Responses observed in individual arterioles and venules of rat skeletal muscle during systemic hypoxia.

Mian, Rubina; Marshall, Janice M.

doi:10.1113/jphysiol.1991.sp018562

Cited by 25 publications

(56 citation statements)

References 19 publications

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“…On balance, dilator responses are more common than constrictor responses and dilator responses are more common and larger in the distal, or terminal arterioles, than in the proximal arterioles (85). Thus, the fact that gross muscle vascular conductance increases during systemic hypoxia disguises the fact that within muscle some vessels constrict while a majority dilate.…”

Section: Interactions Between Reflex and Local Effects Of Hypoxia In mentioning

confidence: 94%

“…Experiments of this type have shown that systemic hypoxia induces both increases and decreases in the diameter, dilatation and constriction, respectively, of individual arterioles of the spinotrapezius muscle (85). On balance, dilator responses are more common than constrictor responses and dilator responses are more common and larger in the distal, or terminal arterioles, than in the proximal arterioles (85).…”

Section: Interactions Between Reflex and Local Effects Of Hypoxia In mentioning

confidence: 99%

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Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Jm¹

1998

Braz J Med Biol Res

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This review describes the ways in which the primary bradycardia and peripheral vasoconstriction evoked by selective stimulation of peripheral chemoreceptors can be modified by the secondary effects of a chemoreceptor-induced increase in ventilation. The evidence that strong stimulation of peripheral chemoreceptors can evoke the behavioural and cardiovascular components of the alerting or defence response which is characteristically evoked by novel or noxious stimuli is considered. The functional significance of all these influences in systemic hypoxia is then discussed with emphasis on the fact that these reflex changes can be overcome by the local effects of hypoxia: central neural hypoxia depresses ventilation, hypoxia acting on the heart causes bradycardia and local hypoxia of skeletal muscle and brain induces vasodilatation. Further, it is proposed that these local influences can become interdependent, so generating a positive feedback loop that may explain sudden infant death syndrome (SIDS). It is also argued that a major contributor to these local influences is adenosine. The role of adenosine in determining the distribution of O 2 in skeletal muscle microcirculation in hypoxia is discussed, together with its possible cellular mechanisms of action. Finally, evidence is presented that in chronic systemic hypoxia, the reflex vasoconstrictor influences of the sympathetic nervous system are reduced and/or the local dilator influences of hypoxia are enhanced. In vitro and in vivo findings suggest this is partly explained by upregulation of nitric oxide (NO) synthesis by the vascular endothelium which facilitates vasodilatation induced by adenosine and other NO-dependent dilators and attenuates noradrenaline-evoked vasoconstriction. Correspondence

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Section: Interactions Between Reflex and Local Effects Of Hypoxia In mentioning

confidence: 94%

Section: Interactions Between Reflex and Local Effects Of Hypoxia In mentioning

confidence: 99%

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Jm¹

1998

Braz J Med Biol Res

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“…Experiments were performed on seventy-four of the male Sprague-Dawley and Wistar rats whose responses to systemic hypoxia were described in the preceding paper (Mian & Marshall, 1991), plus an additional six rats. The details of the anaesthesia, surgical preparation, arrangement of the spinotrapezius muscle for in vivo microscopy and the methods of recording and administering hypoxic mixtures were as described previously (Mian & Marshall, 1991).…”

Section: Methodsmentioning

confidence: 99%

“…The details of the anaesthesia, surgical preparation, arrangement of the spinotrapezius muscle for in vivo microscopy and the methods of recording and administering hypoxic mixtures were as described previously (Mian & Marshall, 1991). Vessel diameters were 500 HYPOXIA AND CATECHOLAMINES recorded before hypoxia and at 1, 2, 3, 5, 7, 9 and 10 min after the onset of hypoxia as described previously (Mian & Marshall, 1991), the maximum change in diameter at these times being used for statistical analyses. The values of arterial pressure and heart rate that were used for analysis were taken before hypoxia and at the end of the 2nd min of hypoxia (cf.…”

Section: Methodsmentioning

confidence: 99%

“…Accordingly, we have now observed the responses induced by hypoxia in individual arterioles of the consecutive sections of the arterial tree before and after topical application of a-or ,-adrenoreceptor antagonists to the spinotrapezius and have also examined the effects of these antagonists upon responses induced in individual sections of the venular tree. As diameter changes observed in any individual arteriole or venule were comparable in the first and second periods of hypoxia, but not in subsequent periods (Mian & Marshall, 1991), the antagonist was applied between the first two periods. Some of these findings have already been reported in brief (Marshall & Mian, 1989.…”

Section: Introductionmentioning

confidence: 99%

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The roles of catecholamines in responses evoked in arterioles and venules of rat skeletal muscle by systemic hypoxia.

