scholarly journals Oxygen dependence of respiration in rat spinotrapezius muscle contracting at 0.5–8 twitches per second

2018 ◽  
Vol 125 (1) ◽  
pp. 124-133 ◽  
Author(s):  
Aleksander S. Golub ◽  
Sami C. Dodhy ◽  
Roland N. Pittman

The oxygen dependence of respiration was obtained in situ in microscopic regions of rat spinotrapezius muscle for different levels of metabolic activity produced by electrical stimulation at rates from 0.5 to 8 Hz. The rate of O2 consumption (V̇o2) was measured with phosphorescence quenching microscopy (PQM) as the rate of O2 disappearance in a muscle with rapid flow arrest. The phosphorescent oxygen probe was loaded into the interstitial space of the muscle to give O2 tension (Po2) in the interstitium. A set of sigmoid curves relating the Po2 dependence of V̇o2 was obtained with a Po2-dependent region below a characteristic Po2 (~30 mmHg) and a Po2-independent region above this Po2. The V̇o2(Po2) plots were fit by the Hill equation containing O2 demand (rest to 8 Hz: 216 ± 26 to 636 ± 77 nl O2/cm3 s) and the Po2 value corresponding to O2 demand/2 (rest to 8 Hz: 22 ± 4 to 11 ± 1 mmHg). The initial Po2 and V̇o2 pairs of values measured at the moment of flow arrest formed a straight line, determining the rate of oxygen supply. This line had a negative slope, equal to the oxygen conductance for the O2 supply chain. For each level of tissue blood flow the set of possible values of Po2 and V̇o2 consists of the intersection points between this O2 supply line and the set of V̇o2 curves. An electrical analogy for the intraorgan O2 supply and consumption is an inverting transistor amplifier, which allows the use of graphic analysis methods for prediction of the behavior of the oxygen processing system in organs. NEW & NOTEWORTHY The sigmoidal shape of curves describing oxygen dependence of muscle respiration varies from basal to maximal workload and characterizes the oxidative metabolism of muscle. The rate of O2 supply depends on extracellular O2 tension and is determined by the overall oxygen conductance in the muscle. The dynamics of oxygen consumption is determined by the supply line that intersects the oxygen demand curves. An electrical analogy for the oxygen supply/consumption system is an inverting transistor amplifier.

1989 ◽  
Vol 256 (3) ◽  
pp. H772-H778 ◽  
Author(s):  
R. D. Wangler ◽  
W. P. Peterson ◽  
H. V. Sparks

d-Propranolol eliminates the increased adenine nucleoside release from hypoperfused hearts [R. D. Wangler, D. F. DeWitt, and H. V. Sparks, Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H330-H336, 1984]. To determine whether d-propranolol reduces adenosine formation or adenosine release into the vascular compartment, we measured myocardial tissue adenosine (TADO). Decreased formation would lower TADO, whereas decreased release would elevate TADO. Reduction of perfusion pressure by 50% reduced coronary flow (CF), venous oxygen tension (PVO2), and myocardial oxygen consumption (MVO2) by approximately 40, 25, and 35%, respectively. Total adenosine and inosine released during 30 min of hypoperfusion increased 10- and 5-fold, respectively. Also, TADO increased from 2.68 +/- 0.37 to 5.17 +/- 0.67 nmol/g (P less than 0.05). In the presence of d-propranolol, the same reduction in perfusion pressure caused a similar decrease in CF and MVO2. d-Propranolol eliminated the release of adenosine and inosine associated with hypoperfusion. TADO after 30 min of hypoperfusion plus d-propranolol was not significantly increased (3.27 +/- 0.40 nmol/g) and was significantly less than hypoperfused hearts. When severe hypoperfusion was created by reducing perfusion pressure 75%, adenosine release still did not increase if d-propranolol was present. When adenosine release was plotted as a function of oxygen supply-consumption, they were related in a hyperbolic fashion. Despite the severity of hypoperfusion, in the presence of d-propranolol the supply-to-consumption ratio was similar to that of the control perfusion group (no drug). We conclude that d-propranolol blocks nucleoside formation during hypoperfusion by reducing oxygen demand such that a reduction of oxygen supply no longer stimulates adenosine formation.


