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PubMed1998

Differential glucose tolerance in dipper and nondipper essential hypertension: the implications of circadian blood pressure regulation on glucose tolerance in hypertension.

OBJECTIVE: The goals of this study were to compare glucose tolerance in dipper and nondipper hypertensive patients and to explore the cause of glucose intolerance in essential hypertension. RESEARCH DESIGN AND METHODS: A total of 50 patients <45 years old who had essential hypertension were recruited and studied by 24-h blood pressure monitoring and an oral glucose tolerance test (OGTT). Autonomic function was assessed with spectral analysis of heart rate variability RESULTS: Dipper hypertensive patients (n=25) had lower nocturnal blood pressure than nondipper (n=25) patients. During OGTT, postprandial glucose levels were higher in the nondippers at 0, 90, and 120 min (all P < 0.05). Nondippers had a higher fasting insulin/glucose ratio than was apparent in normal control subjects. Despite higher postprandial glucose levels, nondippers had lower postprandial insulin levels. These results suggest that nondippers were insulin resistant and that their pancreatic beta-cell function was impaired. For all patients, nocturnal reduction of blood pressure was inversely related to total glucose levels under the OGTT curve and was positively related to postprandial insulin levels. Daytime heart rate did not differ between the dippers and nondippers, but nocturnal heart rate was higher in the nondippers, suggesting that nocturnal sympathetic activities were higher among the nondippers. Spectral analysis of heart rate variability suggests that the nondippers had lower parasympathetic activities and unbalanced sympathetic/parasympathetic outflow. CONCLUSIONS: These findings indicate that nondipper hypertensive patients are more glucose intolerant than are dipper patients. The abnormalities of glucose metabolism in nondippers could be explained by insulin resistance and beta-cell dysfunction. The results of spectral analysis suggest that abnormal autonomic outflow may represent a possible link between hypertension and associated metabolic dysfunction.

Adult↗

PubMed1997

Metabolic abnormalities in renal transplant recipients. Risk factors and predictors of chronic graft dysfunction?

In summary, abnormalities in lipid and carbohydrate metabolism, including features of the metabolic risk factor syndrome, are frequently present in patients both before and after renal transplantation. Risk factors of atherosclerosis may not only contribute to increased cardiovascular morbidity and mortality in this patient population, but can also be assumed to contribute to the development and progression of CVR and chronic graft dysfunction. For preventing both early graft losses and the development of graft damage leading to late graft dysfunction and graft loss, it appears to be essential to identify patients at risk early, prior to transplantation. Intervention aiming to reduce overweight, diet and exercise may be of benefit. The role of omega-3 unsaturated fatty acid supplementation remains controversial. Pharmacological intervention by antioxidants or agents to reduce lipids and/or decrease PAI-1 synthesis may prove to be beneficial. Early identification of patients at risk and intervention in due time may improve the results of renal transplantation.

Fibrinolysis↗

PubMed1995

The frequently low cobalamin levels in dementia usually signify treatable metabolic, neurologic and electrophysiologic abnormalities.

Cobalamin levels are frequently low in patients with dementia, but it is unclear if they represent definable deficiency and what the mechanisms are. Therefore, patients being evaluated for dementia who had low cobalamin levels but no obvious evidence of deficiency were studied hematologically, neurologically and with metabolic tests and were re-evaluated after cobalamin treatment. Abnormalities suggestive of or diagnostic for deficiency were documented in most of the 16 demented and nondemented patients. Metabolic results: 50% of patients tested had abnormal deoxyuridine suppression and 44% had increased serum methylmalonic acid and/or homocysteine levels; these test results correlated with each other. Neurologic results: 73% of patients had clinical abnormalities, primarily mild neuropathies, not attributable to other causes, 75% had electroencephalographic abnormalities, 77% had abnormal visual evoked potentials and 33% had abnormal somatosensory potentials. Metabolic and neurologic dysfunction were present together or absent together in all but 2 cases. Cobalamin therapy improved 50-100% of the various types of abnormalities, although it did not improve cognitive function in the 13 demented patients. Food-cobalamin malabsorption was found in 60% of the patients. Despite the absence of megaloblastic anemia and rarity of traditional malabsorption of free cobalamin, low cobalamin levels in demented patients frequently represent mild cobalamin deficiency and are often associated with food-cobalamin malabsorption. Perhaps most importantly, this is accompanied not only by metabolic changes but by evidence of mild neurologic dysfunction. Their frequent reversibility by cobalamin confirms that these defects indeed arise from cobalamin deficiency. Although the long-standing dementia does not improve, treating such patients with cobalamin has other concrete benefits.

Aged↗

PubMed1999

Diastolic dysfunction in hypertensive heart disease is associated with altered myocardial metabolism.

BACKGROUND: Hypertension is an important clinical problem and is often accompanied by left ventricular (LV) hypertrophy and dysfunction. Whether the myocardial high-energy phosphate (HEP) metabolism is altered in human hypertensive heart disease and whether this is associated with LV dysfunction is not known. METHODS AND RESULTS: Eleven patients with hypertension and 13 age-matched healthy subjects were studied with magnetic resonance imaging at rest and with phosphorus-31 magnetic resonance spectroscopy at rest and during high-dose atropine-dobutamine stress. Hypertensive patients showed higher LV mass (98+/-28 g/m2) than healthy control subjects (73+/-13 g/m2, P<0.01). LV filling was impaired in patients, reflected by a decreased peak rate of wall thinning (PRWThn), E/A ratio, early peak filling rate, and early deceleration peak (all P<0. 05), whereas systolic function was still normal. The myocardial phosphocreatine (PCr)/ATP ratio determined in patients at rest (1. 20+/-0.18) and during stress (0.95+/-0.25) was lower than corresponding values obtained from healthy control subjects at rest (1.39+/-0.17, P<0.05) and during stress (1.16+/-0.18, P<0.05). The PCr/ATP ratio correlated significantly with PRWThn (r=-0.55, P<0.01), early deceleration peak (r=-0.56, P<0.01), and with the rate-pressure product (r=-0.53, P<0.001). CONCLUSIONS: Myocardial HEP metabolism is altered in patients with hypertensive heart disease. In addition, there is an association between impaired LV diastolic function and altered myocardial HEP metabolism in humans. The level of myocardial PCr/ATP is most likely determined by the level of cardiac work load.

