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PubMed1998

Hindlimb suspension reduces muscle regeneration.

Exposure of juvenile skeletal muscle to a weightless environment reduces growth and satellite cell mitotic activity. However, the effect of a weightless environment on the satellite cell population during muscle repair remains unknown. Muscle injury was induced in rat soleus muscles using the myotoxic snake venom, notexin. Rats were placed into hindlimb-suspended or weightbearing groups for 10 days following injury. Cellular proliferation during regeneration was evaluated using 5-bromo-2'-deoxyuridine (BrdU) immunohistochemistry and image analysis. Hindlimb suspension reduced (P < 0.05) regenerated muscle mass, regenerated myofiber diameter, uninjured muscle mass, and uninjured myofiber diameter compared to weightbearing rats. Hindlimb suspension reduced (P < 0.05) BrdU labeling in uninjured soleus muscles compared to weight-bearing muscles. However, hindlimb suspension did not abolish muscle regeneration because myofibers formed in the injured soleus muscles of hindlimb-suspended rats, and BrdU labeling was equivalent (P > 0.10) on myofiber segments isolated from the soleus muscles of hindlimb-suspended and weightbearing rats following injury. Thus, hindlimb suspension (weightlessness) does not suppress satellite cell mitotic activity in regenerating muscles before myofiber formation, but reduces growth of the newly formed myofibers.

Animals↗
PubMed1993

Cromakalim does not protect against skeletal muscle fatigue in an anaesthetized rat model of acute hindlimb ischaemia.

The effects of the potassium (K+) channel opener, cromakalim, on skeletal muscle performance were studied in a model of acute hindlimb ischaemia in the anaesthetized rat. Twitch contractions to direct electrical stimulation of the extensor digitorum and tibialis anterior skeletal muscles were recorded following administration of cromakalim (10-100 micrograms kg-1 i.v.) under normal and reduced whole limb blood flow. With normal blood flow, twitch responses (0.5 and 1 Hz) of the hindlimb skeletal muscles were sustained for > 30 min. Controlled adjustment of the perfusion pressure in the contralateral hindlimb to 45, 30 or 0 mm Hg by partial or total occlusion of the abdominal aorta produced a pressure-related fall in flow to the working hindlimb, and a corresponding increase in the rate of muscle fatigue. Cromakalim (10-100 micrograms kg-1 i.v.) produced a dose-dependent reduction in mean carotid arterial blood pressure, femoral arterial pressure and hindlimb vascular resistance together with an increase in iliac artery blood flow and heart rate, but did not attenuate skeletal muscle fatigue under the different conditions of muscle work and ischaemia employed. A similar profile was observed with levcromakalim (15 micrograms kg-1 i.v.), the active enantiomer of cromakalim. These results demonstrate that in the direct muscle-stimulated hindlimb of the anaesthetized rat, the K+ channel opener cromakalim does not prevent acute ischaemia-induced skeletal muscle fatigue. The previous observation that K+ channel openers improve nutritive blood flow in a chronic model of rat hindlimb ischaemia is not reflected by an improvement in muscle function in the present study.

Animals↗
PubMed1992

Neuromuscular specificity following cross-stage hindlimb transplantation.

In order to determine whether spinal motoneurons can regenerate to their proper targets at stages beyond those when such specificity is typically expressed, autologous and homologous (same- and cross-stage) hindlimb transplantations were performed using bullfrog tadpoles (Rana catesbeiana). Neuromuscular specificity was assessed by applying horseradish peroxidase to the ventral thigh of the transplanted hindlimb and mapping the locations of retrogradely labeled motoneurons. Previously, we found that the hindlimb was reinnervated normally in young tadpoles whose motor nerves were transected. However, motor axons in older animals showed no evidence of target specificity when reinnervating the tadpole's own limb. In the present study, innervation was normal in young tadpoles whose hindlimb was removed and replaced in its original position. Axons of older hosts innervating hindlimbs transplanted from young tadpoles distinguished flexor from extensor limb regions, but failed to distinguish thigh from shank, demonstrating that axons in older animals can respond to at least some guidance cues. The lack of specificity along the proximal-distal axis appears to be a consequence of homologous transplantation since limbs transplanted from one young tadpole to another showed the same loss of proximal-distal specificity. One possibility is that the shank degenerates when the hindlimb is transplanted to a different host. Shank motoneurons, lacking their proper target, may then innervate the thigh. However, shank motoneurons did not innervate the thigh when motor nerve transection was combined with amputation of the hindlimb just above the presumptive knee.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Neural mechanism of depressor responses of arterial pressure elicited by acupuncture-like stimulation to a hindlimb in anesthetized rats.

