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At least 19 recordsLinked to original sources
PubMed1990

Flow-induced oxygen uptake by the perfused rat hindlimb is inhibited by vasodilators and augmented by norepinephrine: a possible role for the microvasculature in hindlimb thermogenesis.

Oxygen uptake in the perfused rat hindlimb was studied at 25 degrees C using an artificial perfusate, and the effects of perfusate flow rate, norepinephrine, and vasodilators were compared. Hindlimb oxygen uptake and perfusion pressure each increased as the flow rate was increased stepwise from 2 to 18.5 mL/min per hindlimb. At each flow rate, the rate of oxygen uptake was inhibited by the vasodilator nitroprusside (0.5 mM) and increased by norepinephrine (5 nM). A corresponding change in perfusion pressure also occurred, with norepinephrine leading to a marked increase and nitroprusside leading to a decrease; however, changes in oxygen uptake and pressure were not linearly related. The lactate/pyruvate ratio of the perfusate was used as an index of tissue perfusion and was determined at each flow rate. Lactate and pyruvate efflux increased as the flow rate was increased stepwise from 2 to 18.5 mL/min per hindlimb. At 2 mL/min per hindlimb, the lactate/pyruvate ratio was 15; at flow rates equal or greater than 4 mL/min per hindlimb, the ratio was constant at 9. Nitroprusside had no significant effect on the ratio at any flow rate even though a marked inhibitory effect on oxygen uptake was evident. Muscle content of high energy phosphates at 8 mL/min per hindlimb did not differ before and after treatment with vasodilators. In addition, the vasodilators had no apparent effect on skeletal muscle oxygen uptake or force development during electrical stimulation. The findings indicate that oxygen uptake by the hindlimb is not limited by inadequate perfusion and that oxygen uptake can be further increased by norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

Fictive hindlimb motor patterns evoked by AMPA and NMDA in turtle spinal cord-hindlimb nerve preparations.

Application of the glutamate agonists alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA, 5-10 microM), or N-methyl-D-aspartate (NMDA, 50-100 microM) to the turtle spinal cord produced fictive hindlimb motor patterns in low-spinal immobilized animals (in vivo) and in isolated spinal cord-hindlimb nerve preparations (in vitro). For in vivo experiments, drugs were applied onto the dorsal surface of 2-4 adjacent spinal cord segments in and near the anterior hindlimb enlargement. Motor output was recorded unilaterally or bilaterally from hindlimb muscle nerves. AMPA elicited vigorous motor patterns in vivo that included strict hip flexor-extensor and right-left alternation. In most turtles, the monoarticular knee extensor nerve FT-KE was active during the HE phase of AMPA evoked burst cycles, similar to the timing of pocket scratch motor patterns. NMDA was less effective in vivo, typically producing only weak and irregular bursting from hip nerves and little or no knee extensor (KE) discharge. Sensory stimulation of a rostral scratch reflex in vivo could reset an ongoing AMPA-evoked motor rhythm, indicating that cutaneous reflex pathways interact centrally with the chemically activated rhythm generator. Most in vitro preparations consisted of six segments of spinal cord, including the entire 5-segment hindlimb enlargement (D8-S2) and the segment immediately anterior to the enlargement (D7), with attached hindlimb nerves. In contrast to in vivo experiments, in vitro preparations exhibited highly regular, long-lasting motor rhythms when NMDA was superfused over the spinal cord. AMPA also produced rhythmic motor patterns in vitro, but these lasted only a few minutes before they were replaced with tonic discharge. FT-KE timing during in vitro chemically elicited activity was similar to that of sensory-evoked pocket scratch motor patterns. Some NMDA-evoked rhythmicity persisted even in 3-segment (D6-D8) and 1-segment (D8) in vitro preparations, demonstrating that neural mechanisms for chemically activated rhythmogenesis reside even in a single segment of the hindlimb enlargement.

Animals↗
PubMed1996

Quantitative changes of GABA-immunoreactive cells in the hindlimb representation of the rat somatosensory cortex after 14-day hindlimb unloading by tail suspension.

