Microvascular PO2 Research Articles

Preservation of intestinal microvascular PO2 during normovolemic hemodilution in a rat model

The effect of hemodilution on the intestinal microcirculatory oxygenation is not clear. The aim of this study was to determine the effect of moderate normovolemic hemodilution on intestinal microvascular partial oxygen pressure (Po2) and its relation to the mesenteric venous Po2 (Pmvo2). Normovolemic hemodilution was performed in 13 anesthetized male Wistar rats. Systemic hemodynamic and intestinal oxygenation parameters were monitored. Intestinal microvascular Po2 was measured by using the oxygen-dependent quenching of palladium-porphyrin phosphorescence. Hemodilution decreased systemic hematocrit from 45.0% ± 0.1% (average ± SEM) to 24.6% ± 1.6%. The mesenteric blood flow did not change from baseline values, resulting in a linear decrease in intestinal oxygen delivery (from 2.77 ± 0.15 to 1.42 ± 0.11 mL·kg–1·min–1). The intestinal oxygen extraction ratio increased significantly from 24% ± 1% to 42% ± 4%. Pmvo2 decreased significantly (from 57 ± 2 to 41 ± 2 mm Hg), but intestinal oxygen consumption and microvascular Po2 remained unaffected. As a result, the difference between microvascular Po2 and Pmvo2 increased significantly during hemodilution. Intestinal microvascular Po2 and oxygen consumption were well preserved during moderate normo-volemic hemodilution. These results might be explained by the notion of others that hemodilution induces recruitment of capillaries, resulting in redistribution of the intestinal blood flow in favor of the microcirculation, which allows a more efficient extraction of oxygen. These findings further indicate that the use of venous Po2 values as indicators of microvascular oxygenation may be misleading. (J Lab Clin Med 2000;135:476-83)

Photochemical Oxygen Consumption Sensitized by a Porphyrin Phosphorescent Probe in Two Model Systems

Phosphorescence quenching of certain metalloporphyrins is used to measure tissue and microvascular pO 2. Oxygen quenching of metalloporphyrin triplet states creates singlet oxygen, which is highly reactive in biological systems, and these oxygen-consuming reactions are capable of perturbing tissue oxygenation. Kinetics of photochemical oxygen consumption were measured for a Pd-porphyrin in two model systems in vitro over a range of irradiances (1.34–134 mW cm −2). For a given irradiance, and, after correction for differing porphyrin concentrations, rates of oxygen consumption were similar when the Pd-porphyrin was bound to bovine serum albumin and when it was taken up by tumor cells in spheroids. At irradiances comparable to those used in imaging superficial anatomy, rates of oxygen consumption were sufficiently low (2.5 μM s −1) that tissue oxygenation would be reduced by a maximum of 6%. An irradiance of 20 mW cm −2, however, initiated a rate of oxygen consumption capable of reducing tissue pO 2 by at least 20–40%. These measured rates of consumption impose limitations on the use of phosphorescence quenching in thick tissues. The irreversible photobleaching of the Pd-porphyrin was also measured indirectly. The bleaching branching ratio, 23 M −1, is significantly lower than that of porphyrin photodynamic agents.

Functional heterogeneity of oxygen supply-consumption ratio in the heart.

In this review, the regional heterogeneity of the oxygen supply-consumption ratio within the heart is discussed. This is an important functional parameter because it determines whether regions within the heart are normoxic or dysoxic. Although the heterogeneity of the supply side of oxygen has been primarily described by flow heterogeneity, the diffusional component of oxygen supply should not be ignored, especially at high resolution (tissue regions << 1 g). Such oxygen diffusion does not seem to take place from arterioles or venules within the heart, but seems to occur between capillaries, in contrast to data recently obtained from other tissues. Oxygen diffusion may even become the primary determinant of oxygen supply during obstructed flow conditions. Studies aimed at modelling regional blood flow and oxygen consumption have demonstrated marked regional heterogeneity of oxygen consumption matched by flow heterogeneity Direct, non-invasive indicators of the balance between oxygen supply and consumption include NADH videofluorimetry (mitochondrial energy state) and microvascular PO2 measurement by the Pd-porphyrin phosphorescence technique. These indicators have shown a relatively homogeneous distribution during physiological conditions supporting the notion of regional matching of oxygen supply with oxygen consumption. NADH videofluorimetry, however, has demonstrated large increases in functional heterogeneity of this ratio in compromised hearts (ischemia, hypoxia, hypertrophy and endotoxemia) with specific areas, referred to as microcirculatory weak units, predisposed to showing the first signs of dysoxia. It has been suggested that these weak units show the largest relative reduction in flow (independent of absolute flow levels) during compromising conditions, with dysoxia initially developing at the venous end of the capillary.

