Costal diaphragmatic O2 and lactate extraction in laryngeal hemiplegic ponies during exercise

1988 ◽  
Vol 65 (4) ◽  
pp. 1723-1728 ◽  
Author(s):  
M. Manohar ◽  
T. E. Goetz ◽  
D. Nganwa
Keyword(s):  
Maximal Exercise ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Hemoglobin Concentration ◽  
Insignificant Change ◽  
Resistive Breathing ◽  
O2 Extraction ◽  
Before And After ◽  
Arterial Po2

Diaphragmatic O2 and lactate extraction were examined in seven healthy ponies during maximal exercise (ME) carried out without, as well as with, inspiratory resistive breathing. Arterial and diaphragmatic venous blood were sampled simultaneously at rest and at 30-s intervals during the 4 min of ME. Experiments were carried out before and after left laryngeal hemiplegia (LH) was produced. During ME, normal ponies exhibited hypocapnia, hemoconcentration, and a decrease in arterial PO2 (PaO2) with insignificant change in O2 saturation. In LH ponies, PaO2 and O2 saturation decreased well below that in normal ponies, but because of higher hemoglobin concentration, arterial O2 content exceeded that in normal ponies. Because of their high PaCO2 during ME, acidosis was more pronounced in LH animals despite similar lactate values. Diaphragmatic venous PO2 and O2 saturation decreased with ME to 15.5 +/- 0.9 Torr and 18 +/- 0.5%, respectively, at 120 s of exercise in normal ponies. In LH ponies, corresponding values were significantly less: 12.4 +/- 1.3 Torr and 15.5 +/- 0.7% at 120 s and 9.8 +/- 1.4 Torr and 14.3 +/- 0.6% at 240 s of ME. Mean phrenic O2 extraction plateaued at 81 and 83% in normal and LH animals, respectively. Significant differences in lactate concentration between arterial and phrenic-venous blood were not observed during ME. It is concluded that PO2 and O2 saturation in the phrenic-venous blood of normal ponies do not reach their lowest possible values even during ME. Also, the healthy equine diaphragm, even with the added stress of inspiratory resistive breathing, did not engage in net lactate production.

Diaphragmatic O2 and lactate extraction during submaximal and maximal exertion in ponies

1988 ◽  
Vol 64 (3) ◽  
pp. 1203-1209 ◽  
Author(s):  
M. Manohar ◽  
T. E. Goetz ◽  
L. C. Holste ◽  
D. Nganwa
Keyword(s):  
Maximal Exercise ◽  
Treadmill Exercise ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Rest Period ◽  
Content Difference ◽  
Arterial Concentration ◽  
O2 Extraction ◽  
Lateral Thoracotomy ◽  
Venous O2 Saturation

Diaphragmatic O2 and lactate extraction were studied in 10 healthy ponies at rest and during treadmill exercise. The phrenic vein was aseptically catheterized via a lateral thoracotomy 8-35 days before the study. Arterial and phrenic venous blood samples were obtained simultaneously at rest and at 30-s intervals during 4 min of exertion. Three levels of exertion were studied (moderate, 10 mi/h; heavy, 15 mi/h; maximal, 20 mi/h), and a rest period of at least 90 min was allowed between them. Each pony was studied twice at least 2-3 days apart. At rest the diaphragmatic venous PO2, O2 saturation, arteriovenous O2 content difference, and O2 extraction were 43.2 ± 2.0 Torr, 76.1 ± 3.2%, 3.14 ± 0.43 ml/dl, and 23.60 ± 3.61%, respectively. Significant decrease in phrenic venous PO2 and O2 saturation occurred within 30 s of exercise. Phrenic venous PO2 decreased to 20.3 ± 1.0, 18.9 ± 1.1, and 15.4 ± 0.9 Torr at 120 s of moderate, heavy, and maximal exercise, respectively. Corresponding values of phrenic venous O2 saturation were 33.6 ± 2.2, 25.8 ± 2.1, and 17.9 ± 0.5%, respectively. Diaphragmatic arteriovenous O2 content difference expanded to 13.11 ± 0.49, 15.00 ± 0.60, and 16.90 ± 0.60 ml/dl at 120 s of moderate, heavy, and maximal exercise, respectively, as O2 extraction rose to 65.93 ± 1.98, 73.90 ± 1.99, and 80.95 ± 0.47%, respectively. During heavy and maximal exercise, the diaphragmatic venous lactate concentration remained similar to the arterial concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional lactate production in early canine endotoxin shock

