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D Cotterrell

Publications and source records attributed to D Cotterrell.

16 recordsLinked to original sources
PubMed2007

Effect of wearing personal protective clothing and self-contained breathing apparatus on heart rate, temperature and oxygen consumption during stepping exercise and live fire training exercises.

Fire fighter breathing apparatus instructors (BAIs) must possess the ability to respond to both the extrinsic stress of a high temperature environment and the intrinsic stress from wearing personal protective equipment (PPE) and self-contained breathing apparatus (SCBA), repeatedly and regularly, whilst training recruits in live fire training exercises (LFTEs). There are few previous investigations on BAIs in hot environments such as LFTEs, since the main research focus has been on regular fire fighters undertaking exercises in temperate or fire conditions at a moderate to high exercise intensity. In this study, the intrinsic cardiovascular stress effects of wearing PPE + SCBA were first investigated using a step test whilst wearing gym kit (control), weighted gym kit (a rucksack weighted to the equivalent of PPE + SCBA) and full PPE + SCBA (weight plus the effects of protective clothing). The extrinsic effects of the very hot environment were investigated in BIAs in LFTEs compared to mock fire training exercises (MFTEs), where the fire was not ignited. There was an increase in heart rate due to the modest workload imposed on the BAIs through carrying out the MFTEs (25.0 (18.7)%) compared to resting. However, when exposed to fire during the LFTEs, heat storage appears to be significant as the heart rate increased by up to 39.8 (+/-20.1)% over that of the mock LFTEs at temperate conditions. Thus, being able to dissipate heat from the PPE is particularly important in reducing the cardiovascular responses for BAIs during LFTEs.

Adult↗
PubMed2000

Exercise training for claudicants: changes in blood flow, cardiorespiratory status, metabolic functions, blood rheology and lipid profile.

OBJECTIVE: Exercise training improves the walking distance of claudicants. The aim of this study was to investigate factors associated with the improvement in the maximum walking distance (MWD) in respect to cardiovascular, respiratory and metabolic adaptations. METHODS: Forty claudicants were studied. Common femoral artery blood flow (BF), heart rate (HR), oxygen consumption (VO(2)), respiratory exchange ratio (RER), lactate levels, blood rheology and lipid profiles were measured. Tests were repeated after 3 months of exercise training. RESULTS: Fifteen patients did not complete the exercise program. For patients who did complete the program, MWD improved by 82%. A significant reduction in HR and VO(2)during exercise was demonstrated. No significant changes occurred in BF or RER. Although MWD increased significantly, there was no increase in recovery VO(2)(oxygen debt). A significant reduction in post-exercise lactate levels occurred. Blood rheology was unchanged, but an improvement in HDL levels was noted. CONCLUSIONS: Many claudicants could not complete an exercise program, mainly due to osteoarthritis. Exercise training improved exercise tolerance significantly without any increase in BF. The HR and oxygen cost of similar exercise was reduced. An improved MWD did not correlate with a higher oxygen debt or lactate load. Favourable changes in lipid profiles occurred.

Aged↗
PubMed1993

Grant policy.

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Animals↗
PubMed1989

The influence of blood flow rate on adenosine release from contracting dog skeletal muscle.

The dependence of adenosine release on blood flow was investigated in greyhounds anaesthesized with sodium pentobarbitone and artificially ventilated. The gracilis muscles were neurally and vascularly isolated, and perfused at constant flow rates of 42% (low), 89% (medium) or 132% (high) of their maximum free flow during contraction induced by stimulation of the motor nerve. Stimulation produced contractions whose force declined from 716 +/- 60 to 464 +/- 46 g (100 g)-1 over 10 min. Resting perfusion pressure increased in line with the flow rate, but the fall in resistance accompanying contractions varied reciprocally with the flow (57 +/- 2.9, 39.6 +/- 6.6 and 15.3 +/- 5.6% at low, medium and high flows respectively). Venous PO2 decreased during contraction to 26.6 +/- 6.2 mmHg at 'low', 31.5 +/- 5.1 mmHg at 'medium' and 37.2 +/- 1.7 mmHg at 'high' flows. Venous plasma adenosine concentration increased significantly above resting levels during contraction at all flow rates. Adenosine release at low flow (12.0 +/- 2.7 nmol min-1 (100 g)-1) was significantly greater than that at medium or high flows (5.6 +/- 1.3 and 4.1 +/- 1.3 nmol min-1 (100 g)-1 respectively), but the latter were not different from each other. There was no correlation between adenosine release and either venous oxygen tension during muscle contraction or the ratio of oxygen supply to free-flow oxygen consumption. These data suggest that the mechanism underlying adenosine release during muscle contraction may be independent of oxygen lack.

