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J K Barclay

Publications and source records attributed to J K Barclay.

At least 37 records · Page 2Linked to original sources
PubMed1995

Blood flow and pressure relationships which determine VO2max.

The role of O2 delivery in regulating VO2max has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting in situ; recent data addressing this issue are presented. VO2 increases nonlinearly with stimulation frequency reaching a peak at 5 twitches.s-1 or 1 tet.s-1 (200 ms trains, 50 imp.s-1). Further increases in stimulation frequency result in a lower VO2. Measured VO2 maxima are less than predicted VO2 capacity, and peak VO2 during tetanic contractions is greater than that during twitches. Above 150 imp.min-1, VO2 is directly related to the level of blood flow attained as VO2/Q (arterial-venous O2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during 1.s-1 tetanic contractions increases O2 diffusive conductance and peak VO2. When O2 delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q. 31P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O2. We conclude that VO2max is limited by O2 delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.

Animals↗
PubMed1994

Cultured endothelial cells from distinct vascular areas show differential responses to agonists.

We compared the ability of cultured endothelial cells isolated from rabbit aorta, vena cava, ventricular chamber, and pulmonary microvasculature to produce relaxing factor(s) in response to acetylcholine (ACh) and bradykinin (BK). Endothelium-denuded rabbit aortic rings were precontracted with 1 microM phenylephrine and superfused at 2 mL/min with Krebs-Henseleit bicarbonate buffer. Rings were exposed to 3-mL bolus control challenges of 1 microM ACh or 1 microM BK. Boluses of ACh or BK were added to dishes of cultured endothelial cells that had been incubated for 45 min in media either with or without 10 microM NG-nitro-L-arginine (NNLA). The resulting solution was applied over the rings within 8 s. Only left ventricular endothelial cells stimulated with ACh and BK, and pulmonary microvascular endothelial cells stimulated with BK produced products that relaxed rings by approximately 6 +/- 2%. Incubation with NNLA attenuated these relaxations. Our findings indicate there are differences in the abilities of endothelial cells of different anatomical origins to release nitric oxide derived relaxing factors in response to ACh and BK.

Acetylcholine↗
PubMed1994

Nitric oxide synthase inhibitors do not alter functional hyperemia in canine skeletal muscle.

To test the hypothesis that endothelium-derived products contribute to functional hyperemia in skeletal muscle, we infused nitric oxide synthase inhibitors, either 200 microM N omega-nitro-L-arginine (NNA) (N = 4) or 1 mM N gamma-monomethyl-L-arginine (NMMA) (N = 4), before and during 6 min of 4 Hz stimulation of canine gastrocnemius in situ. We infused saline (N = 4) as a control. NNA significantly decreased steady-level resting flow by 3.8 +/- 0.4 mL.kg-1.s-1. The increase in flow from rest to 5 min of stimulation was not changed by the nitric oxide synthase inhibitors. We also stimulated muscles for 60 min either with saline infusion (N = 4) or with the infusion of saline during the first 15 min and NNA for the remaining 45 min (n = 4). There was no difference in the flow during contractions. To clarify the effect of these inhibitors on canine vessels, we challenged rings of canine femoral artery with and without endothelium with acetylcholine and bradykinin (both 1 microM) before and after the addition of NNA and NMMA (both 10 microM). The nitric oxide synthase inhibitors decreased the relaxation accompanying acetylcholine. Both inhibitors caused only endothelium-intact rings to contract. Thus, the presence of a nitric oxide synthase inhibitor identified an endothelium-dependent contribution to the regulation of blood flow to skeletal muscle at rest but had no effect on functional hyperemia.

Acetylcholine↗
PubMed1994

Effect of nitroprusside and endothelium-derived products on slow-twitch skeletal muscle function in vitro.