Microcirculatory oxygenation and shunting in sepsis and shock.

To review optical spectroscopic techniques for assessment of the determinants of tissue oxygenation and to evaluate the notion that the disturbances in oxygen pathways in sepsis can be accounted for by enhanced functional shunting of parts of the microcirculation. Experimental data from previous research and the literature were analyzed. The data selected pertained to a) whether cellular distress in sepsis is caused by tissue hypoxia or disturbed metabolic pathways, b) optical spectroscopic techniques used to study microcirculatory oxygenation, and c) possible mechanisms underlying shunting of the microcirculation in hypoxemia and sepsis. STUDY SYNTHESIS: Despite resuscitation of oxygen-derived variables, signs of regional tissue hypoxia persist in sepsis. The mechanisms underlying this condition are expected to be associated with oxygen pathways in the microcirculation. Optical spectroscopic techniques are providing new insights into these mechanisms. These include absorption spectroscopy for hemoglobin saturation of erythrocytes, reduced nicotinamide adenine dinucleotide fluorescence for tissue mitochondrial bioenergetics, and palladium-porphyrin phosphorescence for microvascular PO2. Reduced nicotinamide adenine dinucleotide videofluorescence studies have shown the heterogeneous nature of hypoxia. Measurement of gut microvascular PO2 in pigs has shown the development of a PO2 gap between microvascular PO2 and venous PO2 during hemorrhage and endotoxemia, with a larger gap occurring in sepsis than in hemorrhage. It is hypothesized that this difference is caused by the enhanced shunting of the microcirculation present in sepsis. Microcirculatory distress may form one of the earliest stages in the progress of sepsis to multiple organ failure, and shunting of the microcirculation may be an important contributing factor to this development. To evaluate the severity of microcirculatory distress and the effectiveness of resuscitation strategies, new clinical technologies aimed at the microcirculation will need to be developed. It is anticipated that optical spectroscopy will play a major role in the development of such tools.

EVIDENCE FOR A REDUCED DIAPHRAGMATIC MICROVASCULAR PO2 IN EMPHYSEMA

507 Pulmonary emphysema impairs lung and respiratory muscle function leading to restricted physical capacity and accelerated morbidity and mortality consequent to respiratory muscle failure. In the absence of direct evidence, an O2 supply-demand imbalance within the diaphragm and other respiratory muscles in emphysema has been considered the most likely explanation for this failure. To test this hypothesis, we utilized phosphorescence quenching techniques to measure mean microvascular plasma PO2 (PO2dia, [Poole et al. J. Appl. Physiol. 79: 2050-2057, 1995 ]) within the medial costal diaphragms of control (C, n=5) and emphysematous (E, elastase instilled, n=6) hamsters. PO2dia, mean arterial pressure and blood gases were measured in the spontaneously breathing anesthetized hamster at inspired O2 concentrations of 10 and 21%. Arterial PO2 was decreased in the E hamsters at 21% (C, 90±13; E, 48±7 mmHg, P<0.05) and 10% (C, 55±8; E, 30±3 mmHg, P<0.05) inspired O2. At 21% inspired O2, PO2dia was significantly lower in the emphysema animals (C, 33±2; E, 22±3 mmHg, P<0.05). PO2dia decreased significantly at 10% inspired O2 in both C and E animals but remained lower in E (C, 19±3; E, 11±2 mmHg, P<0.05). We conclude that diaphragmatic microvascular plasma PO2 is decreased in emphysematous hamsters. According to Fick's Law, this will mandate a fall in intramyocyte PO2 thereby providing one possible mechanism for respiratory muscle failure in emphysema. Support: NIH HL-50306 and 17731.