Adenosine↗
PubMed1988

Changes in adenosine release and blood flow in the contracting dog gracilis muscle.

Ischaemic contraction of skeletal muscle increases the venous concentration of adenosine. The present investigation was undertaken to determine changes in blood flow and the release of adenosine into venous blood resulting from 5 min of free flow contractions of the isolated gracilis muscle in dogs anaesthetised with pentobarbitone sodium (42 mg.kg-1) and artificially ventilated. Arterial and venous concentrations of adenosine were measured by high performance liquid chromatography. Five-minute-contractions (induced electrically, 6 V, 1.8 ms, 4 Hz) caused significant increases in blood flow (to 304 +/- 33% of control; mean +/- SEM, n = 9) and venous plasma adenosine concentration (from 126 +/- 18 nM to 293 +/- 76 nM, equivalent to an average increase in release of 7.28 +/- 1.89 nmol.min-1 100 g-1 wet weight of muscle). The venous oxygen tension decreased from 8.33 +/- 0.48 to 3.39 +/- 0.31 kPa (62.5 +/- 3.6 to 25.4 +/- 2.3 mm Hg). This small but significant increase in venous adenosine concentration within the vasoactive range, in the face of a concomitant increase in blood flow, suggests that an increase in the interstitial adenosine concentration during free-flow exercise may contribute to the total dilatation of the resistance vessels to increase blood flow and keep its own concentration low. A significant correlation between venous adenosine concentration and vascular conductance is therefore absent. The results suggest that adenosine may contribute to sustained active hyperaemia in skeletal muscle.

Adenosine↗
PubMed1987

Venous adenosine content and vascular responses in dog hind-limb skeletal muscles during twitch contraction.

In dogs anaesthetized with pentobarbitone sodium and chloralose and artificially ventilated, the skeletal muscles of a hind limb were vascularly and neurally isolated and perfused at a constant flow of 150% of the resting blood flow (5.8 +/- 0.3 ml.min-1.100g-1 muscle tissue, mean +/- S.E.M., n = 6) obtained after denervation of the limb. Electrical stimulation of the cut peripheral ends of the femoral and sciatic nerves for 20 min resulted in muscle contraction and a decrease in arterial perfusion pressure to a new steady level (59.7 +/- 8.6% decrease in vascular resistance) within 2 min; the pressure remained constant throughout the remaining 20 min. Similarly venous oxygen tension decreased from 38.2 +/- 1.3 (control) to 16.4 +/- 1.7 mmHg (n = 5) during contractions. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (122.5 +/- 28 nM, n = 8). However, the adenosine concentrations in venous plasma increased significantly (P less than 0.05) from a control value of 94.8 +/- 33 nM (n = 8) to 256 +/- 82 nM (n = 8) after 10 min and 235 +/- 31 nM (n = 8) after 20 min of muscle contraction. During infusion of adenosine into the femoral artery to give a range of arterial plasma concentrations between 0.17 and 90 microM, 89.2 +/- 2.8% (n = 20) of the infused adenosine was removed (taken up by tissues) from the blood before it reached the vein. Infusion of adenosine caused dose-dependent decreases in vascular resistance ranging between 7 and 79%; 5.58 +/- 1.50 microM adenosine caused a decrease in resistance of 36.1 +/- 7.1% (n = 10) and 51.7 +/- 7.4 microM adenosine caused a decrease of 51.2 +/- 4.1% (n = 9). Comparison of venous plasma adenosine concentrations during adenosine infusions with those seen during contractions suggests that the released adenosine can contribute about 60% of the total vasodilatation seen during contractions of the muscle. These results show that adenosine appears in the venous blood during muscle contraction and is likely to contribute to exercise hyperaemia.

Adenosine↗
PubMed1987

Appearance of adenosine in venous blood from the contracting gracilis muscle and its role in vasodilatation in the dog.