1991 ◽  
Vol 260 (4) ◽  
pp. C708-C714 ◽  
Author(s):  
R. T. Smolenski ◽  
J. Schrader ◽  
H. de Groot ◽  
A. Deussen

Adenosine formation by the heart is known to critically depend on the ratio of oxygen supply to oxygen demand, but the sensitivity of cardiomyocytes to defined changes in PO2 is not known. Isolated metabolically stable rat cardiomyocytes were incubated up to 45 min at constant PO2 values ranging from 0.1 to 100 mmHg using a feedback-controlled incubation system (oxystat system). Changes of the free intracellular adenosine concentration were measured after trapping of adenosine by cytosolic S-adenosylhomocysteine (SAH) hydrolase in the presence of 200 microM L-homocysteine thiolactone. Rate of SAH formation was constant at a PO2 between 3 and 100 mmHg and gradually increased at PO2 less than 3 mmHg. Cellular ATP decreased only at PO2 less than 1 mmHg, and this was accompanied by a decline of oxygen consumption. Treatment of cells with 5.5 mM deoxyglucose and 4 micrograms/ml oligomycin increased SAH formation 60-fold and was associated with elevated intra- and to a lesser extent extracellular adenosine levels. Inhibition of nucleoside transport with 20 microM S-(p-nitrobenzyl)-6-thioinosine steepened the transmembrane adenosine gradient. Our findings suggest that the cardiomyocyte responds to metabolic poisoning and oxygen deprivation with an enhanced formation of adenosine. This adenosine is mainly formed intracellularly and reaches the extracellular space by diffusion. Threshold for adenosine formation is as low as 3 mmHg.


2001 ◽  
Vol 281 (2) ◽  
pp. H823-H830 ◽  
Author(s):  
Bradley J. Hart ◽  
Xiaoming Bian ◽  
Patricia A. Gwirtz ◽  
Srinath Setty ◽  
H. Fred Downey

This is the first investigation of right ventricular (RV) myocardial oxygen supply/demand balance in a conscious animal. A novel technique developed in our laboratory was used to collect right coronary (RC) venous blood samples from seven instrumented, conscious dogs at rest and during graded treadmill exercise. Contributions of the RV oxygen extraction reserve and the RC flow reserve to exercise-induced increases in RV oxygen demand were measured. Strenuous exercise caused a 269% increase in RV oxygen consumption. Expanded arteriovenous oxygen content difference (A-VΔO2) provided 58% of this increase in oxygen demand, and increased RC blood flow (RCBF) provided 42%. At less strenuous exercise, expanded A-VΔO2 provided 60–80% of the required oxygen, and increases in RCBF were small and driven by increased aortic pressure. RC resistance fell only at strenuous exercise after the extraction reserve had been mobilized. Thus RC resistance was unaffected by large decreases in RC venous Po 2 until an apparent threshold at 20 mmHg was reached. Comparisons of RV findings with published left ventricular data from exercising dogs demonstrated that increased O2 demand of the left ventricle is met primarily by increasing coronary flow, whereas increased O2extraction makes a greater contribution to RV O2 supply.


2015 ◽  
Vol 752-753 ◽  
pp. 1073-1077
Author(s):  
Ying Jie Zhao ◽  
Hui Xiang Wu

Based on the analysis of the aircrafts oxygen supply performance, an new electronic oxygen supply regulator is designed. Meanwhile, the design calculation work is conducted and the structure parameters is obtained. From the results we can see that the designed oxygen regulator can satisfy the pilot’s oxygen demand under designed heights and that oxygen flow rise under different outlet pressures is not boundless as the valve opening width is increasing .Furthermore, when the valve opens to the half of its radius, the oxygen flow no longer changes as the opening width is increasing. Also, when it opens to the maximum, the peak demand under emergency can be satisfied.


1942 ◽  
Vol 44 (3) ◽  
pp. 321-332 ◽  
Author(s):  
Otto Rahn ◽  
G. L. Richardson
Keyword(s):  

2020 ◽  
Vol 6 (7) ◽  
pp. 1218-1226 ◽  
Author(s):  
Renata Mirra ◽  
Christian Ribarov ◽  
Dobril Valchev ◽  
Irina Ribarova

The objective of this work is to demonstrate that some weaknesses of the onsite packaged WWTP associated with high operational costs and energy inefficiency could be overcome by improved management. The research methodology consists of series of batch studies with sludge from municipal or onsite WWTP, which simulate different working regimes of the onsite WWTPs – daily operation, toilet flushing and dishwasher machine. A simple classical tool, Oxygen Uptake Rate (OUR) is used to prove the hypothesis that regardless the specificity of the onsite WWTPs, namely the irregularity of the flow and load, three parameters follow similar increasing and decreasing trends – inflow rate, inflow pollution load and oxygen demand in the reactor. The literature review has not shown research publication about applicability of (OUR) for management of onsite WWTPs, but has shown experience and knowledge with municipal WWTPs, which were utilized in our study. The results prove that when there is no wastewater generation in the household, the (OUR) in the reactor is very low, 0.0007 to 0.0015 mg/l.s, thus do not require high oxygen supply. However, when wastewater flushes into the onsite WWTP, the oxygen demand increases rapidly and (OUR) reaches the range of 0.0040 to 0.0063 mg/l.s depending on the type and the quantity of the incoming substrate (pollution load). These results, if verified in filed experiments will enable optimization of the energy use during onsite WWTP operation.  The suggestion is that the oxygen supply in the reactor should be adjusted according to the demand, respectively proportional to the inflow rate. In addition to the benefit of saving energy, the comprehensive sensors for dissolved oxygen monitoring, which require qualified maintenance could be avoided and replaced by simple sensors for level, which are anyway part of the equipment of most of the onsite packaged WWTP.