The effects of acupuncture-like stimulation of a hindlimb on renal sympathetic nerve activity (RNA) as well as mean arterial blood pressure (MAP) were examined in anesthetized rats. An acupuncture needle (diameter of 160 microns) was inserted into the skin of a hindlimb and underlying muscles to a depth of 5 mm and was twisted at about 1 Hz. Under deep anesthetic condition, in about 70% of trials, acupuncture-like stimulation for 60 s induced a decrease in MAP which was accompanied by a decrease in RNA. Acupuncture-like stimulation applied to the muscles alone, but not to the skin alone, induced inhibition of RNA and MAP. Transection of sciatic and femoral nerves ipsilateral to the hindlimb stimulation completely abolished the responses of RNA and MAP. The hindlimb stimulation excited the femoral and common peroneal afferent nerves. In spinalized animals, the hindlimb stimulation did not produce any changes in RNA and MAP. The results indicate that the decrease in MAP induced by acupuncture-like stimulation of a hindlimb is a reflex response. The afferent pathway is composed of hindlimb muscle afferents while the efferent pathway is composed of sympathetic vasoconstrictors including the renal nerves. Endogenous opioids may not be involved in the present reflex, because an intravenous injection of naloxone, an antagonist of the opioid receptors, did not influence the reflex.

Acupuncture Therapy↗
PubMed1996

Stimulation of lumbar sympathetic nerves may produce hindlimb vasodilation via the release of pre-formed stores of nitrosyl factors.

The physiological activation of lumbar sympathetic nerves by air-jet stress produces a hindlimb vasodilation in conscious rats. Although the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester markedly reduces the duration of this air-jet stress-induced vasodilation, it does not prevent the initial fall in resistance. These data suggest that the vasodilation is initiated by the release of an as yet unidentified factor, whereas the vasodilation is sustained by the release of nitric oxide or newly synthesized nitrosyl factors such as S-nitrosothiols. At present, the possibility that neurogenic vasodilation may be initiated by the release of pre-formed pools of nitrosyl factors from storage sites within the hindlimb vasculature has not been addressed. We reasoned that if nitrosyl factors do exist in storage pools, then we should be able to demonstrate a "use-dependent" loss of vasodilation after nitric oxide synthesis inhibition which would be the result of a gradual depletion of the releasable pools of these nitrosyl factors. In the present study, we examined the effects of repeated episodes of direct electrical stimulation of the lumbar sympathetic chain on ipsilateral hindlimb vascular resistance in pentobarbital-anesthetized rats prior to and following administration of the nitric oxide synthesis inhibitors N(G)-nitro-L-arginine methyl ester (10, 25 or 100 mumol/kg i.v.) or N(G)-nitro-L-arginine (50 mumol/kg i.v.). Three episodes of electrical stimulation of 3.2 +/- 0.4 V (20 Hz, 5 ms duration, 5 ms delay for 10 s given 5 min apart) produced pronounced and reproducible reductions in hindlimb vascular resistance in the ipsilateral hindlimb (-56 +/- 5%, -55 +/- 5% and -53 +/- 6%, respectively), but no changes in mean arterial pressure. Three episodes of electrical stimulation at 4.8 +/- 0.4 V also caused reproducible decreases in hindlimb resistance (-59 +/- 7%, -61 +/- 9% and -64 +/- 12%) and minor but reproducible decreases in blood pressure. The vasodilation produced by the first electrical stimulation at 3.2 +/- 0.4 V was completely abolished by a 25 mumol/kg dose of N(G)-nitro-L-arginine methyl ester (-11 +/- 9%). The initial episode of electrical stimulation at 4.8 +/- 0.4 V produced a pronounced fall in ipsilateral hindlimb resistance in the N(G)-nitro-L-arginine methyl ester-treated animals whereas the second and third stimulations produced progressively smaller vasodilations (-55 +/- 4%, -34 +/- 3% and -19 +/- 2%, respectively). The 10 mumol/kg dose of N(G)-nitro-L-arginine methyl ester was not effective whereas the 100 mumol/kg dose produced similar effects as the 25 mumol/kg dose. The 50 mumol/kg dose of N(G)-nitro-L-arginine produced similar effects as the higher doses of N(G)-nitro-L-arginine methyl ester. Those results suggest that lower intensity electrical stimulation of the lumbar sympathetic nerves produces vasodilation via the release of nitric oxide or newly synthesized nitrosyl factors such as S-nitrosothiols. In contrast, the vasodilation produced by higher intensity electrical stimulation may involve the mobilization and release of pre-formed pools of nitrosyl factors which undergo a "use-dependent" depletion in the absence of nitric oxide synthesis. These pre-formed pools of nitrosyl factors may exist within the sympathetic nerves themselves. In addition, they may be stored within the vascular endothelium and released by neurogenically-derived neurotransmitters/neuromodulators.