We tested the hypothesis that the products of endothelial cells alter the force developed by skeletal muscle. Since these products have a very short half-life and are produced in a low concentration, we developed a superfused muscle preparation in which the mouse soleus (SOL) was superfused at 10.5 mL/min with Krebs-Henseleit buffer (KH) (27 degrees C; pH 7.4), gassed with 95% O2-5% CO2. To evaluate this preparation, we compared the superfused muscles with muscles submerged in a bath. All muscles were stimulated at 50 Hz for 500 ms once every 30 s. Submerged SOL developed 275 +/- 15 mN/mm2, while the superfused muscles developed 271 +/- 15 mN/mm2. Both submerged and superfused SOL consistently increased rest tension to a 3-mL bolus of 25 mM caffeine and decreased developed force when exposed to a 3-mL bolus of 30 mM diprotonated phosphate (pH 6.4). We then exposed superfused SOL to 3 mL bolus injections of KH, 1 microM acetylcholine, 30 mM nitroprusside (a source of nitric oxide), and the supernatant from dishes of cultured endothelial cells from rabbit aorta challenged with acetylcholine. Nitroprusside and the supernatant significantly improved force maintenance, compared with KH and acetylcholine, respectively. Since the supernatant should contain products of endothelial cells, these products appear to have a positive effect on contractile function in slow-twitch skeletal muscle that is similar to the effect of nitric oxide.

Acetylcholine↗
PubMed1991

Free radicals may contribute to oxidative skeletal muscle fatigue.

We used mouse soleus in vitro (n = 30) and canine gastrocnemius-plantaris preparations (n = 20) pump-perfused at the animal's blood pressure to establish if free radicals contribute to fatigue in oxidative skeletal muscle. The soleus from each leg contracted for 200 ms (70 Hz) once every minute for 60 min in Hepes buffer gassed with 100% oxygen at 27 degrees C. When contracting in Hepes alone, both muscles fatigued at 0.9 mN/mm2.min over the 60 min. The addition of purines to the bath increased the rate to 1.4 mN/mm2.min and the addition of xanthine oxidase to generate free radicals increased the rate again to 1.9 mN/mm2.min. Thus free radicals appeared to attenuate oxidative skeletal muscle function. Each canine muscle contracted isometrically at 4 Hz for 30 min and then rested for 45 min before contracting for a second 30 min at 4 Hz. In each experiment, we infused saline at 0.76 mL/min into resting muscle and at 1.91 mL/min during the first contraction period. During the remainder of the experiment, we infused, at the same rates, saline (n = 4), 10 microM dimethyl sulfoxide (DMSO) (n = 4) to identify the effect of scavenging hydroxyl radicals, 1 mM allopurinol to establish the effect of blocking xanthine oxidase (n = 4), or 200 microM desferoxamine to determine the effect of chelating iron (n = 4). With saline, the fatigue rate over the 30 min of contractions increased from 5.0 +/- 0.2 to 6.3 +/- 0.5 N/kg.min from the first to the second stimulation period. The fatigue rate was slower in the second period with each of the three experimental substances (DMSO, 5.9 +/- 0.8 to 3.2 +/- 0.3; allopurinol, 7.3 +/- 1.1 to 4.6 +/- 0.6; desferoxamine, 6.8 +/- 0.8 to 4.4 +/- 0.8 N/kg.min). The fatigue rate was the same as control when DMSO was infused only during the second contraction period. Therefore, free radicals appeared to contribute to fatigue in oxidative skeletal muscle.

Animals↗
PubMed1991

Differences between VO2 maxima of twitch and tetanic contractions are related to blood flow.

The purpose of this investigation was to compare oxygen uptake (VO2) and fatigue characteristics of isotonic tetanic contractions with those observed during isotonic twitches in dog gastrocnemius-plantaris muscle. Tetanic contractions (1/s, 200-ms trains of 50 impulses/s) elicited a peak VO2 of 9.01 +/- 0.42 mumol.g-1.min-1, which declined 29% in 30 min. The peak was significantly lower during 4/s twitches (6.23 +/- 0.36 mumol.g-1.min-1), but the rate of decline was similar. Peak blood flow (Q) was 37% higher and decreased more slowly during tetanic than twitch contractions. VO2/Q and VO2/venous PO2 were similar in both groups at peak VO2 and later declined or remained constant over time. Power was significantly greater with tetanic contractions with the relative decline between 3 and 30 min similar in both groups (32 and 37%). In conclusion, tetanic contractions result in significantly higher VO2 and power than do twitch contractions. This was derived primarily from increased Q because the arteriovenous O2 difference was similar. A significant determinant of the difference in Q between twitch and tetanic contractions is mechanical hindrance of Q. There is relatively more time for unhindered flow in the tetanic contractions. In electrically stimulated muscles, maximal VO2 is related to Q and reflects mainly Q through the muscle rather than the VO2 capacity of the muscle.

