Decrease In Oxygen Utilization Research Articles

Formation of initial changes in hemodynamics and fluid compartments in high surgical risk patients under the influence of acute abdominal pathology

Among the main factors of pathological changes that accompany acute abdominal pathology are the inflammatory process of the peritoneum and fluid deficiency due to its pathological losses. The aim of our study was to analyze the initial state of fluid compartments of the body and hemodynamics in high surgical risk patients with acute surgical abdominal pathology. There were examined 157 patients with acute abdominal pathology who underwent emergency laparotomy. The presence and severity of fluid deficiency were determined clinically by tissue hydrophilicity test by P.I. Shelestiuk, biochemically – by assessing the levels of hematocrit, hemoglobin, erythrocytes, blood electrolytes, vasopressin (ADH) and brain natriuretic propeptide (proBNP), as well as the mean erythrocyte volume and plasma osmolarity. Variables of fluid compartments of the body and central hemodynamics were studied using the non-invasive bioimpedancemetry. Based on the values of oxygen concentration in arterial and venous blood, total oxygen consumption (VO2) and delivery of oxygen (DO2), oxygen extraction ratio (O2ER) were calculated. The detected changes indicate intravascular fluid deficiency and concomitant hemoconcentration with normal electrolytes levels and plasma osmolarity. In patients with high surgical risk and moderate dehydration according to P.I. Shelestiuk, urgent surgical pathology of the abdominal cavity reduces extracellular fluid volume by 19.1% (p=0.019) of the reference by reducing the volume of the interstitium and intravascular fluid respectively by 20.7% (p=0.002) and 16.3% (p=0.001) of regional values, which forms in patients a state of "volume depletion" of moderate severity. This is accompanied by an increase in the ADH concentration by 16.7% (p=0.041) above reference and normal proBNP levels. Stroke volume decreases by 28.8% (p=0.021) against tachycardia (increase in heart rate by 39.7% (p=0.001) above normal) and vascular spasm (increase in systemic vascular resistance by 86.9% (p=0.001) above reference), which supports the normodynamic type of blood circulation (cardiac index – 3.2 (0.4) l/min/m2) with the decrease in stroke index and peripheral perfusion index by 41.3% (p=0.002) and 55.2% (p=0.002) from reference, respectively. DO2 decreases by 11.1% (p=0.011) from reference with VO2 increased by 16.3% (p=0.004) above reference, which leads to a decrease in oxygen utilization by 7.2% (p=0.041) from reference.

Coenzyme Q10reverses mitochondrial dysfunction in atorvastatin-treated mice and increases exercise endurance

Statins are cholesterol-lowering drugs widely used in the prevention of cardiovascular diseases; however, they are associated with various types of myopathies. Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and thus decrease biosynthesis of low-density lipoprotein cholesterol and may also reduce ubiquinones, essential coenzymes of a mitochondrial electron transport chain, which contain isoprenoid residues, synthesized through an HMG-CoA reductase-dependent pathway. Therefore, we hypothesized that statin treatment might influence physical performance through muscular mitochondrial dysfunction due to ubiquinone deficiency. The effect of two statins, atorvastatin and pravastatin, on ubiquinone content, mitochondrial function, and physical performance was examined by using statin-treated mice. Changes in energy metabolism in association with statin treatment were studied by using cultured myocytes. We found that atorvastatin-treated mice developed muscular mitochondrial dysfunction due to ubiquinone deficiency and a decrease in exercise endurance without affecting muscle mass and strength. Meanwhile, pravastatin at ten times higher dose of atorvastatin had no such effects. In cultured myocytes, atorvastatin-related decrease in mitochondrial activity led to a decrease in oxygen utilization and an increase in lactate production. Conversely, coenzyme Q(10) treatment in atorvastatin-treated mice reversed atorvastatin-related mitochondrial dysfunction and a decrease in oxygen utilization, and thus improved exercise endurance. Atorvastatin decreased exercise endurance in mice through mitochondrial dysfunction due to ubiquinone deficiency. Ubiquinone supplementation with coenzyme Q(10) could reverse atorvastatin-related mitochondrial dysfunction and decrease in exercise tolerance.

Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease

The use of sodium bicarbonate (NaHCO3) in cardiopulmonary arrest has been questioned, but the effects of NaHCO3 in patients with heart disease are not known. We therefore prospectively evaluated the effects of NaHCO3 in patients with congestive heart failure. Ten patients received NaHCO3 and control infusions of equimolar sodium chloride (NaCl). Measurements were made of blood gases, 2,3-diphosphoglyceric acid (2,3-DPG), glucose, lactate, cardiac hemodynamics, and oxygen consumption. The arterial oxygen tension (pO2) fell an average of 10 mm Hg after NaHCO3 administration in patients with congestive heart failure, whereas it rose with NaCl (p less than 0.005). Myocardial oxygen consumption decreased by 17% (p less than 0.002) without an accompanying change in oxygen demand. Systemic oxygen consumption fell by 21%. Red blood cell 2,3-DPG levels were elevated at baseline, but did not change with NaHCO3 administration. The oxygen pressure at 50% hemoglobin saturation (P50) was correspondingly elevated at baseline in these patients and decreased significantly with NaHCO3 (Bohr effect) (p less than 0.003). The arterial and mixed venous carbon dioxide tensions increased with NaHCO3 but decreased with NaCl administration (p less than 0.05). Blood glucose concentrations fell by 1.7 mmol/L with NaHCO3 (p less than 0.003) and blood lactate concentrations increased uniformly (p less than 0.001). Three patients developed net myocardial lactate generation during NaHCO3 administration; two of these three developed symptoms of angina. Coronary blood flow did not change with NaHCO3 but increased with NaCl (p less than 0.04). Two patients developed transient pump failure. These data demonstrate that NaHCO3 impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption. The decrease in oxygen utilization is associated with anaerobic metabolism, enhanced glycolysis, and elevation of the blood lactate level, and may lead to transient myocardial ischemia in some patients. Thus, the use of NaHCO3 in such patients warrants re-evaluation.

