV sensory neurons in the muscles leading to the sensation of DOMS.
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