Animals↗
PubMed1990

A comparison of midazolam with and without nalbuphine for intravenous sedation.

The introduction of nalbuphine to intravenous sedation with midazolam added little to the quality of sedation for short operative procedures. There was a greater tendency for patients who received nalbuphine and midazolam to sleep in the afternoon after treatment compared with those who received only midazolam. Significantly more patients had nausea and vomiting in the midazolam/nalbuphine group than did patients in the midazolam-only group.

Adolescent↗
PubMed1990

Effect of acidosis on skeletal muscle metabolism with and without propranolol.

Does the stimulatory effect of circulating catecholamines counteract the inhibitory effect of acidosis on skeletal muscle metabolism? To investigate this possibility, we studied gastrocnemii in dogs breathing either air (n = 10) or 4% carbon dioxide in air (n = 10) at rest and during contractions. In five dogs from each group, we infused propranolol into the arterial supply of the right and left muscles for 40 min. After 30 min of infusion, the left muscle was stimulated at 3 Hz for 10 min. During the 10th min of contractions, we removed and froze both muscles in liquid nitrogen. Oxygen uptake and blood flow to the left muscle prior to or during stimulation was not affected by acidosis either with or without propranolol. Glycogen concentration in resting muscle was unaffected by acidosis with or without propranolol. There was an acidosis related decrease of approximately 50% in the glycolytic intermediates (glucose 6-phosphate, fructose 1,6-diphosphate, alpha-glycerol phosphate, and dihydroxyacetone phosphate) in unstimulated muscles without beta-blockade. At rest, acidosis decreased muscle lactate by 50% with and 64% without propranolol, but lactate release was decreased only with acidosis without propranolol (1.4-0.1 mumols/kg.s). Acidosis without propranolol had no effect on the changes in glycogen concentration or the change in the concentration of glycolytic intermediates resulting from contractions. In beta-blocked muscle, the difference between stimulated and unstimulated concentrations of glycogen and glycolytic intermediates including lactate was 20-50% smaller with acidosis. Thus, with beta-blockade, the acidotic effects at rest disappeared and an inhibition of the metabolic adjustment to contractions appeared, indicating that circulating catecholamines do modify some metabolic effects of acidosis.

Acidosis↗
PubMed1990

Effects of ischemic and hypoxic hypoxia on VO2 and lactic acid output during tetanic contractions.

We measured O2 uptake (VO2), CO2 output (VCO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxia hypoxia (hypoxia), and free-flow normoxia (control). The major goal was to assess the effects of these perturbations on L during contractions. Ischemia and hypoxia were initiated just before the start of the contractions and at minute 7 of contractions in separate groups of experiments. Whenever applied, both ischemia and hypoxia reduced VO2 compared with the control values. When ischemia was initiated at the start of contractions, L was reduced transiently compared with the controls. When ischemia began at minute 7, L was increased modestly but transiently compared with the controls. When hypoxia was initiated at the start of contractions, L was increased during the entire period of contractions. The L pattern was the same as in the controls, rising to a maximal value at 3 min and declining steadily to a lower value at 30 min. When hypoxia began at minute 7, L declined initially at a slower rate than it did in the controls and was thereby elevated above the controls from 9 to 30 min. Ischemia was associated with a more rapid reduction in mechanical performance than hypoxia. The data suggest that the mechanisms of the decreased mechanical performance and VO2 are different for ischemia and hypoxia.

Animals↗
PubMed1990

Antibiotics revisited.