2011 ◽  
Vol 1 ◽  
pp. 10-15
Author(s):  
Ashfaq Ahmad ◽  

Myocardial infarction is simply due to decreased supply of oxygen and blood to the particular tissue of heart which ultimately leads to the death of tissue. Naturally heart is quite stable in its involuntary action due to balance between oxygen supply and oxygen demand of the cardiac muscle. when this balance is disturbed by the clot formation(atherosclerosis) in coronary artery or increased demand of oxygen due to increased heart rate then clinical situation arises as tightening of chest,laboured breathing, sweating and radiating pain originating form chest and terminating to left arm and jaws as well. A male of 55 years was hospitalized in one of the most well reputed hospital of Federal area of Pakistan. The patients was nimble due to cold sweating, sever radiating left sided chest pain and was in the state of fear and apprehension.


1990 ◽  
Vol 258 (6) ◽  
pp. G910-G918 ◽  
Author(s):  
K. Nagano ◽  
S. Gelman ◽  
E. L. Bradley ◽  
D. Parks

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.


2004 ◽  
Vol 100 (1) ◽  
pp. 70-76 ◽  
Author(s):  
Jens Meier ◽  
Gregor I. Kemming ◽  
Hille Kisch-Wedel ◽  
Stefan Wölkhammer ◽  
Oliver P. Habler

Background Acute normovolemic hemodilution reduces the circulating erythrocyte mass and, thus, the hemoglobin concentration. After extreme acute normovolemic hemodilution to the critical hemoglobin concentration (Hbcrit), oxygen demand of the tissues is no longer met by oxygen supply, and death occurs with increasing oxygen debt. The aim of the current study was to investigate whether ventilation with 100% oxygen (fraction of inspired oxygen [FiO2] = 1.0; hyperoxic ventilation) initiated at Hbcrit could restore adequate tissue oxygenation and prevent death. Methods Fourteen anesthetized pigs ventilated with room air (FiO2 = 0.21) were hemodiluted by exchange of whole blood for 6% hydroxyethyl starch (200,000:0.5) until the individual Hbcrit was reached. Hbcrit was defined as the onset of oxygen supply dependency of oxygen consumption and was identified with indirect calorimetry. For the next 6 h, animals were either ventilated with an FiO2 of 0.21 (n = 7) or an FiO2 of 1.0 (n = 7). Results All animals in the 0.21 FiO2 group died within the first 3 h at Hbcrit (i.e., 6-h mortality 100%). Death was preceded by an increase of serum concentrations of lactate and catecholamines. In contrast to that, six of the seven animals of the 1.0 FiO2 group survived the complete 6-h observation period without lactacidosis and increased serum catecholamines (i.e., 6-h mortality 14%; FiO2 0.21 vs. FiO2 1.0, P < or = 0.05). After 6 h at Hbcrit, the FiO2 was reduced from 1.0 to 0.21, and five of the six animals died within the next 3 h. Conclusion In anesthetized pigs submitted to lethal anemia, hyperoxic ventilation enabled survival for 6 h without signs of circulatory failure.


1982 ◽  
Vol 243 (4) ◽  
pp. H628-H633 ◽  
Author(s):  
A. N. Bacchus ◽  
S. W. Ely ◽  
R. M. Knabb ◽  
R. Rubio ◽  
R. M. Berne

The role of adenosine in matching myocardial oxygen supply to demand by regulating coronary blood flow has been the subject of intensive study. The present experiments were designed to determine the relationship among myocardial oxygen consumption, coronary blood flow, and adenosine production as estimated by pericardial adenosine accumulation under several physiological conditions in the same animal. Conscious chronically instrumented dogs were used to measure changes in coronary blood flow, myocardial oxygen consumption, and pericardial adenosine accumulation during two levels of treadmill exercise, excitement caused by loud noises, and feeding (the presentation and consumption of a meal). The results show significant increases in the adenosine production with all experimental procedures and significant linear correlations between myocardial oxygen consumption and coronary blood flow (r = 0.78), myocardial oxygen consumption and adenosine production (r = 0.73), and adenosine production and coronary blood flow (r = 0.88). These data show that increases in adenosine production by the normally oxygenated myocardium can be the physiological mechanism for matching oxygen supply to increased oxygen demand in the conscious dog.


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