Microvascular oxygen delivery and interstitial oxygenation during sodium pentobarbital anesthesia.

Anesthesia may represent a considerable bias in experimental medicine, particularly in conditions of stress (such as hemorrhage). Sodium pentobarbital (PB), widely used for cardiovascular investigations, may impair oxygen delivery by hemodynamic and respiratory depression. The critical issue, however, is whether the microcirculation can still maintain tissue oxygenation during anesthesia. To answer this question, the authors studied the effect of PB anesthesia on subcutaneous microvascular oxygen delivery and interstitial oxygenation in Syrian golden hamsters. Sodium pentobarbital anesthesia was induced by intravenous injection (30 mg/kg body weight) and maintained by a 15-min infusion (2 mg.kg-1.min-1), with animals breathing spontaneously (PB-S) or ventilated with air (PB-V). Systemic parameters evaluated were mean arterial pressure (MAP), heart rate, cardiac index (CI), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), base excess, and pH. Microvascular and interstitial oxygen tension (PO2), vessel diameter, red blood cell velocity (vRBC), and blood flow (Qb) were measured in a dorsal skinfold preparation. Microcirculatory PO2 values were determined by phosphorescence decay. Sodium pentobarbital anesthesia significantly decreased CI, MAP, vRBC, and Qb. During PB infusion, PaO2 values were 56 +/- 12.8 mmHg (PB-S) and 115.9 +/- 14.6 mmHg (PB-V) compared with 69.4 +/- 18.2 mmHg and 61.4 +/- 12.6 mmHg at baseline. However, microvascular PO2 was reduced by 25-55% in both groups, resulting in an interstitial PO2 decrease from 23.9 +/- 5.6 mmHg (control) to 13.1 +/- 9.1 mmHg (PB-S) and 15.2 +/- 7 mmHg (PB-V). Microcirculatory PO2 values were restored 30 min after PB infusion, even though hemodynamic depression and a light anesthetic plane were maintained. Sodium pentobarbital anesthesia caused impairment of microvascular oxygen delivery and interstitial oxygenation, effects that were not prevented by mechanical ventilation. Although these effects were restricted to deep anesthetic planes, prolonged hemodynamic depression suggests that caution is warranted when using PB as an anesthetic in cardiovascular investigations.

Microvascular gut oxygenation measured by Pd-porphyrin phosphorescence during severe hemorrhagic shock and low volume resuscitation with DCLHb™ in pigs

Diaspirin crosslinked hemoglobin (DCLHb™, Baxter Healthcare Corp) is a hemoglobin based blood substitute which has been demonstrated to restore systemic blood pressure following hypovolemic shock at a low dose in pigs. In this study microvascular pO2 of the pig gut (pO2microv) was measured with a light guide attached to a phosphorimeter and using Pd-porphyrin quenching of phosphorescence [1], during shock and resuscitation. Resuscitation with DCLHb™ was compared to resuscitation with a combination of crystalloid and colloid.

Systemic and subcutaneous microvascular Po2 dissociation during 4-h hemorrhagic shock in conscious hamsters.

The relationship between systemic and microvascular Po2 in subcutaneous connective tissue and hemodynamics was investigated during 4-h hemorrhagic shock (40 mmHg) in conscious Syrian hamsters (n = 66) fitted with a dorsal skinfold window. Systemic blood gases, metabolic parameters, arteriolar, venular, and tissue Po2, microvascular red blood cell velocity, and blood flow were evaluated in survivors (S) and nonsurvivors (NS). Surviving animals were resuscitated with shed blood. Microvascular and tissue Po2 were measured by phosphorescence decay of Pd-meso-tetra (4-carboxyphenyl) porphyrin (30 mg/kg body wt iv). Shock caused a significant dissociation between systemic arterial and microvascular arteriolar Po2 levels. Arterial Po2 increased from 59.7 +/- 12.0 to 110.8 +/- 19.7 mmHg (S) and from 64.0 +/- 13.7 to 128.5 +/- 10.1 mmHg (NS), whereas Po2 in large arterioles decreased from 56.9 +/- 5.5 (control) to 29.5 +/- 20.1 (S) and 6.0 +/- 5.7 mmHg (NS). Correspondingly, tissue Po2 fell from 24.1 +/- 6.8 (control) to 0.9 +/- 0.6 (S) and 0.4 +/- 0.3 mmHg (NS). Venous Po2 decreased from 28.8 +/- 3.7 to 20.4 +/- 4.1 (S) and from 28.0 +/- 2.9 to 16.3 +/- 0.5 mmHg (NS). Shock outcome and tissue oxygenation were predicted by arterial blood gases and metabolic and microcirculatory conditions but not by central venous Po2.