The present study was aimed at evaluating quantitatively gamma-aminobutyric acid (GABA) immunoreactivity in the hindlimb representation of the rat somatosensory cortex after 14 days of hindlimb unloading by tail suspension. A reduction in the number of GABA-immunoreactive cells with respect to the control animals was observed in layer Va and Vb. GABA-containing terminals were also reduced in the same layers, particularly those terminals surrounding the soma and apical dendrites of pyramidal cells in layer Vb. On the basis of previous morphological and behavioral studies of the neuromuscular system of hindlimb-suspended animals, it is suggested that the unloading due to hindlimb suspension alters afferent signaling and feedback information from intramuscular receptors to the cerebral cortex due to modifications in the reflex organization of hindlimb muscle groups. We propose that the reduction in immunoreactivity of local circuit GABAergic neurons and terminals is an expression of changes in their modulatory activity to compensate for the alterations in the afferent information.

Animals↗
PubMed2007

Tbx4 is not required for hindlimb identity or post-bud hindlimb outgrowth.

Tbx4 is a crucial gene in the initiation of hindlimb development and has been reported as a determinant of hindlimb identity and a presumptive direct regulator of Fgf10 in the limb. Using a conditional allele of Tbx4, we have ablated Tbx4 function before and after limb initiation. Ablation of Tbx4 before expression in the hindlimb field confirms its requirement for limb bud outgrowth. However, ablation of Tbx4 shortly after onset of expression in the hindlimb field, during limb bud formation, alters neither limb outgrowth nor expression of Fgf10. Instead, post-limb-initiation loss of Tbx4 results in reduction of limb core tissue and hypoplasia of proximal skeletal elements. Loss of Tbx4 during later limb outgrowth produces no limb defects, revealing a brief developmental requirement for Tbx4 function. Despite evidence from ectopic expression studies, our work establishes that loss of Tbx4 has no effect on hindlimb identity as assessed by morphology or molecular markers.

Alleles↗
PubMed2005

Hindlimb unweighting for 2 weeks alters physiological properties of rat hindlimb motoneurones.

We sought to determine whether decreased neuromuscular use in the form of hindlimb unweighting (HU) would affect the properties of innervating motoneurones. Hindlimb weight-bearing was removed in rats for a period of 2 weeks via hindlimb suspension by the tail. Following this the electrophysiological properties of tibial motoneurones were recorded under anaesthesia in situ. After HU, motoneurones had significantly (P < 0.05) elevated rheobase currents, lower antidromic spike amplitudes, lower afterhyperpolarization (AHP) amplitudes, faster membrane time constants, lower cell capacitances, and depolarized spike thresholds. Frequency-current (f-I) relationships were shifted significantly to the right (i.e. more current required to obtain a given firing frequency), although there was no change in f-I slopes. 'Slow' motoneurones (AHP half-decay times, > 20 ms) were unchanged in proportions in HU compared to weight-bearing rats. Slow motoneurones had significantly lower minimum firing frequencies and minimum currents necessary for rhythmic firing than 'fast' motoneurones in weight-bearing rats; these differences were lost in HU rats, where slow motoneurones resembled fast motoneurones in these properties. In a five-compartment motoneurone model with ion conductances incorporated to resemble firing behaviour in vivo, most of the changes in passive and rhythmic firing properties could be reproduced by reducing sodium conductance by 25% and 15% in the initial segment and soma, respectively, or by increasing potassium conductance by 55% and 42%, respectively. This supports previous conclusions that changes in chronic neuromuscular activity, either an increase or decrease, may result in physiological adaptations in motoneurones due to chronic changes in ion conductances.

Action Potentials↗
PubMed1997

Effect of hindlimb unloading on two hindlimb muscles during treadmill locomotion in rats.

The purpose of the study was to examine the pattern of electromyographic (EMG) activity of the rat soleus (SOL) and tibialis anterior (TA) muscles during treadmill locomotion at various speeds after 7 days of hindlimb unloading (HU). Raw EMG signals were processed to determine cycle duration, burst duration and mean EMG (burst surface divided by its duration). Cycle duration and SOL burst duration increased after HU (+7% and +5%, respectively) while TA burst duration decreased (-16%). After HU, the alternating pattern of activity between extensor and flexor muscles was maintained. Nevertheless, a co-activation of the two muscles was sometimes observed. The EMG pattern revealed no difference in the timing of the coordination between flexor and extensor muscles after HU. The delay between TA offset and SOL onset was increased (+12 ms), but this increase could be explained by the decrease in TA burst duration. Neither TA burst duration nor TA mean EMG were changed with increased treadmill speed, so that the flexor muscle activity was not related to speed of locomotion. These results would suggest that SOL activity is centrally programmed. Moreover, it is proposed that a decline in afferent feedback from SOL in rats which are suspended has an effect upon the locomotor pattern, leading to an hyperexcitability of SOL motoneurons and, via reciprocal inhibition, to a reduction in TA activity.