Adrenergic Fibers↗
PubMed2006

Biomechanical capabilities influence postural control strategies in the cat hindlimb.

During postural responses to perturbations, horizontal plane forces generated by the cat hindlimb are stereotypically directed either towards or away from the animal's center of mass, independent of perturbation direction. We used a static, three-dimensional musculoskeletal model of the hindlimb to investigate possible biomechanical determinants of this "force constraint strategy." We hypothesized that directions in which the hindlimb can produce large forces are preferentially used in postural control. We computed feasible force sets (FFSs) based on hindlimb configurations of three cats during postural equilibrium tasks and compared them to horizontal plane postural force directions. The grand mean FFS was bimodal, with maxima near the posterior-anterior axis (-86+/-8 degrees and 71+/-4 degrees ), and minima near the medial-lateral axis (177+/-8 degrees and 8+/-8 degrees ). Experimental postural force directions clustered near both maxima; there were no medial postural forces near the absolute minimum. However, the medians of the anterior and posterior postural force direction histograms in the right hindlimb were rotated counter-clockwise from the FFS maxima (p<0.05; Wilcoxon signed-rank test). Because the posterior-anterior alignment of the FFS is consistent with a hindlimb structure optimized for locomotion, we conclude that the biomechanical capabilities of the hindlimb strongly influence, but do not uniquely determine the force directions observed in the force constraint strategy. Forces used in postural control may reflect a balance between a neural preference for using forces in the directions of large feasible forces and other criteria, such as the stabilization of the center of mass, and muscular coordination strategies.

Animals↗
PubMed2004

Experimental hindlimb ischemia leads to neutrophil-mediated increases in gastrocnemius MMP-2 and -9 activity: a potential mechanism for ischemia induced MMP activation.