1988 ◽  
Vol 254 (1) ◽  
pp. E45-E51 ◽  
Author(s):  
A. A. van Lambalgen ◽  
H. C. Runge ◽  
G. C. van den Bos ◽  
L. G. Thijs
Keyword(s):  
Blood Flow ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Endotoxin Shock ◽  
Serum Lactate ◽  
High Serum ◽  
Arterial Lactate ◽  
Endotoxin Challenge ◽  
O2 Extraction ◽  
Anesthetized Dogs

High serum lactate may not reflect the severity of endotoxin shock: the lactate load could even be formed immediately after the endotoxin challenge. During the first 30 min after endotoxin injection (Escherichia coli; 1.5 mg/kg iv) into anesthetized dogs (4 mg.kg-1.h-1 etomidate, n = 19) we studied arterial lactate concentration; contributions of portal and splanchnic (n = 6), renal and pulmonary (n = 7), and femoral (n = 6) vascular beds to the early lactate rise; and regional O2 extraction and blood flow (microspheres). In control dogs (n = 5, no endotoxin), we found no significant hemodynamic and biochemical changes. Endotoxin caused an immediate decrease in blood pressure, cardiac output, and organ perfusion, followed by recovery after approximately 5 min to approximately 75% of preshock values at t = 30 min (except for renal blood flow, which remained low). Arterial lactate concentration started to increase almost immediately after endotoxin and increased rapidly until t = 15 min (to 300%) and then leveled off, but in spite of the hemodynamic recovery it remained elevated. A major part of the early increase in lactate concentration can be explained by splanchnic lactate production. The total splanchnic bed released more lactate than the portal bed, indicating that the liver produces lactate. We conclude that the lactate concentration later in canine endotoxin shock depends on events that occur during early shock in which the liver may play a crucial role.

scholarly journals Increased Pentose Phosphate Pathway Flux after Clinical Traumatic Brain Injury: A [1,2-13C2]glucose Labeling Study in Humans

2007 ◽  
Vol 27 (9) ◽  
pp. 1593-1602 ◽  
Author(s):  
Joshua R Dusick ◽  
Thomas C Glenn ◽  
WN Paul Lee ◽  
Paul M Vespa ◽  
Daniel F Kelly ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Jugular Bulb ◽  
Pentose Phosphate ◽  
Severe Tbi ◽  
The Difference ◽  
Gas Chromatography Mass Spectroscopy

Patients with traumatic brain injury (TBI) routinely exhibit cerebral glucose uptake in excess of that expected by the low levels of oxygen consumption and lactate production. This brings into question the metabolic fate of glucose. Prior studies have shown increased flux through the pentose phosphate cycle (PPC) during cellular stress. This study assessed the PPC after TBI in humans. [1,2-13C2]glucose was infused for 60 mins in six consented, severe-TBI patients (GCS < 9) and six control subjects. Arterial and jugular bulb blood sampled during infusion was analyzed for 13C-labeled isotopomers of lactate by gas chromatography/mass spectroscopy. The product of lactate concentration and fractional abundance of isotopomers was used to determine blood concentration of each isotopomer. The difference of jugular and arterial concentrations determined cerebral contribution. The formula PPC = ( m1/ m2)/(3 + ( m1/ m2)) was used to calculate PPC flux relative to glycolysis. There was enrichment of [1,2-13C2]glucose in arterial-venous blood (enrichment averaged 16.6% in TBI subjects and 28.2% in controls) and incorporation of 13C-label into lactate, showing metabolism of labeled substrate. The PPC was increased in TBI patients relative to controls (19.6 versus 6.9%, respectively; P = 0.002) and was excellent for distinguishing the groups (AUC = 0.944, P < 0.0001). No correlations were found between PPC and other clinical parameters, although PPC was highest in patients studied within 48 h of injury (averaging 33% versus 13% in others; P = 0.0006). This elevation in the PPC in the acute period after severe TBI likely represents a shunting of substrate into alternative biochemical pathways that may be critical for preventing secondary injury and initiating recovery.

scholarly journals GLUCOSE METABOLISM OF THE SWIMBLADDER TISSUE OF THE EUROPEAN EEL ANGUILLA ANGUILLA

1993 ◽  
Vol 185 (1) ◽  
pp. 169-178 ◽  
Author(s):  
B. Pelster ◽  
P. Scheid
Keyword(s):  
Glucose Uptake ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Anguilla Anguilla ◽  
Pentose Phosphate ◽  
Co2 Production ◽  
European Eel ◽  
O2 Uptake ◽  
Lactate Release