Animals↗
PubMed2005

The effect of gradual or acute arterial occlusion on skeletal muscle blood flow, arteriogenesis, and inflammation in rat hindlimb ischemia.

BACKGROUND: Current experimental models of critical limb ischemia are based on acute ischemia rather than on chronic ischemia. Human peripheral vascular disease is largely a result of chromic ischemia. We hypothesized that a model of chronic hindlimb ischemia would develop more collateral arteries, more blood flow, and less necrosis and inflammation than would acute hindlimb ischemia. We therefore developed a rat model of chronic hindlimb ischemia and compared the effects of chronic ischemia with those of acute ischemia on hindlimb skeletal muscle. METHODS: Acute or chronic ischemia was induced in 36 male Sprague-Dawley rats. Chronic ischemia caused blood flow, as measured by laser Doppler scanning and confirmed by muscle oxygen tension measurements, to gradually decrease over 1 to 2 weeks after operation. RESULTS: Histologic analysis showed chronic hindlimb ischemia better preserved muscle mass and architecture and stimulated capillary angiogenesis, while lacking the muscle necrosis and inflammatory cell infiltrate seen after acute ischemia. Surprisingly, the chronic ischemia group recovered dermal blood flow more slowly and less completely than did the acute ischemia group, as measured by laser Doppler (0.66 +/- 0.02 vs 0.76 +/- 0.04, P < .05) and tissue oxygen tension (0.61 +/- 0.06 vs 0.81 +/- 0.05, P < .05) at 40 days postoperatively. Consistent with poorer blood flow recovery, chronic ischemia resulted in smaller diameter collateral arteries (average diameter of the five largest collaterals on angiogram was 0.01 +/- 0.0003 mm vs 0.013 +/- 0.0007 mm for acute, P < .005 at 40 days postoperatively). Acute ischemia resulted in decreased tissue concentrations of vascular endothelial growth factor (VEGF) (0.96 +/- 0.23 pg/mg of muscle for acute vs 4.4 +/- 0.75 and 4.8 +/- 0.75 pg/mg of muscle for unoperated and chronic, respectively, P < .05 acute vs unoperated), and in increased tissue concentrations of interleukin (IL)-1beta (7.3 +/- 4.0 pg/mg of muscle for acute vs undetectable and 1.7 +/- 1.6 pg/mg of muscle for unoperated and chronic, respectively, P < 0.05 acute vs unoperated). CONCLUSIONS: We describe here the first model of chronic hindlimb ischemia in the rat. Restoration of blood flow after induction of hindlimb ischemia is dependent on the rate of arterial occlusion. This difference in blood flow recovery correlates with distinct patterns of muscle necrosis, inflammatory cell infiltration, and cytokine induction in the ischemic muscle. Differences between models of acute and chronic hindlimb ischemia may have important consequences for future studies of mechanisms regulating arteriogenesis and for therapeutic approaches aimed at promoting arteriogenesis in humans suffering from critical limb ischemia. CLINICAL RELEVANCE: Despite the substantial clinical differences between acute and chronic ischemia, researchers attempting to develop molecular therapies to treat critical limb ischemia have only tested those therapies in experimental models of acute hindlimb ischemia. We present here a novel model of chronic hindlimb ischemia in the rat. We further demonstrate that when hindlimb ischemia is developed chronically, collateral artery development is poorer than when hindlimb ischemia is developed acutely. These findings suggest that further tests of molecular therapies for critical limb ischemia should be performed in chronic hindlimb ischemia models rather than in acute hindlimb ischemia models.

Acute Disease↗
PubMed1993

Brachially innervated ectopic hindlimbs in the chick embryo. I. Limb motility and motor system anatomy during the development of embryonic behavior.