INTRODUCTION: Matrix metalloproteinases (MMP)-2 and -9 are Type 4 collagenases instrumental in basement membrane degradation, a process necessary for angiogenesis to occur. Polymorphonuclear leukocytes (PMNs) contain MMP-9, and in the presence of both PMN-derived serine protease and membrane type 1 (MT1)-MMP, are able to activate pro-MMP-2 following hindlimb ischemia. We hypothesized that neutrophil depletion (ND) of animals prior to hindlimb ischemia (HI) would abrogate the activation of pro-MMP-2 and decrease the level of MMP-9 MATERIALS AND METHODS: 12 FVB/N Tie2/LacZ-182 SATO female mice were randomly divided into four blinded groups; HI + PBS, HI + anti-PMN antibody (GR-1), HI + isotype matched control antibody (IgG(2b,K)), and no HI + PBS. PMN depletion was achieved prior to the time of ischemia and maintained until sacrifice. HI was achieved by unilateral femoral artery ligation. Three days postligation the animals were sacrificed and the gastrocnemius muscle from each hindlimb was harvested. MMP-2 and -9 (gelatin zymography) and MT1-MMP (Western blot) expression and activation were quantified by densitometry and NIH Image Analysis software. MMP values were expressed as a ratio of ischemic-to-nonischemic hindlimbs and compared between groups. Statistical significance was determined with analysis of variance (ANOVA) RESULTS: Zymograms revealed a greater than 10-fold increase in active MMP-9 and greater than 4-fold increase in active MMP-2 from HI + PBS compared to no HI + PBS (P < 0.05). HI + anti-PMN antibody demonstrated reduction of both active MMP-2 and -9 levels to that of the nonischemic group. Pro-MMP-2 was constitutively expressed in all four groups with no significant differences between any group (P = NS). There was no difference between the HI + isotype-matched antibody group and the HI + PBS group throughout the experiments (P = NS). ND did not affect MT1-MMP activation or expression CONCLUSIONS: Limb ischemia causes activation of MMP-2 and -9, which is eliminated by ND. ND animals undergoing hindlimb ischemia exhibit identical levels of active MMP-2 and -9 as animals that did not have hindlimb ischemia. Neutrophils may be an important activator of MMP-2 and the suppliers of MMP-9 in the ischemic hindlimb and may be essential for tissue remodeling, basement membrane degradation, and angiogenesis in ischemic limbs

Acute Disease↗
PubMed2004

Responses to bradykinin are mediated by NO-independent mechanisms in the rat hindlimb vascular bed.

The vasodilator response to bradykinin (BK) appears to be mediated by a number of different endothelium-derived relaxing factors (EDRFs). The EDRFs mediating the response depend on the species and vascular bed studied. The mechanism by which BK dilates the hindlimb vascular bed was investigated in the anesthetized rat. BK produced dose-dependent increases hindlimb blood flow. The NOS antagonist L-NAME had little effect on the magnitude of the increase in flow when baseline hemodynamic parameters were corrected by an NO donor infusion. However, the duration of the response was slightly shortened by L-NAME. Charybdotoxin (Chtx) and apamin nearly abolished the L-NAME resistant component of the hindlimb vasodilator response to BK, but did not affect the hindlimb vasodilator response to the sodium nitroprusside (SNP). The cyclooxygenase inhibitor meclofenamate and the K+-ATP channel blocker U37883A, in the presence of L-NAME, did not alter the vasodilator response to BK. These results suggest that a significant portion of the hindlimb vasodilator response to BK is mediated by the activation of KCa channels, and independent of NO synthesis, cyclooxygenase products, and activation of K+-ATP channels. The present data suggest that the mechanisms mediating the vasodilator response to BK in the hindlimb vascular bed of the rat are complex, consisting of a Chtx and apamin sensitive, L-NAME resistant phase and a minor phase mediated by NO. In contrast, NO accounts for about half of the hindlimb vasodilator response to acetylcholine (ACh), with the other half of the response mediated by a Chtx and apamin sensitive mechanism. Additionally, the present results demonstrate that the NO donor infusion technique is able to compensate for the loss of basal NO production following inhibition of NOS, and to restore hemodynamic parameters to pre-L-NAME levels, making it a useful technique for the investigation of the role of NO in mediating vascular responses.

Animals↗
PubMed2006

Pitx1 determines the morphology of muscle, tendon, and bones of the hindlimb.