1. In dogs anaesthetized with sodium pentobarbitone and artificially ventilated, the gracilis muscles were vascularly isolated and perfused at a constant flow rate of 51.2 +/- 9.8 ml min-1 100 g-1 muscle tissue (183 +/- 17.8% of resting blood flow; mean +/- S.E.; n = 13). 2. Electrical stimulation of the cut peripheral end of the obturator nerve (6 V, 4 Hz) resulted in muscle contraction (658 +/- 118 g 100 g-1 force after 5 min), and an immediate decrease in arterial perfusion pressure from 179 +/- 15.7 mmHg to 87 +/- 10.0 mmHg (51.4 +/- 4.5% decrease in vascular resistance after 2 min of contraction). Venous oxygen tension decreased from 69.2 +/- 5.1 mmHg to 18.5 +/- 1.4 mmHg (n = 6). These values did not significantly alter during the remaining period of stimulation (10-20 min). 3. The concentration of adenosine in arterial plasma did not change significantly during muscle contraction (137 +/- 23 nM; n = 10). However, the adenosine concentrations in venous plasma showed a significant (P less than 0.01) increase from a control value of 164 +/- 55 nM to 455 +/- 77 nM (n = 9) after 5 min of muscle contraction and remained high during the rest of the 20 min contraction. In six of the dogs adenosine concentrations were determined after 1 and 3 min of contraction and showed a smaller but statistically significant (P less than 0.05) rise in venous concentration. 4. During infusion of adenosine into the artery to give plasma concentrations between 0.3 microM and 1 mM, 72.6 +/- 2.1% (n = 29) of the infused adenosine was taken up by the tissues before it reached the vein. Comparison of vasodilatation and venous adenosine concentrations during adenosine infusion and muscle contractions showed that the released adenosine could contribute about 15% to the total vasodilatation after 1 min and about 40% between 5 and 20 min of contractions. Released adenosine could contribute about 80% to the vasodilatation that remained 5 min after the withdrawal of stimulation. Arterial perfusion pressure took 22 min to return to control, whereas adenosine release had fallen to zero within 10 min. 5. These data suggest that the released adenosine could contribute to exercise hyperaemia, but is unlikely to be the main factor, particularly in the initial stage.

Adenosine↗
PubMed1986

Analysis of submicromolar concentrations of adenosine in plasma using reversed phase high-performance liquid chromatography.

A method is described for the determination of adenosine in small samples of plasma (< 1 ml) using reversed-phase high-performance liquid chromatography (HPLC) in either a simple isocratic or a gradient elution system which gives a clear separation of adenosine from other plasma constituents. Acetone is used to deproteinize plasma and chloroform to remove unwanted lipid soluble material prior to HPLC. 6-Methyladenosine is used as an internal standard for making corrections for changes in concentration during sample processing. Adenosine in plasma could be reliably detected at concentrations lower than its minimum effector concentration as a vasodilator (4 x 10(-8) Mol l(-1) using the isocratic system and 1.9 x 10(-8) Mol l(-1) with gradient elution). The recoveries of adenosine added to blood at concentrations ranging from 2 x 10(-8) Mol l(-1) to 1.4 x 10(-6) Mol l(-1) were from 101.4 +/- 16.9% (n = 4) to 100.0 +/- 3.6% (n = 5). The present method provides a simple, sensitive and selective assay for submicromolar concentrations of adenosine in plasma with good recovery.

Journal Article↗
PubMed1982

Effects of adenosine and its analogues on the perfused hind limb artery and vein of anaesthetized dogs.

1. The effects of infusion of adenosine and its analogues on arterial and venous resistance have been studied in the vascularly and sympathetically isolated hind limb of chloralose-anaesthetized dogs. Resistance changes have been assessed by monitoring changes in perfusion pressures at constant flow through the femoral artery and metatarsal vein.2. With sympathetic stimulation (10 V, 2 msec, 0.5-2 Hz applied to the cut peripheral end of the lumbar sympathetic trunk), continuous infusion of adenosine, to produce a concentration of approximately 2 x 10(-5)m, resulted in a near maximal sustained decrease in arterial perfusion pressure of 35.3+/-3.6%, and a decrease of about half this in venous perfusion pressure.3. Bolus injections of adenosine into the artery, to produce a concentration of about 7 x 10(-5)m, caused a transient decrease in resistance similar to that observed with continuous infusion. However, the venous response was smaller than that induced by continuous infusion.4. Withdrawal of sympathetic stimulation to the limb had little effect on adenosine-induced vasodilatation in the artery, but abolished the small response of the vein.5. Less than 5% vasodilatation was produced in the artery and vein by 2-deoxyadenosine, inosine, guanosine, xanthosine, cytidine or uridine when infused in amounts up to ten times, or by sodium phosphate (pH 7.4) in amounts one hundred times the maximal amounts of adenosine given.6. These results suggest that adenosine caused vasodilatation, at least in arterioles, largely by acting directly on vascular muscle rather than via presynaptic inhibition of noradrenaline release.