The choice of an antibiotic for the management of an acute dental infection should be made from a relatively small range of agents. There is little evidence for prescribing the newer, more expensive, wide-spectrum, antibiotics. Failure to respond to therapy is usually due to inadequacy of dose, or failure to eliminate aggravating factors. The temptation to use antibiotics for the management of trivial infections should be resisted, and such problems managed by careful attention to first principles. The prophylactic use of antibiotics is less clear cut. Guidelines have been produced by expert committees that cover some situations, but such guidelines cannot be all-embracing. By weighing individual factors, the dentist should be able to reach a decision as to when antibiotic cover is indicated. This can only be done by maintaining contact with the literature in order to note changing recommendations, and drawing conclusions from conflicting opinions.

Anti-Bacterial Agents↗
PubMed1990

Hypothesis: local vascular regulation is a key to flow limited muscle function.

The ability of canine oxidative skeletal muscle in situ to maintain developed isometric force is flow limited during twitch contractions at greater than 3 Hz. This limitation implies a mismatching of blood flow and the metabolic rate. The blood flow past a muscle cell is determined by the number of capillaries per fibre, the vascular conductance, the capillaries perfused and vascular autoregulation. Of these, capillary number is regulated on a time scale of days while the other three require seconds to minutes. Each of the regulatory systems involves hypoxia, adenosine and the eicosanoids as contributing factors which would predict that regulatory systems working on the same time scale should change in parallel. This does not appear to be the case at high metabolic rates. The resulting mismatching of flow and metabolism accelerates the fatigue process. This peripheral vascular limitation can exist without a central cardiovascular limit being reached.

Animals↗
PubMed1989

Oxidation/reduction state of cytochrome oxidase during repetitive contractions.

There is disagreement regarding whether inadequate O2 determines maximal O2 uptake (VO2max) and lactic acid output (L) during muscular activity. Direct assessment of mitochondrial cytochrome oxidase (cytochrome a-a3) oxidation/reduction (O/R) state should provide an unequivocal answer for this issue. A new near-infrared spectrophotometric method was used to measure the O/R state of cytochrome a-a3 of dog gastrocnemius-plantaris muscle in situ during repetitive isotonic twitch and tetanic contractions. Three contraction frequencies were used for each contraction type in alternating sequence to provide a wide range of VO2 up to VO2max. VO2 and L were measured after 3 and 9 min of a 10-min contraction period, and 15 min were allowed for recovery between contraction periods. VO2 increased with contraction frequency. L was variably increased with contraction frequency at 3 min and uptake usually occurred at 9 min, except at the highest tetanic frequency. The O/R span of cytochrome a-a3 was determined by respiring the animals with 100% N2 to determine the most reduced state. This was followed by respiration with 100% O2, which gave the most oxidized state transiently during recovery. Within this span in muscles at rest, cytochrome a-a3 was 50-80% oxidized. During contractions of both types at all frequencies, cytochrome a-a3 always became more oxidized by an additional 10-20%. These findings should put to rest any arguments that inadequate O2 is a determinant of VO2max or L under the conditions of these experiments: repetitive contractions with free flow in self-perfused muscles and normoxia.

Animals↗
PubMed1989

Facial abscess: a case report.

This report describes a patient with a migratory abscess as a sequel to the surgical removal of a mandibular third molar tooth. Culture of pus drained from the abscess revealed no growth, probably because of previous management with antibiotics.

Abscess↗
PubMed1988

Effects of ischemia on VO2, tension, and vascular resistance in contracting canine skeletal muscle.