Diaphragm microvascular plasma PO2 measured in vivo.

Phosphorescence quenching techniques measure microvascular PO2 without direct surgical manipulation of the tissue. At a given arterial PO2, microvascular PO2 reflects the local O2 uptake-to-O2 delivery ratio, i.e., VO2/QO2. We evaluated the potential of phosphorescence quenching to determine microvascular PO2 in the rat costal diaphragm (PdiaO2). PdiaO2 and arterial blood gases were monitored across transient changes of inspired O2 among 21, 10, and 100% and also during hypotensive states evoked by progressive phlebotomy. After a transit delay, PdiaO2 responded rapidly to alterations of inspired and thus arterial PO2, with half times of the response averaging 5-7 s for switches to a lower inspired O2 (i.e., from 21 to 10%, from 100 to 21%, and from 100 to 10%) and also from 10 to 21%. By comparison, half times of the 10 to 100% and 21 to 100% switches were longer [11 s (P = 0.085) and 21 s (P < 0.05), respectively]. Below a mean arterial blood pressure (BP) of 120-130 mmHg, PdiaO2 decreased as a linear function of BP, with these variables being significantly correlated in each instance (n = 5, r = 0.851-0.937, P < 0.01 for all animals). From these results, it appears feasible to measure PdiaO2 in the spontaneously breathing rat in vivo under steady-state and transient conditions. Also, during progressive hypotension, the fall in PdiaO2 is significantly related to falling BP, likely as a consequence of an increased metabolic demand (increased ventilation and diaphragm VO2) concomitant with decreased blood flow. We conclude that phosphorescence quenching techniques offer a powerful tool for assessing diaphragm physiology and pathophysiology.

Systemic and subcutaneous microvascular oxygen tension in conscious Syrian golden hamsters.

Arteriolar and venular oxygen tension distribution was studied in the subcutaneous connective tissue of the chamber window preparation in conscious Syrian golden hamsters as a function of the systemic PO2, PCO2, pH, arterial pressure and hematocrit, microvascular red blood cell (RBC) velocity, vessel diameter, and blood flow in the same microvessels. PO2 was measured with the phosphorescence decay technique using Pd-meso-tetra(4-carboxyphenyl)porphyrin (30 mg/kg body wt iv). Systemic arterial and venous PO2s were 71.6 +/- 13.1 and 28.4 +/- 5.1 mmHg, while oxygen tension was 45.1 +/- 13.3 mmHg in arterioles and 30.1 +/- 10.7 mmHg in venules. The relatively low arteriolar PO2 and the small arteriolar-venular PO2 gradient indicate that some blood oxygen exits directly to the tissue or is shunted before reaching the capillaries. RBC velocity was the strongest correlate of microvascular PO2 (arterial correlation coefficient = 0.503 and venous correlation coefficient = 0.560, P < 0.001). Microvascular PO2 was also correlated with blood flow, vessel diameter, blood pH, and PCO2 but not with systemic PO2. Arterial oxygen tension was only significantly related to PCO2, pH, and hematocrit. These findings suggest that oxygen delivery to the tissue improves with increasing blood flow velocity and that microvascular PO2 is a locally regulated parameter in the absence of major systemic perturbations.

Noninvasive measurement of microvascular and interstitial oxygen profiles in a human tumor in SCID mice.