The vertebrate forelimb and hindlimb are serially homologous structures; however, their distinctive morphologies suggest that different mechanisms are associated with each limb type to give rise to limb-type identity. Three genes have been implicated in this process; T-box transcription factors Tbx5 and Tbx4, which are expressed in the forelimb and hindlimb, respectively, and a paired-type homeodomain transcription factor Pitx1, expressed in the hindlimb. To explore the roles of Pitx1 and Tbx4 in patterning the hindlimb, we have ectopically misexpressed these genes in the mouse forelimb using transgenic methods. We have developed a novel technique for visualising the structure and organisation of tissues in limbs in 3D using optical projection tomography (OPT). This approach provides unparalleled access to understanding the relationships between connective tissues during development of the limb. Misexpression of Pitx1 in the forelimb results in the transformation and translocation of specific muscles, tendons, and bones of the forelimb so that they acquire a hindlimb-like morphology. Pitx1 also upregulates hindlimb-specific factors in the forelimb, including Hoxc10 and Tbx4. In contrast, misexpression of Tbx4 in the forelimb does not result in a transformation of limb-type morphology. These results demonstrate that Pitx1, but not Tbx4, determines the morphological identity of hindlimb tissues.

Animals↗
PubMed1993

Hindlimb loading, morphology and biochemistry of articular cartilage in the ACL-deficient cat knee.

The cat hindlimb is the best studied animal model of neuromuscular control, muscle mechanics/muscle morphology, and locomotor kinematics. Therefore, this model offers itself for intervention studies, where a musculoskeletal parameter is perturbed and the effects of this perturbation are compared with normal function. The objective of this study was to describe the effects of anterior cruciate ligament (ACL) transection in the cat knee and to correlate hindlimb loading with morphological and biochemical changes of articular cartilage. A distinct unloading of the deficient hindlimb was found when compared with the nonoperated hindlimb immediately after ACL transection, and persisted for about 16-18 weeks. Beyond about 18 weeks post-ACL transection, hindlimb loading returned to the symmetric pattern observed before surgery. In accordance with the expectations from the force-platform results, a decrease in muscle mass was found from muscles of the experimental hindlimb when compared to the mass of muscles from the contralateral hindlimb. This decrease of muscle mass was largest at 4 weeks and smallest at 35 weeks post-ACL transection. At 12 and 35 weeks post-ACL transection, cell density was increased and absolute amounts of hexuronic acid were elevated in the articular cartilage of the experimental knee compared with the corresponding values of the contralateral knee. Progressive changes of the articular cartilage towards osteoarthritis (OA) were not observed in the time frame of this experiment. The results suggest that anterior cruciate ligament transection in the cat produces initial changes in the knee that are similar to those observed previously in the dog and rabbit.

Animals↗
PubMed1993

Hindlimb protein turnover and muscle protein synthesis in lambs: a comparison of techniques.

A combination of arterio-venous difference, kinetic isotope transfer and blood flow rate techniques were used to measure tyrosine metabolism across hindlimb tissues of nine growing lambs (average live weight 36.5 kg) fed on a range of dry matter intakes. Muscle protein synthesis was measured using a continuous infusion technique and compared with simultaneous estimates of hindlimb protein turnover calculated from the values for tyrosine metabolism. When the specific radioactivity (SRA) of tyrosine in the arterial plasma free pool was assumed to be the same as the SRA of tyrosine in the direct precursor pool of protein synthesis, hindlimb protein synthesis (ksav; 3.66 (SEM 0.50) %/d) was significantly (P < 0.001) higher (68%) than muscle protein synthesis (ksp; 2.18 (SEM 0.31) %/d) but was similar to the value for muscle protein synthesis calculated using the homogenate free tyrosine SRA (ksh; 3.35 (SEM 0.42) %/d). Hindlimb and muscle protein synthesis (y) were both significantly related to dry matter intake (chi) (ksav, r2 0.667, P = 0.007; ksh, r2 0.968, P < 0.001) and there was no significant difference between the slopes (P = 0.532) and intercepts (P = 0.945) of the two regression lines. The results demonstrate that hindlimb protein turnover cannot be quantitatively compared with muscle protein synthesis, probably due to high protein metabolic activity in non-muscular tissues within the hindlimb, although similar responses in protein synthetic rate to the level of feed intake were observed between hindlimb and muscle tissues.