This study examined the changes in O2 consumption (VO2), vascular resistance, and tension development during skeletal muscle contractions at reduced flow. We tested the hypothesis that when VO2 is limited by O2 supply, the skeletal muscle vasculature is not maximally dilated because of the fall in contractile force that accompanies the decrease in O2 supply. During 30 min of ischemic contractions, tension fell by 45 +/- 4% and VO2 fell 54 +/- 1% from preischemic levels. The O2 cost per unit tension did not change compared with nonischemic muscles. After the initial flow reduction, flow fell an additional 16 +/- 3% over 30 min. Adenosine infusion after 30 min of ischemic contractions increased flow by 42 +/- 3% but increased VO2 by only 9.8 +/- 2.3% and had no effect on tension development. When perfusion pressure was returned to normal after 30 min of ischemic contractions, twitch tension did not begin to recover within 20 min but tetanic tension showed a small improvement. VO2, although increased, remained well below the preischemic level. These results suggest that because of the reduced tension during ischemic contractions, the O2 supply-to-consumption ratio is nearly normal, which could explain the presence of the vasodilator reserve. The defect in tension development is long lived, producing a "stunned" muscle in which excess O2 supply does not restore function or VO2 to normal.

Adenosine↗
PubMed1988

Physiological determinants of Qmax in contracting canine skeletal muscle in situ.

Canine skeletal muscle preparations in situ contain varying mixtures of fast and slow fatigue resistant fibers. All vessels on the arterial side of the vascular bed in these preparations from the conduit arteries to the arterioles contribute to the vascular resistance. The vascular beds autoregulate at rest and during contractions, indicating that the effects of the surgery are minimal. Stimulation frequency and pattern, i.e., twitch or brief tetanic contractions, the force exerted, and the length at which the muscle contracts, combine to determine the metabolic rate, which in turn, establishes the blood flow at a given perfusion pressure. When blood flow is normalized for oxygen uptake, the ratio is similar for twitch and rhythmic brief tetanic contractions. The ratio stays constant over a wide range of frequencies even though the flow increases and is greater than the theoretical minimum set by the maximum arteriovenous oxygen concentration difference. The infusion of vasodilators such as adenosine results in higher flows than those obtained with 6 Hz stimulation alone, indicating the presence of a "pharmacological reserve". The peak blood flow measured with isometric twitch contractions at 6 Hz in constant pressure pump perfused muscles at the optimum length for tension development averages 19.7 +/- 1.1 ml.kg-1.s-1. The pharmacological maximum at 6 Hz averages 25.9 +/- 1.6 ml.kg-1.s-1 with an observed maximum of 33.2 ml.kg-1.s-1.

Animals↗
PubMed1987

Root in the maxillary sinus.

The accidental displacement of a root into the maxillary sinus is a recognized complication of exodontia. Such roots should normally be removed early rather than late in order to minimize the likelihood of maxillary sinus complications. A root left within the maxillary sinus may, on occasion, pass spontaneously into the nose. Appropriate treatment and possible complications are discussed.

Foreign Bodies↗
PubMed1987

Carbonic anhydrase III inhibition in normocapnic and hypercapnic contracting mouse soleus.

The physiological role of carbonic anhydrase III in slow-twitch skeletal muscle was investigated using isolated mouse soleus (N = 30) contracting once every 1.7 min for 75 min in Krebs-Henseleit solution gassed with either 95% oxygen - 5% carbon dioxide (normocapnia) or 90% oxygen - 10% carbon dioxide (hypercapnia). Each contraction was 500 ms in duration at 50 Hz. When muscles contracted in normocapnic solution (pH 7.42), the developed tension decreased an average of 6.1 +/- 0.8% over 25 min. For the next 50 min, 15 muscles remained normocapnic, while the remainder contracted in hypercapnic solution (pH 7.20). Tension decreased significantly more with hypercapnia. For the last 25 min, both normocapnic and hypercapnic muscles were divided into three treatment groups (N = 5). One group continued in the same environment, while acetazolamide (final concentration of 10(-5) M) was added to the bath of the second and sodium cyanate (final concentration of 10(-5) M) was added to the bath of the third group. Acetazolamide had no effect on tension in either carbon dioxide environment. Sodium cyanate significantly decreased tension from the hypercapnic control but had no effect in normocapnia. Thus carbonic anhydrase III inhibition with sodium cyanate increased the effect of hypercapnia implying that carbonic anhydrase III assists in the regulation of free hydrogen ion concentration in slow-twitch skeletal muscle.

Acetazolamide↗