Studies on Oxidative Phosphorylation and Steroidogenesis by Ovarian Mitochondria after Gonadotropic Stimulation

No differences in oxidative phosphorylation or in the per cent of [4-14C]progesterone were found in ovarian mitochondria of immature rats after treatment with 20 IU of pregnant mare serum gonadotropin (PMSG) iv 30 min before killing. However, treatment of immature rats with 20 IU of PMSG sc 54 h prior to killing decreased the ADP:O ratio and increased the per cent of [4-14C]cholesterol conversion. Electron microscopic studies showed that mitochondria with lamellar cristae were prominent in ovaries of untreated rats, while large pleomorphic mitochondria and mitochondria with tubulovesicular cristae dominated in ovaries of PMSG-treated rats. Ovarian homogenates separated by zonal centrifugation showed three peaks od cytochrome oxidase activity which shifted to the heavier end of the gradient after PMSG treatment. These studies suggest that PMSG treatment influences ovarian mitochondria, possibly by stimulating the synthesis of additional functional components and/or the biogenesis of new mitochondria. Aminoglutethimide addition to bovine luteal mitochondria decreased steroidogenesis by 60% when succinate was used as substrate. However, there was a 16% increase in the ADP:O ratio, apparently due to a decrease in oxygen utilization. When oligomycin was added to luteal mitochondria, there was a 30% decrease in the ACP:O ratio but a 300% increase in [4-14C]cholesterol conversion. Dinitrophenol also decreased mitochondrial steroidogenesis. These results suggest that energy obtained from succinate oxidation can be diverted from phosphorylation to support steroidogenesis.

ALVEOLAR-ARTERIAL OXYGEN TENSION DIFFERENCES IN ANAESTHETIZED HORSES

Anaesthetized, laterally recumbent horses were found to have large alveolar-arterial oxygen tension differences. These differences had a rapid onset following the induction of anaesthesia and remained constant during the anaesthetic period both in horses breathing spontaneously and in those subjected to intermittent positive pressure ventilation. It is suggested that the differences may result from mismatching of ventilation and perfusion due to the effect of gravity on the pulmonary circulation and restricted ventilation of the lower lung. The large fall in cardiac output found may, if unaccompanied by a decrease in oxygen utilization, augment the alveolar-arterial oxygen tension differences by causing a decrease in the mixed venous oxygen tension.

Diminished Blood Flow and Oxygen Deprivation as Principal Factors in Progression of Shock.

s1 October 1964Diminished Blood Flow and Oxygen Deprivation as Principal Factors in Progression of Shock.Arthur C. Guyton, M.D.Arthur C. Guyton, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-798_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMany different research workers in the field of shock have recently come to the conclusion that one of the major factors that causes progression of shock is the deprivation of oxygen to the tissues resulting from diminished blood flow. This concept is supported by two primary types of evidence as follows: First, transport of oxygen to the tissues is even normally nearly "flow-limited." That is, a slight diminishment in cardiac output immediately begins to decrease the amount of oxygen used by the body. Thus, a 25% diminishment in cardiac output causes about 10% decrease in oxygen utilization; 50% decrease in... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Arthur C. Guyton, M.D.Affiliations: Jackson, Miss. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 798-798KeywordsBlood flowCardiac outputOxygenShock ePublished: 1 December 2008 Issue Published: 1 October 1964 PDF downloadLoading ...

Electronic evaluation of the fetal and maternal heart rate during hypothermia in a pregnant woman

I N D u c E D hypothermia has been employed with increasing frequency in recent years as an adjunct to surgery and in the treatment of a variety of medical conditions. Due to decrease in oxygen utilization, anesthesia requirements, and circulatory stress it is believed that hypothermia is of value particularly when renal, hepatic, or pulmonary disease complicates the necessity for operative interventi0n.l It is inevitable that instances requiring this accessory procedure may occur when the patient is concomitantly pregnant. Numerous observations have been made of the profound effects upon physiologic processes intimately related to the cardiovascular and metabolic systems which may accompany surface cooling methods that lower the total body temperature. The potential influence of the maternal hypothermic state on the fetus is less well documented. Only a few reports concerning results of the employment of this technique for patients during the period of gestation have appeared in the literature.