The functional status of brachially innervated hindlimbs, produced by transplanting hindlimb buds of chick embryos in place of forelimb buds, was quantified by analyzing the number and temporal distribution of spontaneous limb movements. Brachially innervated hindlimbs exhibited normal motility until E10 but thereafter became significantly less active than normal limbs and the limb movements were more randomly distributed. Contrary to the findings with axolotls and frogs, functional interaction between brachial motoneurons and hindlimb muscles cannot be sustained in the chick embryo. Dysfunction is first detectable at E10 and progresses to near total immobility by E20 and is associated with joint ankylosis and muscular atrophy. Although brachially innervated hindlimbs were virtually immobile by the time of hatching (E21), they produced strong movements in response to electrical stimulation of their spinal nerves, suggesting a central rather than peripheral defect in the motor system. The extent of motoneuron death in the brachial spinal cord was not significantly altered by the substitution of the forelimb bud with the hindlimb bud, but the timing of motoneuron loss was appropriate for the lumbar rather than brachial spinal cord, indicating that the rate of motoneuron death was dictated by the limb. Measurements of nuclear area indicated that motoneuron size was normal during the motoneuron death period (E6-E10) but the nuclei of motoneurons innervating grafted hindlimbs subsequently became significantly larger than those of normal brachial motoneurons. Although the muscle mass of the grafted hindlimb at E18 was significantly less than that of the normal hindlimb (and similar to that of a normal forelimb), electronmicroscopic examination of the grafted hindlimbs and brachial spinal cords of E20 embryos revealed normal myofiber and neuromuscular junction ultrastructure and a small increase in the number of axosomatic synapses on cross-sections of motoneurons innervating grafted hindlimbs compared to motoneurons innervating normal forelimbs. The anatomical data indicate that, rather than being associated with degenerative changes, the motor system of the brachial hindlimb of late-stage embryos is intact, but inactive.

Animals↗
PubMed2003

Hindlimb glucose and lactate metabolism during umbilical cord compression and acute hypoxemia in the late-gestation ovine fetus.

The metabolic adaptation of the hindlimb in the fetus to a reversible period of adverse intrauterine conditions and, subsequently, to a further episode of acute hypoxemia has been examined. Sixteen sheep fetuses were chronically instrumented with vascular catheters and transit-time flow probes. In nine of these fetuses, umbilical blood flow was reversibly reduced by 30% from baseline for 3 days (umbilical cord compression), while the remaining fetuses acted as sham-operated, age-matched controls. Acute hypoxemia was subsequently induced in all fetuses by reducing maternal fractional inspired oxygen concentration for 1 h. Paired hindlimb arteriovenous blood samples were taken at appropriate intervals during cord compression and acute hypoxemia, and by using femoral blood flow and the Fick principle, substrate delivery, uptake, and output were calculated. Umbilical cord compression reduced blood oxygen content and delivery to the hindlimb and increased hindlimb oxygen extraction and blood glucose and lactate concentration in the fetus. However, hindlimb glucose and oxygen consumption were unaltered during umbilical cord compression. In contrast, hindlimb oxygen delivery and uptake were significantly reduced in all fetuses during subsequent acute hypoxemia, but glucose extraction, oxygen extraction, and hindlimb lactate output significantly increased in sham-operated control fetuses only. Preexposure of the fetus to a temporary period of adverse intrauterine conditions alters the metabolic response of the fetal hindlimb to subsequent acute stress. Additional data suggest that circulating blood lactate may be derived from sources other than the fetal hindlimb under these circumstances. The lack of hindlimb lactate output during acute hypoxemia in umbilical cord-compressed fetuses, despite a significant fall in oxygen delivery to and uptake by the hindlimb, suggests that the fetal hindlimb may not respire anaerobically after exposure to adverse intrauterine conditions. hypoxia

Acid-Base Equilibrium↗
PubMed1999

Evidence of a nonendothelial source of nitric oxide in the isolated perfused hindlimb vasculature of the pregnant rat.

