Experimental physiology
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Oxidative stress plays an important role in the pathophysiology of vascular diseases. Reactive oxygen species, especially superoxide anion and hydrogen peroxide, are important signalling molecules in cardiovascular cells. Enhanced superoxide production increases nitric oxide inactivation and leads to an accumulation of peroxynitrites and hydrogen peroxide. ⋯ Potential sources of vascular superoxide production include NADPH-dependent oxidases, xanthine oxidases, lipoxygenases, mitochondrial oxidases and nitric oxide synthases. Studies performed during the last decade have shown that NADPH oxidase is the most important source of superoxide anion in phagocytic and vascular cells. Evidence from experimental animal and human studies suggests a significant role of NADPH oxidase activation in the vascular remodelling and endothelial dysfunction found in cardiovascular diseases.
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Experimental physiology · Nov 2004
ReviewMuscle afferent contributions to the cardiovascular response to isometric exercise.
The cardiovascular response to isometric exercise is governed by both central and peripheral mechanisms. Both metabolic and mechanical stresses on the exercising skeletal muscle produce cardiovascular change, yet it is often overlooked that the afferent signal arising from the muscle can be modified by factors other than exercise intensity. This review discusses research revealing that muscle fibre type, muscle mass and training status are important factors in modifying this peripheral feedback from the active muscles. ⋯ Thus it appears that training may decrease the metabolic stimulation of muscle afferents and in some instances chronic exposure to the products of anaerobic metabolism may blunt the sensitivity of the muscle metaboreflex. There may be surprising parallels between the local muscle conditions induced in athletes training for longer sprint events (e.g. 400 m) and by the low-flow conditions in, for example, the muscles of chronic heart failure patients. Whether their similar attenuations in muscle afferent feedback during exercise are due to decreased metabolite accumulation or to a desensitization of the muscle afferents is not yet known.
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Experimental physiology · Nov 2004
Comparative StudyComparison of thermoregulatory responses to exercise in dry heat among prepubertal boys, young adults and older males.
The purpose of this investigation was to compare the thermoregulatory responses during exercise in a hot climate among three age categories. Eight prepubertal (PP), eight young adult (Y) and eight elderly (O) male subjects cycled at an intensity of 50 +/- 1% of their maximum oxygen uptake (V(O2peak)) for 85 min (three 20 min bouts with three 7 min rest periods) in hot and dry conditions (41 +/- 0.67 degrees C, 21 +/- 1% relative humidity). During the exercise-in-heat protocol, rectal temperature (T(re)) skin temperatures (T(sk)), heart rate (HR), V(O2), V(CO2) V(E), RER, sweat rate, and the number of heat activated sweat glands (HASG) were determined. ⋯ Furthermore, it was calculated that while the O group required only 4.1 +/- 0.5 W of heat energy to raise their body core temperature by 1 degrees C, and the Y group needed 6.9 +/- 0.9 W (1 degrees C)(-1), the PP group required as much as 12.3 +/- 0.7 W to heat up their body core temperature by 1 degrees C. These results suggest that in conditions similar to those imposed during this study, age and age-related characteristics affect the overall rate of heat gain as well as the mechanisms through which this heat is being dissipated. While prepubertal boys seem to be the most efficient thermoregulators, the elderly subjects appear to be the least efficient thermoregulators.
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Experimental physiology · Sep 2003
Isolation of the arterial supply to the carotid and central chemoreceptors in the sheep.
The aim of our study was to develop and validate a simple surgical model in the sheep which allows control of the gas composition of the blood supplying the carotid and central chemosensitive area independently of the rest of the body. This approach was made possible due to the specific features of the cranial circulation in the sheep. An extracorporeal circuit, consisting of a pump and a gas exchanger, was placed at the level of the two common carotid arteries to create a pressure gradient between the carotid and the systemic systems and to reverse blood flow in the vertebral vessels via the occipital arteries. ⋯ The slope of the relationship between minute ventilation (V(E)) and systemic arterial P(CO2) (P(a,CO2)) during high CO(2) inhalation in seven hyperoxic vagotomised and anaesthetised sheep was dramatically reduced, but remained above zero, when P(a,CO2) was maintained constant in the cephalic circuit (0.11 +/- 0.15 vs. 0.70 +/- 0.35 l min(-1) Torr(-1) for the control tests). This residual V(E) response to CO(2) inhalation remains to be explained since it could not be accounted for by any of the chemical or circulatory changes occurring in the cephalic circulation. Nevertheless, this preparation provides an easy method of maintaining chemical and circulatory homeostasis at the chemoreceptor level.
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Experimental physiology · Nov 2002
The effects of primary thoracic blast injury and morphine on the response to haemorrhage in the anaesthetised rat.
Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea mediated in part via a vagal reflex. Blast casualties may also suffer blood loss, and the response to progressive simple haemorrhage is biphasic: an initial tachycardia followed by a vagally mediated reflex bradycardia which can be attenuated by micro opioid agonists. The aims of this study were to determine the effects of thoracic blast injury on the response to subsequent haemorrhage, and the effects of morphine, administered after blast, on the response to blood loss. ⋯ Mean arterial blood pressure (MBP) began to fall as soon as haemorrhage commenced and was significant after the loss of 10 % BV. Morphine (Group III) prevented the haemorrhage-induced bradycardia and delayed the significant fall in MBP until the loss of 30 % BV. It is concluded that the response to thoracic blast injury augments the depressor response to haemorrhage while morphine attenuates this response.