Glucose uptake from, and lactate release into, the blood have been analysed in the active gas- depositing swimbladder of the immobilized European eel Anguilla anguilla. Under normoxic conditions, 0.72 micromole min-1 glucose was removed from the blood supply, while lactate was released into it at a rate of 1.16 micromole min-1. The rate of gas deposition into the swimbladder was significantly correlated with the rate of lactate production. Under hypoxic conditions, glucose consumption by, and lactate production of, the swimbladder tissue were reduced, as was the rate of gas deposition. Compared with normoxic conditions, lactate concentration in the swimbladder tissue was elevated after 1 h of hypoxia, indicating a decrease in lactate release. No difference in the osmolality of arterial and venous blood could be detected in these experiments. Combining the data for glucose uptake and lactate release measured under normoxic conditions with the values for O2 uptake and CO2 production of the swimbladder tissue measured under similar conditions in a previous study, a quantitative evaluation of glucose catabolism was performed. According to the O2 uptake of the tissue, only about 1 % of the glucose was oxidized, while about 80 % was fermented to lactic acid. The remaining 0.14 micromole min-1 glucose was presumably catabolized through the pentose phosphate shunt, as indicated by the CO2 production of 0.16 micromole min-1 that cannot be explained by aerobic metabolism.

scholarly journals Down regulating PHGDH affects the lactate production of Sertoli cells in varicocele

2020 ◽  
Author(s):  
Wen-bin Guo ◽  
Zhen-hui Huang ◽  
Cheng Yang ◽  
Xian-yuan Lv ◽  
Hui Xia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Male Infertility ◽  
Western Blot ◽  
Sertoli Cells ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Down Regulation ◽  
Regulation Model

Abstract Background: Although varicocele is considered to be one of the leading causes of male infertility, the precise mechanism underlying how varicocele leads to male infertility is not completely understood. We found the lactate concentration on the varicocele side of the patients was decreased compare with peripheral venous blood. In the testicles, the lactate produced by the sertoli cells (TM4) through the glycolysis pathway provides most of the energy needed for spermatogenesis, the reduction of lactate will affect spermatogenesis. The objective of this study was to investigate the mechanism of this abnormal energy metabolism phenomenon in varicocele.Methods: In this study, we collected the testicular tissue from patients with varicocele, the glycolysis related proteins PHGDH was identified by iTRAQ proteomics technology. Experimental rat varicocele model was constructed according to our new clip technique, the mRNA and protein expression levels of PHGDH were examined with qRT-PCR and Western blotting. We constructed a TM4 cell of PHGDH down-regulation model, and then detected the glucose consumption, LDH activities and lactate production in the TM4 cells. Western blot was conducted to investigate the effects of PHGDH on the expression of phosphoserine phosphatase (PSPH) and Pyruvate kinase M2 (PKM2). Flow cytometry was used to detect the cell apoptosis and cell cycle in TM4 cells.Results: The results showed that testicular protein PHGDH was down-regulated in varicocele. Down-regulation of PHGDH in TM4 cells significantly decreased the glucose consumption, LDH activities and lactate production in the TM4 cells, indicating that the low expression of PHGDH ultimately led to a decrease in lactate production by affecting the glycolysis. The Western blot results showed that the down-regulation of PHGDH significantly reduced the expression of pathway protein PSPH and PKM2, leading to the reduction of lactate production. Moreover, PHGDH knockdown can promote apoptosis and inhibit cell cycle to affect cell growth.Conclusions: Overall, we conformed that varicocele lead to the decreasing of testis lactate production. Down-regulation of PHGDH in TM4 cells may mediate the process of abnormal glucose metabolism. Our study provide new insight into the mechanisms underlying metabolism-associated male infertility and suggests a novel therapeutic target for male infertility.