OBJECTIVE: This study was undertaken to further elucidate the roles of the vascular endothelium and nitric oxide (NO) in the regulation of vascular tone and constrictor responsiveness in pregnancy. METHODS: The perfusion pressure-flow relationship was measured in isolated, perfused, norepinephrine-constricted (1) endothelium-intact, (2) endothelium-denuded, and (3) N omega-nitro-L-arginine methyl ester (L-NAME)-treated hindlimbs from nonpregnant and term-pregnant rates. RESULTS: Baseline perfusion pressure at a flow rate of 2 mL/min was similar (approximately 20 min Hg) in all hindlimbs. Norepinephrine (0.5 muM) increased perfusion pressure in both nonpregnant (+21.6 +/- 2.4 mm Hg) and pregnant (+13.6 +/- 0.9 mm Hg) endothelium-intact rat hindlimbs. In nonpregnant rat hindlimbs, endothelium removal and L-NAME increased norepinephrine vasoconstriction similarly (+44.3 +/- 4.0 mm Hg and +46.4 +/- 8.6 mm Hg, respectively). In pregnant-rat hindlimbs, L-NAME increased norepinephrine vasoconstriction by 43.5 +/- 10.8 mm Hg, similar to that in nonpregnant-rat hindlimbs, but endothelium removal only increased norepinephrine vasoconstriction by 28.0 +/- 2.2 mm Hg. Perfusion pressure increased linearly as the flow rate was increased from 2 to 4 mL/min, and the slope of the regression line of the endothelium-intact pregnant-rat hindlimbs (7.0 +/- 0.6) was slightly, but not significantly, lower than that of the nonpregnant-rat hindlimbs (9.6 +/- 0.9). Endothelium removal increased the slopes of the regression lines, but that of pregnant-rat hindlimbs (12.8 +/- 1.6) was significantly lower (p < or = 0.05) than that of the nonpregnant-rat hindlimbs (23.8 +/- 1.8). L-NAME caused a similar increase in the pressure-flow slopes of nonpregnant-rat (36.5 +/- 3.4) and pregnant-rat (32.1 +/- 5.3) hindlimbs. CONCLUSIONS: These results suggest that nonendothelial nitric oxide production may be increased in the hindlimb resistance vasculature of the pregnant rat, which may play a role in the normal pregnancy blunting of constrictor responsiveness and reduction of vascular resistance.

Acetylcholine↗
PubMed1991

A peripheral 5-HT1D-like receptor involved in serotonergic induced hindlimb scratching in rats.

The pharmacological characteristics of hindlimb scratching induced by serotonergic compounds were studied. We conclude that hindlimb scratching induced by serotonergic compounds is mediated by a serotonin1D (5-HT1D) or 5-HT1D-like receptor outside the blood-brain barrier because hindlimb scratching could be induced by s.c. injection of 5-methoxytryptamine (5-MeOT), 5-carboxamidotryptamine (5-CT), bufotenine, 5-hydroxytryptamine (5-HT) and tryptamine. These compounds have high affinity for 5-HT1A and 5-HT1D receptors. The 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5-HT1C receptor agonist MK 212, and the mixed 5-HT1C/5-HT2 receptor agonists (dl)-1-(2,5 dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and quipazine did not induce hindlimb scratching. Rather, the latter compounds attenuated 5-MeOT-induced hindlimb scratching. The 5-HT releasing compounds fenfluramine and p-chloroamphetamine (PCA) inhibited whereas the 5-HT re-uptake inhibitors fluvoxamine and indalpine potentiated 5-MeOT-induced hindlimb scratching. 5-MeOT-induced hindlimb scratching could be inhibited dose dependently by the alpha 2-adrenoceptor blockers yohimbine and rauwolsince, which also have high affinity for 5-HT1D receptors, whereas the alpha 2-adrenoceptor blocker piperoxan only weakly counteracted hindlimb scratching. Haloperidol, apomorphine, morphine, clonidine and methiothepin strongly attenuated hindlimb scratching, atropine, naloxone and ICS 205930 attenuated it weakly whereas domperidone, methylatropine and mepyramine were inactive in doses up to 10 mg/kg. Hindlimb scratching induced by 5-MeOT was potentiated by the 5-HT receptor antagonists metergoline, methysergide, mesulergine, mianserin, ritanserin and xylamidine. Hindlimb scratching was not induced by i.c.v. injection of 5-MeOT.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Methoxytryptamine↗
PubMed2006

Hindlimb claudication reflects impaired nitric oxide-dependent revascularization after ischemia.