Animals↗
PubMed1994

Nutrient utilization and protein turnover in the hindlimb of cattle treated with bovine somatotropin.

Our objectives were to assess the effects of chronic administration of recombinant bovine somatotropin (bST) on nutrient utilization and protein turnover in the hindlimb of growing Holstein steers. External iliac vessels were catheterized to allow for hindlimb measurements of arteriovenous differences and blood flow. Animals were used in a single-reversal design with 16-d treatment periods of daily intramuscular injection of either excipient or 120 micrograms/kg body wt of bST. On d 11 and 13 of each period, a primed-continuous infusion of L-[sidechain-2,3-3H]tyrosine was initiated, followed by a 4-h sampling period to assess hindlimb nutrient utilization and protein kinetics. Somatotropin did not alter blood flow or the consumption of acetate and oxygen across the hindlimb. In contrast, glucose uptake was reduced by 22% despite increases in arterial concentrations of glucose and insulin of 10 and 114%, respectively. Treatment with bST increased hindlimb protein accretion (estimated from net uptake of tyrosine) and whole-body N balance, each by approximately 40%. A modest increase (10%) in the absolute rate of protein synthesis seemed to account for the improved N retention in the hindlimb with no change in the rate of protein degradation. Thus, bST reduced the responses of the hindlimb to insulin, and a small alteration in protein synthesis was sufficient to explain substantial improvement in protein deposition.

Amino Acids↗
PubMed1993

Effects of high salt intake on control of hindlimb vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats.

1. This study aimed to examine whether a high salt diet alters control of vascular resistance by arterial baroreflex and vagal afferents in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). 2. SHR and WKY aged 8 weeks were fed either high (8%) or normal salt (0.4%) diet for 4 weeks. Arterial baroreflex control of hindlimb vascular resistance was assessed by examining reflex-induced vasodilation and vasoconstriction in response to phenylephrine and nitroprusside, respectively, in the constant-flow perfused hindlimb of urethane-anesthetized rats. 3. Tonic influence of the cardiopulmonary vagal afferents was evaluated by examining the effects of vagotomy on hindlimb vascular resistance and on the gain of arterial baroreflex control of hindlimb vascular resistance. 4. The gain of the arterial baroreflex control of hindlimb vascular resistance in response to both phenylephrine and nitroprusside were not significantly different between SHR receiving high and normal salt diets, and between WKY receiving high and normal salt diets. 5. Vagotomy increased hindlimb vascular resistance in all four groups of rats. However the high salt diet than those in SHR on a normal salt diet but similar between the two groups of WKY. Vagotomy increased the slope of arterial baroreflex control of hindlimb vascular resistance in SHR receiving a normal salt diet and the two groups of WKY but not in SHR receiving a high salt diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed2004

Mitochondrial KATP channels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction.