Simultaneous measurements of intravascular and interstitial oxygen partial pressure (PO2) in any tissue have not previously been reported, despite the importance of oxygen in health and in disease. This is due to the limitations of current techniques, both invasive and noninvasive. We have optically measured microscopic profiles of PO2 with high spatial resolution in subcutaneous tissue and transplanted tumors in mice by combining an oxygen-dependent phosphorescence quenching method and a transparent tissue preparation. The strengths of our approach include the ability to follow PO2 in the same location for several weeks and to relate these measurements to local blood flow and vascular architecture. Our results show that (i) PO2 values in blood vessels in well-vascularized regions of a human colon adenocarcinoma xenograft are comparable to those in surrounding arterioles and venules, (ii) carbogen (95% O2/5% CO2) breathing increases microvascular PO2 in tumors, and (iii) in unanesthetized and anesthetized mice PO2 drops to hypoxic values at < 200 microns from isolated vessels but drops by < 5 mmHg (1 mmHg = 133 Pa) in highly vascularized tumor regions. Our method should permit noninvasive evaluations of oxygen-modifying agents and offer further mechanistic information about tumor pathophysiology in tissue preparations where the surface of the tissue can be observed.

Microvascular PO2 regulation and chemoreception in the cat carotid body.

Regulation of carotid body microcirculation and microvascular PO2 is in itself of great physiological interest, and understanding their roles in the integrated cellular and sensory functions is critical. Now that a sensitive optical method, based on quenching of phosphorescence of lumiphors is available (Vanderkooi et al., 1987; Wilson et al., 1988), we investigated the effects of arterial PCO2 and PO2 changes on the cat carotid body microvascular PO2 (CBM PO2) simultaneously with the chemosensory activity in vivo. The working hypothesis was that PCO2 -pH changes do not change CBM PO2 but affects the sensory discharge directly.

Contribution of in vivo microvascular PO2 in the cat carotid body chemotransduction.

To understand the interplay between microcirculatory control and carotid body (CB) function, we simultaneously measured carotid body microvascular PO2 (CBM PO2) and chemosensory activity in the cat in vivo under several experimental conditions. Cats were anesthetized with pentobarbital sodium, paralyzed, and artificially ventilated. CBs were exposed, and steady-state CBM PO2 was measured by the O2-dependent quenching of the phosphorescence of Pd-meso-tetra-(4-carboxyphenyl)porphine, which was administered intravenously. A few fibers of the carotid sinus nerve were used to record chemosensory discharges. At arterial PO2 (PaO2) of 103.4 +/- 4.1 Torr, CBM PO2 was 52.5 +/- 3.6 Torr (n = 9). Graded lowering of PaO2 from 160 to 50 Torr resulted in nearly proportional decreases in CBM PO2, but at lower PaO2 the decrease in CBM PO2 became more substantial. As PaO2 decreased, chemosensory discharge increased in parallel with CBM PO2. Hypercapnia and hypocapnia did not significantly change the relationship between PaO2 and CBM PO2, although the chemosensory discharge responded significantly. CBM PO2 and chemosensory discharge were not affected by hemorrhagic hypotension until arterial blood pressure fell below approximately 50 Torr and then CBM PO2 decreased and chemosensory discharge increased. The lack of a significant effect of hemorrhagic hypotension indicated that O2 delivery to CB was almost independent of the systemic blood pressure. Taken together, the observations suggest that CB microcirculation and PO2 are subject to control by intrinsic mechanisms and that CBM PO2 is compatible with oxidative metabolism playing a role in O2 chemoreception during hypoxia.

Optical measurements of the dependence of chemoreception on oxygen pressure in the cat carotid body