Although vascular remodeling is important in preventing tissue damage and restoring muscle function, there is no evidence of a relationship between vascular remodeling and muscle function after peripheral vascular occlusion. Nitric oxide (NO) has been implicated in the process of vascular remodeling in hindlimb ischemia. Thus, development of alterations in hindlimb gait after ischemia may be associated with impaired nitric oxide-dependent, vascular blood flow recovery. We evaluated hindlimb gait as an index of ischemia-induced revascularization and tested the effects of NO synthase inhibition on both hindlimb blood flow and hindlimb gait locomotion. After 14 days of ischemia, the ischemic hindlimb showed no significant differences in gait locomotion compared to the sham-operated hindlimb. However, hindlimb ischemia drastically reduced hindlimb blood flow from 46+/-3 mL/min/100 g to 12+/-2 mL/min/100 g which reverted to 33+/-5 mL/min/100 g after 14 days of ischemia. eNOS mRNA expression levels at 3, 7, 14, and 28 days after initiation of ischemia, were increased by 50+/-5%, 100+/-10%, 140+/-8% and 270+/-12% respectively and eNOS protein expression levels at 7, 14, and 28 days, were increased by 28+/-3%, 62+/-6% and 80+/-16% respectively. However, eNOS inhibition caused by l-NAME treatment prevented blood flow recovery and correction of abnormal gait locomotion in rats. Thus, the duration of the stride-swing phase increased and the stride length decreased. The knee joint angle decreased during flexion and extension with eNOS inhibition. In conclusion, ischemia-induced revascularization is associated with recovery of both hindlimb blood flow and normal gait locomotion. Moreover, prevention of NO synthesis, a key messenger in ischemia-induced revascularization, is associated with impairment in hindlimb locomotion. Thus, gait locomotion represents a functional model that could be used to evaluate the degree of ischemia-induced revascularization.

Animals↗
PubMed2003

Hindlimb unloading increases oxidative stress and disrupts antioxidant capacity in skeletal muscle.

Skeletal muscle disuse with space-flight and ground-based models (e.g., hindlimb unloading) results in dramatic skeletal muscle atrophy and weakness. Pathological conditions that cause muscle wasting (i.e., heart failure, muscular dystrophy, sepsis, COPD, cancer) are characterized by elevated "oxidative stress," where antioxidant defenses are overwhelmed by oxidant production. However, the existence, cellular mechanisms, and ramifications of oxidative stress in skeletal muscle subjected to hindlimb unloading are poorly understood. Thus we examined the effects of hindlimb unloading on hindlimb muscle antioxidant enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase), nonenzymatic antioxidant scavenging capacity (ASC), total hydroperoxides, and dichlorohydrofluorescein diacetate (DCFH-DA) oxidation, a direct indicator of oxidative stress. Twelve 6 month old Sprague Dawley rats were divided into two groups: 28 d of hindlimb unloading (n = 6) and controls (n = 6). Hindlimb unloading resulted in a small decrease in Mn-superoxide dismutase activity (10.1%) in the soleus muscle, while Cu,Zn-superoxide dismutase increased 71.2%. In contrast, catalase and glutathione peroxidase, antioxidant enzymes that remove hydroperoxides, were significantly reduced in the soleus with hindlimb unloading by 54.5 and 16.1%, respectively. Hindlimb unloading also significantly reduced ASC. Hindlimb unloading increased soleus lipid hydroperoxide levels by 21.6% and hindlimb muscle DCFH-DA oxidation by 162.1%. These results indicate that hindlimb unloading results in a disruption of antioxidant status, elevation of hydroperoxides, and an increase in oxidative stress.

Animals↗
PubMed1990

Adenosine is not essential for exercise hyperaemia in the hindlimb in conscious dogs.

1. The contribution of endogenous adenosine to the increase in hindlimb blood flow that occurs during treadmill exercise was evaluated in conscious dogs. We postulated that if adenosine is essential for the hindlimb hyperaemic response, then pharmacological treatment of the animals with adenosine receptor antagonists should decrease hindlimb blood flow during treadmill exercise. 2. A total of twenty-three dogs were chronically instrumented for measurement of aortic blood pressure and hindlimb blood flow using electromagnetic or Doppler flow probes on the left external iliac artery. Measurements of arterial blood pressure, hindlimb blood flow and heart rate were made during steady-state treadmill exercise in both the presence and the absence of adenosine receptor antagonists. Four different protocols were performed using different routes of administration of two adenosine receptor antagonists. Aminophylline was used in most of the experiments, and the effects of the more potent antagonist, 8-phenyltheophylline, were also evaluated. In addition, the dogs exercised at varying intensities ranging from a low level of 5.5 km h-1 at 0% gradient to a high intensity of 5.5 km h-1 at 21% gradient. 3. Aminophylline given as a single intravenous dose, or as a constant infusion either intravenously or directly into the hindlimb artery, did not decrease hindlimb blood flow at low, moderate or high intensities of exercise. Likewise, the blockade of adenosine receptors with 8-phenyltheophylline, given systemically or as a bolus injection administered directly into the hindlimb circulation during moderate exercise, did not attenuate the hindlimb blood flow response. 4. Our data demonstrate that exercise hyperaemia of the hindlimb is not reduced by antagonism of adenosine receptors. These findings are consistent with the hypothesis that adenosine is not an essential mediator of hindlimb vasodilatation during exercise.