Adenosine infusion does not improve maximal O2 uptake in isolated working dog muscle

1994 ◽  
Vol 76 (6) ◽  
pp. 2820-2824 ◽  
Author(s):  
S. S. Kurdak ◽  
M. C. Hogan ◽  
P. D. Wagner
Keyword(s):  
Vascular Resistance ◽  
Gastrocnemius Muscle ◽  
Venous Blood ◽  
Blood Gases ◽  
O2 Uptake ◽  
Vascular Perfusion ◽  
Fick Principle ◽  
O2 Extraction ◽  
Before And After ◽  
O2 Delivery

We asked whether maximally working muscle could increase O2 extraction at fixed O2 delivery [i.e., improve maximal O2 uptake (VO2max)] when vascular resistance was decreased with adenosine (A) infusion. We postulated that a reduction in vascular resistance at the same blood flow (Q) might result in more uniform vascular perfusion and also possibly increase red blood cell transit time, thereby potentially improving the ability of the tissue to extract O2. Pump-perfused isolated dog gastrocnemius muscle (n = 6) was stimulated maximally at each of two levels of Q: 110 +/- 3 and 54 +/- 4 (SE) ml.100 g-1.min-1 [normal control (C) and ischemia (I), respectively], both before and after giving 10(-2) M of A solution in each case. Arterial and venous blood samples were taken to measure blood gases, and the Fick principle was used to calculate O2 uptake. Resistance decreased significantly after A treatment in both groups (1.2 +/- 0.1 vs. 0.9 +/- 0.1 and 1.3 +/- 0.1 vs. 1.1 +/- 0.1 mmHg.ml-1.100 g.min for C vs. C + A and I vs. I + A, respectively; P < 0.01). O2 delivery was lower with I but did not change at either perfusion rate when A was infused. VO2max also decreased significantly with I but was no different when A was added (13.8 +/- 0.7 vs. 13.8 +/- 0.9 and 8.4 +/- 0.5 vs. 8.2 +/- 0.6 ml.100 g-1.min-1 for C vs. C + A and I vs. I + A, respectively). These results show that the decrease in resistance with A did not lead to changes in VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of long-term anemia and retransfusion on central circulation during exercise

1986 ◽  
Vol 61 (4) ◽  
pp. 1358-1362 ◽  
Author(s):  
F. Celsing ◽  
J. Nystrom ◽  
P. Pihlstedt ◽  
B. Werner ◽  
B. Ekblom
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Maximal Exercise ◽  
Hemoglobin Concentration ◽  
Close Correlation ◽  
O2 Uptake ◽  
Exercise Tests ◽  
O2 Extraction ◽  
Male Subjects

The purpose of this study was to evaluate the effect of long-term anemia and subsequent retransfusion of erythrocytes on various circulatory parameters. Anemia was induced in nine healthy male subjects by repeated venesections. The stored blood was retransfused after 9 wk (range 8–11 wk). Exercise tests were performed before venesection in the control state (C), in the anemic state (A), and 48 h after retransfusion (R). Hemoglobin concentration levels were 146 +/- 10 g/l in C, 110 +/- 7 g/l in A, and 145 +/- 9 g/l in R. Maximal O2 uptake was 4.55 +/- 0.6, 3.74 +/- 0.7, and 4.45 +/- 0.6 l/min in C, A, and R, respectively. A decrease in heart rate of 7 beats/min (P less than 0.01) and in cardiac output of 2 l/min (P less than 0.05) at maximal exercise occurred in the anemic state compared with control values. These decreases were not reversed but, rather, were further accentuated after retransfusion. The adaptive response to submaximal exercise (cycling at 150–175 W) in anemia was mediated to the amount of 50% by an increase in cardiac output (mainly an increase in heart rate) and 50% was due to increased O2 extraction in the peripheral tissue. In conclusion, long-term anemia was found to decrease the heart rate and cardiac output at maximal exercise. Furthermore the close correlation between hemoglobin concentration and maximal O2 uptake in humans is confirmed.

scholarly journals Down regulating PHGDH affects the lactate production of Sertoli cells in varicocele

2020 ◽  
Author(s):  
Wen-bin Guo ◽  
Zhen-hui Huang ◽  
Cheng Yang ◽  
Xian-yuan Lv ◽  
Hui Xia ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Male Infertility ◽  
Western Blot ◽  
Sertoli Cells ◽  
Venous Blood ◽  
Lactate Concentration ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Down Regulation ◽  
Regulation Model