The relationship between oxygen pressure (PO2) in the carotid body and carotid sinus nerve discharge was evaluated in the isolated perfused/superfused cat carotid body using the oxygen-dependent quenching of phosphorescence. Images of phosphorescence intensity arising from Pd-coproporphyrin within the microcirculation of the carotid body provided measurements of intravascular PO2. These measurements were substantiated by determining phosphorescence life-time. The carotid body was perfused in the isolated state via the common carotid artery with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered Tyrode solution, pH 7.4, at a constant pressure of 80 mmHg. Superfusion was maintained with similar media equilibrated with 100% argon. PO2 in the exchange vessels was markedly less than that in the perfusate entering the carotid artery, 23 +/- 3 and 45 +/- 3 Torr for normoxic (111 +/- 15 Torr) and hyperoxic (345 +/- 72 Torr) perfusates, respectively. Chemosensory discharge rose slowly in response to a brief interruption of perfusate flow as PO2 steadily declined from either of these capillary PO2 values to approximately 10 Torr. Between approximately 10 and 3 Torr, chemosensory discharge increased strikingly, concomitant with an enhanced rate of oxygen disappearance, from -36 +/- 4 to -69 +/- 13 (92% change) and -28 +/- 3 to -48 +/- 3 (71% change) Torr/s for normoxic and hyperoxic perfusates, respectively. As PO2 fell below approximately 3 Torr, oxygen disappearance slowed and neural activity decayed. Thus the relationships between microvascular PO2 and chemosensory discharge and between oxygen disappearance and neural discharge suggest that oxygen metabolism in the carotid body determines the expression of oxygen chemoreception.

Tissue PO2 and functional capillary density in chronically ischemic skeletal muscle.

In order to study changes in functional capillary density and tissue PO2 in chronically ischemic skeletal muscle, a new model, using the Syrian golden hamster was developed. In the hamster dorsal skin fold, which receives its vascular supply from two cranial and two caudal feeding arteries, a double frame chamber was implanted and ischemia was induced in the cranial part by heat coagulation of the cranial arteries outside of the chamber. This technique allows for analysis of microvascular hemodynamics and local tissue PO2 prior to and during a prolonged period of ischemia in skin muscle. As result of ischemia the diameters of the arterioles increased (p less than 0.001) over the whole 11 day observation period. Functional capillary density decreased significantly (p less than 0.01) during the first 7 days, while capillary RBC-velocity was reduced throughout the 11 days of observation. RBC-velocity in collecting venules was diminished significantly throughout the postischemic observation period. The diameters of the collecting venules first increased upon ischemia (p less than 0.001) but were found decreased at 4, 7 and 11 days. Measurements of tissue PO2 demonstrated a marked decrease from a mean PO2 of 20.5 mmHg prior, to 9.5 mmHg following induction of ischemia. The model allows for induction of chronic ischemia and is suitable to study the effect of therapeutic measures on the microcirculation in chronically ischemic skeletal muscle in vivo.

Enhancement of maximal force by contralateral-limb stimulation

We calculated the light absorbing potential (LAP) of hemoglobin (Hb) and myoglobin (Mb) in mammalian skeletal muscle at rest based on analysis of published chemical and morphometric data (Part 1), interpreted changes in total[Hb + Mb] from NIRS during exercise (Part 2), and estimated the potential contribution of Hb and Mb to changes in NIRS from rest to exercise (Part 3). Part 1: [Hb] in skeletal muscle was estimated from microvascular volume, systemic blood [Hb], and microvascular hematocrit and saturation at rest and during exercise. Part 2: Changes in total[Hb + Mb] (as t[Hb + Mb]) during cycling or knee extension exercise were interpreted using the results of Part 1. Part 3: Using estimates of mean microvascular PO2, Hb and Mb contribution at peak exercise was estimated. Across several species, [Mb] contributed ∼50–70% of the total LAP to NIRS at rest in skeletal muscle. With exercise, increases in t[Hb + Mb] of up to 30% could be entirely explained by the predicted increase in microvascular hematocrit with exercise. Finally, Mb was estimated to contribute ∼70% of the changes in NIRS from rest to peak exercise.

Tissue PO2 in normal and denervated cat skeletal muscle.