Adenosine↗
PubMed2002

Functional morphology of the hindlimb of tupaiids (Mammalia, Scandentia) and its phylogenetic implications.

In this study, the hindlimb of 12 species of tupaiids was analyzed functionally and compared to that of primates, dermopterans, and chiropterans. Many aspects of the tupaiid hindlimb vary in relation to differential substrate use. These differences include width of the ilium, shape of the acetabulum, size of the anterior inferior iliac spine, size of the greater and third trochanters, depth of the femoral condyles, shape of the patellar groove, and size of the tibial tuberosity. The hindlimb of the arboreal Ptilocercus lowii, the only ptilocercine, is better adapted for arboreal locomotion, whereas that of tupaiines is better adapted for rapid terrestrial (or scansorial) locomotion. The hindlimb of Ptilocercus seems to be habitually flexed and has more joint mobility, a condition necessary for movement on uneven, discontinuous arboreal supports. The tarsus of Ptilocercus facilitates inversion of the foot and its grasping hallux is capable of a great range of abduction. Tupaiines, on the other hand, are characterized by more extended hindlimbs and less mobility in their joints. These restricted joints limit movements more to the parasagittal plane, which increases the efficiency of locomotion on a more even and continuous surface like the ground. The hindlimb of tupaiines is adapted for powerful flexion and extension. Even the most arboreal tupaiines remain similar to terrestrial tupaiines in their hindlimb morphology, which probably reflects the terrestrial ancestry of Tupaiinae (but not Tupaiidae). Many attributes of the tupaiid hindlimb, especially those of the foot, reflect the arboreal ancestry of Tupaiidae and it is proposed that the ancestral tupaiid was arboreal like Ptilocercus. Also, compared to the hindlimb character states of tupaiines, those of Ptilocercus are more similar to those of other archontans, and it is proposed that the hindlimb features of Ptilocercus are primitive for the Tupaiidae. Hence, Ptilocercus should be considered in any phylogenetic analysis that includes Scandentia.

Animals↗
PubMed1993

Brachially innervated ectopic hindlimbs in the chick embryo. II. The role of supraspinal input in the loss of limb motility.

Brachially innervated grafted hindlimbs display a progressive loss of motility as development proceeds. However, the virtually immobile grafted hindlimbs of E20 embryos exhibited strong, synchronous contractions of gastrocnemius and tibialis muscles upon intraperitoneal injection of strychnine nitrate (20 micrograms). This result indicated that the marked behavioral deficit was not due to an inability of the motoneurons that innervate the immobile grafted hindlimbs to initiate and propagate action potentials, but was probably the result of an effective loss of motoneuron excitation. To examine the hypothesis that interaction with the supraspinal nervous system is involved in the reduction of grafted hindlimb activity, the normal forelimb and grafted hindlimb movements of chronic spinal embryos were examined. The normal forelimbs of chronic spinal embryos exhibited the same number of movements as normal embryos at all stages examined. Thus the deficit in grafted hindlimb motility is not comparable to the behavior of the normal forelimb in chronic spinal embryos and is, therefore, unlikely to be due to a lack of excitation from the supraspinal nervous system. The possibility of an inhibitory influence via supraspinal projections was examined in chronic spinal embryos that had brachially innervated grafted hindlimbs. After E12, the grafted hindlimbs of chronic spinal embryos displayed significantly fewer movements than the normal forelimbs of chronic spinal embryos but significantly more movements than the brachial hindlimb of embryos with intact spinal cords. By E18, however, both spinal and nonspinal brachial hindlimbs, were equally dysfunctional.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