We previously demonstrated in the pig that instigation of three cycles of 10 min of occlusion and reperfusion in a hindlimb by tourniquet application (approximately 300 mmHg) elicited protection against ischemia-reperfusion injury (infarction) in multiple distant skeletal muscles subsequently subjected to 4 h of ischemia and 48 h of reperfusion, but the mechanism was not studied. The aim of this project was to test our hypothesis that mitochondrial ATP-sensitive potassium (KATP) (mKATP) channels play a central role in the trigger and mediator mechanisms of hindlimb remote ischemic preconditioning (IPC) of skeletal muscle against infarction in the pig. We observed in the pig that hindlimb remote IPC reduced the infarct size of latissimus dorsi (LD) muscle flaps (8 x 13 cm) from 45 +/- 2% to 22 +/- 3% (n = 10; P < 0.05). The nonselective KATP channel inhibitor glibenclamide (0.3 mg/kg) or the selective mKATP channel inhibitor 5-hydroxydecanoate (5-HD, 5 mg/kg), but not the selective sarcolemmal KATP (sKATP) channel inhibitor HMR-1098 (3 mg/kg), abolished the infarct-protective effect of hindlimb remote IPC in LD muscle flaps (n = 10, P < 0.05) when these drugs were injected intravenously at 10 min before remote IPC. In addition, intravenous bolus injection of glibenclamide (1 mg/kg) or 5-HD (10 mg/kg) at the end of hindlimb remote IPC also abolished the infarct protection in LD muscle flaps (n = 10; P < 0.05). Furthermore, intravenous injection of the specific mKATPchannel opener BMS-191095 (2 mg/kg) at 10 min before 4 h of ischemia protected the LD muscle flap against infarction to a similar extent as hindlimb remote IPC, and this infarct-protective effect of BMS-191095 was abolished by intravenous bolus injection of 5-HD (5 mg/kg) at 10 min before or after intravenous injection of BMS-191095 (n = 10; P < 0.05). The infarct protective effect of BMS-191095 was associated with a higher muscle content of ATP at the end of 4 h of ischemia and a decrease in muscle neutrophilic myeloperoxidase activity at the end of 1.5 h of reperfusion compared with the time-matched control (n = 10, P < 0.05). These observations led us to conclude that mKATP channels play a central role in the trigger and mediator mechanisms of hindlimb remote IPC of skeletal muscle against infarction in the pig, and the opening of mKATP channels in ischemic skeletal muscle is associated with an ATP-sparing effect during sustained ischemia and attenuation of neutrophil accumulation during reperfusion.

Adenosine Triphosphate↗
PubMed1981

Reflex control of canine hindlimb resistance under different modes of perfusion.

The carotid sinus control of hindlimb hemodynamics was determined in halothane-anesthetized vagotomized dogs. The carotid sinuses were bilaterally isolated and perfused under controlled conditions. The hindlimb was perfused under conditions of 1) physiological inflow, 2) constant pressure, and 3) constant flow. The variation of hindlimb resistance with mean carotid sinus perfusion pressure was largest under conditions of constant-pressure perfusion and smallest with physiological inflow. Values for constant-flow perfusion were intermediate. The effects of different values of constant-flow perfusion on the carotid sinus control of hindlimb hemodynamics was also determined. Values of hindlimb resistance increased with decreasing flow rate as did the variation with carotid sinus perfusion pressure. No evidence of a contribution of local control mechanisms related to changes in perfusion pressure or bed inflow could be demonstrated. The differences in the variation of hindlimb resistance with carotid sinus pressure under the various perfusion conditions can be explained on the basis of the mechanics of vascular smooth muscle. The amount of lumen constriction associated with changes in degree of activation depends on the conditions under which shortening occurs as well as upon the initial muscle length. It appears that local factors do not contribute to the control of hindlimb hemodynamics under the conditions in which these studies were performed.

Animals↗
PubMed2000

NTS A(2a) purinoceptor activation elicits hindlimb vasodilation primarily via a beta-adrenergic mechanism.

Previously, we have shown that activation of adenosine A(2a) receptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of the selective A(2a) receptor agonist CGS-21680 elicits potent, dose-dependent decreases in mean arterial pressure and preferential, marked hindlimb vasodilation. Although A(2a) receptor activation does not change lumbar sympathetic nerve activity, it does markedly enhance the preganglionic adrenal sympathetic nerve activity, which will increase epinephrine release and could subsequently elicit hindlimb vasodilation via activation of beta(2)-adrenergic receptors. Therefore we investigated whether this hindlimb vasodilation was due to neural or humoral mechanisms. In chloralose-urethan-anesthetized male Sprague-Dawley rats, we monitored cardiovascular responses to stimulation of NTS adenosine A(2a) receptors (CGS-21680, 20 pmol/50 nl) in the intact control animals; after pretreatment with propranolol (2 mg/kg iv), a beta-adrenergic antagonist; after bilateral lumbar sympathectomy; after bilateral adrenalectomy; and after combined bilateral lumbar sympathectomy and adrenalectomy. After beta-adrenergic blockade, stimulation of NTS adenosine A(2a) receptors produced a pressor response and a hindlimb vasoconstriction. Lumbar sympathectomy reduced the vasodilation seen in the intact animals by approximately 40%, and adrenalectomy reduced it by approximately 80%. The combined sympathectomy and adrenalectomy virtually abolished the hindlimb vasodilation evoked by NTS A(2a) receptor activation. We conclude that the preferential, marked hindlimb vasodilation produced by stimulation of NTS adenosine A(2a) receptors is mediated by both the efferent sympathetic nerves directed to the hindlimb and the adrenal glands via primarily a beta-adrenergic mechanism.