Abstract Background: Although varicocele is considered to be one of the leading causes of male infertility, the precise mechanism underlying how varicocele leads to male infertility is not completely understood. We found the lactate concentration on the varicocele side of the patients was decreased compare with peripheral venous blood. In the testicles, the lactate produced by the sertoli cells through the glycolysis pathway provides most of the energy needed for spermatogenesis, the reduction of lactate will affect spermatogenesis. The objective of this study was to investigate the mechanism of this abnormal energy metabolism phenomenon in varicocele.Methods: In this study, we collected the testicular tissue from patients with varicocele, the glycolysis related proteins PHGDH was identified by iTRAQ proteomics technology. Experimental rat varicocele model was constructed according to our new clip technique, the mRNA and protein expression levels of PHGDH were examined with qRT-PCR and Western blotting. We constructed a sertoli cell of PHGDH down-regulation model, and then detected the glucose consumption, LDH activities and lactate production in the sertoli cells. Western blot was conducted to investigate the effects of PHGDH on the expression of phosphoserine phosphatase (PSPH) and Pyruvate kinase M2 (PKM2). Flow cytometry was used to detect the cell apoptosis and cell cycle in sertoli cells.Results: The results showed that testicular protein PHGDH was down-regulated in patients with varicocele and in experimental rat varicocele model. Down-regulation of PHGDH in sertoli cells significantly decreased the glucose consumption, LDH activities and lactate production in the sertoli cells, indicating that the low expression of PHGDH ultimately led to a decrease in lactate production by affecting the glycolysis. The Western blot results showed that the down-regulation of PHGDH significantly reduced the expression of pathway protein PSPH and PKM2, leading to the reduction of lactate production. Moreover, PHGDH knockdown can promote apoptosis and inhibit cell cycle to affect cell growth.Conclusions: Overall, we conformed that varicocele lead to the decreasing of testis lactate production. Down-regulation of PHGDH in sertoli cells may mediate the process of abnormal glucose metabolism. Our study provide new insight into the mechanisms underlying metabolism-associated male infertility and suggests a novel therapeutic target for male infertility.

scholarly journals The Effect of Maximal Exercise on Matrix Metalloproteinase, its Inhibitor (MMP9 and TIMP1), and the Role of MMP9 -1562 C/T and TIMP1 372 T/C Polymorphisms

2021 ◽  
Author(s):  
Merve Koca Kosova ◽  
Faruk Turgay ◽  
Oya Yigittürk ◽  
Semih Aşıkovalı ◽  
Sercin Kosova ◽  
...  
Keyword(s):  
Genetic Polymorphisms ◽  
Acute Exercise ◽  
Maximal Exercise ◽  
Low Density Lipoprotein ◽  
Venous Blood ◽  
Density Lipoprotein ◽  
Post Exercise ◽  
Sedentary Group ◽  
Before And After

Abstract To investigate the levels of MMP9 and TIMP1 before and after acute maximal exercise and the role of MMP9 -1562 C/T and TIMP1 372 T/C polymorphisms in athletes and sedentary individuals. The athlete group (n = 43) and sedentary group (n = 43) performed the Yo-Yo intermittent recovery test level 1. A blood sample was taken before and after the test. MMP9, TIMP1, MMP9/TIMP1 ratio, blood lipids, and lipoproteins (total cholesterol, high and low-density lipoprotein cholesterol) and indicators of muscle damage (creatine kinase, aspartate aminotransferase, alanine aminotransferase) were determined from postprandial venous blood samples. Genetic polymorphisms were determined from DNA samples obtained from peripheral blood. MMP9 levels were found higher in both groups after the YOYO IR-1 test (exercise) (sedentary group, pre-exercise: 1771.15 ± 862.17 pg/mL, post-exercise: 2172.18 ± 680.93 pg/mL; athletic group, pre-exercise: 1373.57 ± 705.16 pg/mL, post-exercise: 1723.72 ± 733.88 pg/mL, p < 0.05). TIMP1 levels were also found higher in both groups after exercise (sedentary group, pre-exercise: 4.63 ± 3.99 ng/mL, post-exercise: 5.3 ± 3.51 ng/mL; athletic group, pre-exercise: 3.26 ± 2.34 ng/mL, post-exercise: 3.59 ± 1.99 ng/mL, p < 0.05). Basal serum MMP9 levels were significantly higher in sedentary individuals as compared with athletes (p = 0.046). MMP9 -1562 C/T and TIMP1 372 T/C polymorphisms had no effect on MMP9 and TIMP1 levels (p > 0.05). As a conclusion acute exercise increases MMP9 and TIMP1 levels in male athletes and sedentary individuals. Chronic anaerobic exercises performed by the athletic group may caused lower MMP9 levels. MMP9 -1562 C/T and TIMP1 372 T/C genetic polymorphisms are not associated with MMP9 and TIMP1 activation.

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