Adenosine↗
PubMed1972

The uptake and hydrolysis of p-nitrophenyl phosphate by red cells in relation to ATP hydrolysis by the sodium pump.

1. The hydrolysis of p-nitrophenyl phosphate has been studied in human red cells, ghosts and haemoglobin-free membranes to see whether hydrolysis was related to the functioning of the sodium pump.2. The cell membrane restricted p-nitrophenyl phosphate entry into cells and was rate-limiting for hydrolysis by the large amount of intracellular soluble phosphatase. The uptake was inversely proportional to the external chloride concentration, and inhibitors (phloretin and persantin) of inorganic phosphate uptake also reduced p-nitrophenyl phosphate uptake and hydrolysis. The entry mechanism of p-nitrophenyl phosphate appears to be similar to that of inorganic phosphate.3. p-Nitrophenyl phosphate was hydrolysed in cells almost entirely by ouabain-insensitive phosphatases, both soluble and membrane bound. In ghosts containing less soluble enzyme than cells there was still no component of p-nitrophenyl phosphate hydrolysis that was related to the sodium pump in being sensitive to external potassium or ouabain.4. Haemoglobin-free membranes lacking soluble p-nitrophenyl phosphatase required potassium for optimum p-nitrophenyl phosphate hydrolysis and this part was inhibited by ouabain as was also ATP hydrolysis by the sodium pump. The rates of potassium-dependent and potassium-independent hydrolysis were each increased about threefold on decreasing the electrolyte concentration from 150 to 25 mM. The response was found whether the main electrolyte was potassium chloride, sodium chloride, choline chloride or Tris chloride. In contrast, the changes were not found when the osmotic pressure was varied to the same extent with non-electrolytes. p-Nitrophenyl phosphate hydrolysis was thus activated on lowering the ionic strength. The soluble enzyme was similarly affected and the effect was reversible.5. The membrane ATPase activity was unaffected by the changes in ionic strength which markedly altered p-nitrophenyl phosphate hydrolysis.6. These results with red cell membranes show that the ionic strength under physiological conditions largely prevents the hydrolysis of p-nitrophenyl phosphate, but not of ATP. A possible mechanism is discussed in terms of the effect of different structures of water in electrolyte and non-electrolyte solutions on the enzymic activity of the sodium pump.

Adenosine Triphosphatases↗
PubMed1971

The influence of the chloride gradient across red cell membranes on sodium and potassium movements.

1. A study has been made to see whether active and passive movements of sodium and potassium in human red blood cells are influenced by changing the chloride gradient and hence the potential difference across the cell membrane.2. Chloride distribution was measured between red cells and isotonic solutions with a range of concentrations of chloride and non-penetrating anions (EDTA, citrate, gluconate). The cell chloride concentration was greater than that outside with low external chloride, suggesting that the sign of the membrane potential was reversed. The chloride ratio (internal/external) was approximately equal to the inverse of the hydrogen ion ratio at normal and low external chloride, and inversely proportional to external pH. These results show that chloride is passively distributed, making it valid to calculate the membrane potential from the chloride ratio.3. Ouabain-sensitive (pump) potassium influx and sodium efflux were decreased by not more than 20 and 40% respectively on reversing the chloride gradient, corresponding to a change in membrane potential from -9 to +30 mV. In contrast, passive (ouabain-insensitive) movements were reversibly altered - potassium influx was decreased about 60% and potassium efflux was increased some tenfold. Sodium influx was unaffected by the nature of the anion and depended only on the external sodium concentration, whereas ouabain-insensitive sodium efflux was increased about threefold. When external sodium was replaced by potassium there was a decrease in ouabain-insensitive sodium efflux with normal chloride, but an increase in low-chloride medium.4. Net movements of sodium and potassium were roughly in accord with the unidirectional fluxes.5. The results suggest that reversing the chloride gradient and, therefore, the sign of the membrane potential, had little effect on the sodium pump, but caused a marked increase in passive outward movements of both sodium and potassium ions.

Biological Transport, Active↗