Mian¹,

Marshall²

1991

The Journal of Physiology

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SUMMARY1. Studies have been made in the anaesthetized rat of the roles played by a-and /8-adrenoreceptor stimulation in determining diameter changes induced in individual arterioles and venules of the spinotrapezius muscle during systemic hypoxia (breathing 6% 02 for 3 min).2. Topical application to the spinotrapezius of phentolamine, the cz-adrenoreceptor antagonist, or sotalol, the ,3-adrenoreceptor antagonist, had no effect on the fall in systemic arterial pressure and tachyeardia induced by hypoxia.3. All arterioles and venules showed a decrease in diameter in response to topical application of noradrenaline (10-6 g ml-1): these responses were abolished by topical application of phentolamine. Moreover, those arterioles and venules that showed a decrease in diameter during hypoxia before phentolamine, showed a significantly smaller decrease, or an increase in diameter after phentolamine. This effect was most marked in primary and secondary arterioles (13-50 4am diameter).4. All arterioles and venules showed an increase in diameter in response to topical application of isoprenaline (10-6 g ml-1); these responses were abolished by topical application of sotalol. Moreover, these arterioles and venules that showed an increase in diameter during hypoxia before sotalol, showed a significantly smaller increase or even a decrease in diameter after sotalol. 5. These results suggest that during hypoxia the arterioles of skeletal muscle, especially primary and secondary arterioles, are under the constrictor influence of a reflex increase in sympathetic nerve activity while the venules, which have no sympathetic innervation, are under the constrictor influence of circulating catecholamines. They also suggest that in individual arterioles and venules, these constrictor influences may be overcome by dilatation mediated by the fi-adrenoreceptor influence of circulating catecholamines.6. Since some arterioles and venules still showed constriction during hypoxia after phentolamine and some still showed dilatation during hypoxia after sotalol, it seems that factors other than catecholamines contribute to the diameter changes. It is suggested that locally released metabolites exert a substantial dilator influence, particularly on terminal arterioles and collecting venules, those vessels nearest to the capillary bed. MS 8638 R. MIAN AND J. M. MARSHALL 7. These findings are discussed in relation to responses recorded during hypoxia in gross flow studies on hindlimb muscles and in view of the functional roles of the consecutive sections of muscle microcirculation.

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Intravital microscopy evaluation of angiogenesis and its effects on glucose sensor performance

Koschwanez¹,

Reichert²,

Klitzman³

2009

J Biomedical Materials Res

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An optical window model for the rodent dorsum was used to perform chronic and quantitative intravital microscopy and laser Doppler flowmetry of microvascular networks adjacent to functional and non-functional glucose sensors. The one-sided configuration afforded direct, realtime observation of the tissue response to bare (unmodified, smooth surface) sensors and sensors coated with porous poly-L-lactic acid (PLLA). Microvessel length density and red blood cell flux (blood perfusion) within 1mm of the sensors were measured bi-weekly over two weeks. When non-functional sensors were fully implanted beneath the windows the porous coated sensors had twofold more vasculature and significantly higher blood perfusion than bare sensors on Day 14. When functional sensors were implanted percutaneously, as in clinical use, no differences in baseline current, neovascularization or tissue perfusion were observed between bare and porous coated sensors. However, percutaneously implanted bare sensors had two-fold more vascularity than fully implanted bare sensors by Day 14, indicating other factors, such as micromotion, might be stimulating angiogenesis. Despite increased angiogenesis adjacent to percutaneous sensors, modest sensor current attenuation occurred over 14 days, suggesting that factors other than angiogenesis may play a dominant role in determining sensor function.

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Responses observed in individual arterioles and venules of rat skeletal muscle during systemic hypoxia.

Cited by 25 publications

References 19 publications

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

Chemoreceptors and cardiovascular control in acute and chronic systemic hypoxia

The roles of catecholamines in responses evoked in arterioles and venules of rat skeletal muscle by systemic hypoxia.

Intravital microscopy evaluation of angiogenesis and its effects on glucose sensor performance

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