ARTICLESTissue PO2 in normal and denervated cat skeletal muscleWJ Whalen, P Nair, D Buerk, and CA ThuningWJ Whalen, P Nair, D Buerk, and CA ThuningPublished Online:01 Dec 1974https://doi.org/10.1152/ajplegacy.1974.227.6.1221MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByQuantitative Assessment of Blood Lactate in Shock: Measure of Hypoxia or Beneficial Energy SourceBioMed Research International, Vol. 2020August Krogh's theory of muscle microvascular control and oxygen delivery: a paradigm shift based on new data12 September 2020 | The Journal of Physiology, Vol. 598, No. 20Edward F. Adolph Distinguished Lecture. Contemporary model of muscle microcirculation: gateway to function and dysfunctionDavid C. Poole14 October 2019 | Journal of Applied Physiology, Vol. 127, No. 4Skeletal muscle interstitial O 2 pressures: bridging the gap between the capillary and myocyte10 October 2018 | Microcirculation, Vol. 26, No. 5Skeletal muscle microvascular and interstitial PO2 from rest to contractions30 January 2018 | The Journal of Physiology, Vol. 596, No. 5Arteriolar oxygen reactivity: where is the sensor and what is the mechanism of action?21 July 2016 | The Journal of Physiology, Vol. 594, No. 18Measuring Intracellular Oxygenation with Myoglobin MRS10 September 2015Effects of perfluorocarbon emulsions on microvascular blood flow and oxygen transport in a model of severe arterial gas embolismJournal of Surgical Research, Vol. 187, No. 1Skeletal muscle capillary function: contemporary observations and novel hypotheses10 October 2013 | Experimental Physiology, Vol. 98, No. 12Dynamics of muscle microcirculatory and blood-myocyte O2 flux during contractions1 March 2011 | Acta Physiologica, Vol. 202, No. 3Phosphorescence quenching microrespirometry of skeletal muscle in situAleksander S. Golub, Michael A. Tevald, and Roland N. Pittman1 January 2011 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 300, No. 1Local Regulation of Microvascular Perfusion1 January 2011Blood flow and metabolic regulation in seal muscle during apneaJournal of Experimental Biology, Vol. 211, No. 20Local Regulation of Microvascular PerfusionIn vivo Tissue pO 2 Measurements in Hamster Skinfold by Recessed pO 2 Microelectrodes and Phosphorescence Quenching Are in Agreement26 January 2010 | Microcirculation, Vol. 5, No. 2‐3Capillary blood flow and tissue metabolism in skeletal muscle during sympathetic trunk stimulationMiklós Pál, András Tóth, Peipei Ping, and Paul C. Johnson1 February 1998 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 274, No. 2Comparing Tissue PO2 Measurements by Recessed Microelectrode and Phosphorescence QuenchingOxygen sensitivity of mitochondrial metabolic state in isolated skeletal and cardiac myocytesKeith Neu Richmond, Steven Burnite, and Ronald M. Lynch1 November 1997 | American Journal of Physiology-Cell Physiology, Vol. 273, No. 5Microelectrode Studies of Facilitated O2 Transport Across Hemoglobin and Myoglobin LayersAn examination of the measurement of flow heterogeneity in striated muscle.Circulation Research, Vol. 60, No. 1Autoregulation of blood flow.Circulation Research, Vol. 59, No. 5Microcirculatory responses to carotid sinus nerve stimulation at various ambient O2 tension in the rabbit tenuissimus muscleMicrovascular Research, Vol. 30, No. 3Blood flow in the rabbit tenuissimus muscle Influence of preparative procedures for intravital microscopic observationActa Physiologica Scandinavica, Vol. 114, No. 1Influence of oxygen on perfused capillary density and capillary red cell velocity in rabbit skeletal muscleMicrovascular Research, Vol. 19, No. 2Oxygen requirement for prostaglandin biosynthesisProstaglandins and Medicine, Vol. 1, No. 2Relative importance of tissue oxygenation and vascular smooth muscle hypoxia in determining arteriolar responses to occlusion in the hamster cheek pouch.Circulation Research, Vol. 41, No. 4Hypoxia in skeletal muscle at rest and during the transition to steady workMicrovascular Research, Vol. 13, No. 3Oxygen pressure in small lymphaticsPflügers Archiv European Journal of Physiology, Vol. 366, No. 1The effect of oxygen on arteriolar red cell velocity and capillary density in the rat cremaster muscleMicrovascular Research, Vol. 12, No. 1 More from this issue > Volume 227Issue 6December 1974Pages 1221-1225 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.6.1221PubMed4440766History Published online 1 December 1974 Published in print 1 December 1974 Metrics