Adenosine↗
PubMed1990

Influence of single hindlimb support during simulated weightlessness in the rat.

Mature male rats (n = 16) were assigned to either 14 days of head-down suspension with one hindlimb supported (HDS) or to control cages (C) of similar dimensions. Hindlimb support during HDS preserved the muscle mass-to-body mass ratio (mg/100g) compared with C conditions for the soleus (48.3 +/- 1.0 to 41.7 +/- 1.0), plantaris (98.4 +/- 3.4 to 103.3 +/- 4.1), and gastrocnemius (484.7 +/- 18.5 to 507.2 +/- 13.9). However, the muscle mass-to-body mass ratio was significantly lower for the soleus (28.9 +/- 1.5), plantaris (83.9 +/- 3.6), and gastrocnemius (411.9 +/- 24.2) muscles from the freely hanging hindlimbs compared with the contralateral muscles from the supported hindlimbs or muscles from C animals. Citrate synthase activity (mumol.g-1.min-1) was significantly lower in soleus muscles from HDS rats in both the supported (19.4 +/- 2.3) and freely hanging (20.0 +/- 1.6) hindlimbs compared with C (28.5 +/- 3.1), whereas soleus muscle glycogen concentration (mg/g) was significantly higher in the freely hanging limbs from HDS rats (5.90 +/- 0.31) but not in the supported limbs (3.80 +/- 0.61) compared with C (4.34 +/- 0.50). Doppler flow probes were used to determine that iliac blood flow to freely hanging hindlimbs was significantly decreased after 48 (-19 +/- 5%) and 72 (-20 +/- 6%)h of HDS compared with presuspension values. In addition, iliac vascular resistance was significantly elevated at most time points during the 72 h of HDS in the freely hanging limbs but not the supported hindlimbs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Muscle glucose uptake in the rat after suspension with single hindlimb weight bearing.

This study was designed to examine the effect of non-weight-bearing conditions and the systemic influences of simulated microgravity on rat hindlimb muscles. For this purpose, rats were suspended (SUS) in a head-down position (45 degrees) with the left hindlimb non-weight bearing (NWB) and the right hindlimb bearing 20% of presuspension body mass (WB). Weight bearing by the SUS-WB limb was accomplished by using a platform connected to a rod in sleeve, cable, and pulley apparatus to which weight could be added. Rats (250-325 g) were assigned to SUS or cage control (CC) conditions for 14 days. The angle between the foot and leg for SUS-WB and CC remained similar (20-30 degrees) throughout the experiment while the SUS-NWB hindlimbs extended to approximately 140 degrees by day 12. On day 14, the soleus, plantaris, and gastrocnemius muscles from the SUS-NWB limbs exhibited significantly lower (P < or = 0.05) masses than presuspension mass values (29, 11, and 21%, respectively). Weight bearing by the SUS-WB limbs prevented the loss of mass by these muscles. In separate groups of SUS and CC rats, 2-deoxyglucose uptake during hindlimb perfusion was significantly higher in both SUS-NWB and SUS-WB hindlimbs at 24,000 microU/ml of insulin compared with CC for all the muscles examined (21-80%). In addition, extracellular space (ml/g) was significantly greater in the soleus muscles from both the SUS-NWB and SUS-WB hindlimbs (64%) compared with CC muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