Adenosine Triphosphate↗

PubMed2001

Induced mitochondrial failure in the feline brain: implications for understanding acute post-traumatic metabolic events.

OBJECTIVE: Recently, evidence has become available implicating mitochondrial failure as a crucial factor in the pathogenesis of acute brain damage following severe traumatic brain injury (TBI). However, it remains unclear how mitochondrial dysfunction affects cerebral metabolism. Therefore the aim of the study was to evaluate the impact of 'isolated' mitochondrial failure on local cerebral metabolism. METHODS: Cerebral mitochondrial metabolism was blocked by local microdialysis perfusion with cyanide in seven cats. Local brain tissue oxygen tension (p(tiO(2))), carbon dioxide tension (p(tiCO(2))) and pH, as well as extracellular cerebral fluid, glucose, lactate, pyruvate and glutamate were monitored, using a Neurotrend sensor and microdialysis, respectively. Tissue oxygen consumption was measured in a microrespirometric system, and ultrastructural changes evaluated via electron microscopy. RESULTS: Brain tissue oxygen tension increased from a baseline of 31+/-9 mmHg to 84+/-30 mmHg after 60 min of cyanide perfusion (P<0.05), concomitant a decrease in oxygen consumption from 14.45+/-3.91 microl/h/mg to 10.83+/-1.74 microl/h/mg (P<0.05). Brain tissue pH was decreased after 60 min of cyanide perfusion (6.83+/-0.16) compared to baseline (7.07+/-0.39) (P<0.05), whereas p(tiCO(2)) did not show significant changes. Lactate massively increased from a baseline of 599+/-270 micromol/l to 2609+/-1188 micromol/l immediately after cyanide perfusion (P<0.05). The lactate:glucose ratio increased from 0.79+/-0.15 before cyanide perfusion to 6.40+/-1.44 at 40 min after cyanide perfusion (P<0.05), while no significant changes in the lactate:pyruvate ratio could be observed. Glutamate increased from a baseline of 11.6+/-7.2 micromol/l to 61.4+/-44.7 micromol/l after cyanide perfusion (P<0.05). CONCLUSION: The results of this study show that 'isolated' cerebral mitochondrial failure initiates changes in cerebral substrates and biochemistry, which are very similar to most of the changes seen after severe human head injury, except for the early fall in p(tiO(2)), further indicating a crucial involvement of mitochondrial impairment in the development of brain damage after TBI.

Animals↗

PubMed1997

Enterocyte viability and mitochondrial function after graded intestinal ischemia and reperfusion in rats.

Ischemia/reperfusion of the small intestine can lead to metabolic and structural alterations in the mucosa. Cellular dysfunction occurs when mitochondrial metabolism is compromised, which may ultimately lead to impaired organ function. The aims of this study were to assess the suppression of cellular and mitochondrial oxidative metabolism and involvement of mitochondria in the ischemia/reperfusion injury. The mitochondria were prepared from isolated enterocytes obtained from the small intestine of anesthetized adult rats following different time periods of ischemia and ischemia followed by 5 min reperfusion. Cellular and mitochondrial function were assessed using MTT (3-(4,5-Dimethylthiazol-2-yl) -2,5-diphenyl tetrazolium bromide) reduction assay. Ischemia of increasing time periods caused a progressive decrease in cellular and mitochondrial MTT reduction in enterocytes and reperfusion showed further decrease of MTT formazan formation. Inclusion of 1 mM succinate, as respiratory substrate, showed reversal of suppression of mitochondrial function in 30-60 min ischemia whereas 90 min ischemia or short time period ischemia followed by 5 min reperfusion indicated an irreversible damage to mitochondria. This study indicated that mitochondria are a sensitive target of damage due to oxygen deficiency and possibly due to sudden burst of oxygen free radicals. Mitochondria can withstand short periods of ischemia whereas long duration ischemia or reperfusion results in irreversible damage to mitochondrial function.

Animals↗

PubMed2005

RSA 2004: combined basic research satellite symposium - session three: alcohol and mitochondrial metabolism: at the crossroads of life and death.

This article summarizes the proceedings of the RSA 2004 Combined Basic Research Satellite Meeting convened at the Westin Bayshore Resort and Marina, Vancouver, CA. One of the sessions "Alcohol and mitochondrial metabolism: At the crossroads of life and death" featured five speakers and was chaired by Drs. Jan Hoek and Sam Zakhari. The presentations were 1) INTRODUCTION: Alcohol and cellular energy metabolism by Jan Hoek, 2) Ethanol-dependent dysfunction of mitochondrial energy metabolism: the role of NO by Victor Darley-Usmar, 3) Ethanol and apoptosis in the heart by Gyorgy Hajnoczky, 4) Alcohol and mitochondrial biogenesis in development by Thomas Knudsen, and 5) Alcohol, mitochondrial function and cardiac preconditioning by Daria Mochly-Rosen.

Animals↗

PubMed2005

Cyclic AMP-phosphodiesterases inhibitor improves sodium excretion in rats with cirrhosis and ascites.

BACKGROUND: The mechanisms responsible for renal dysfunction and sodium retention in cirrhosis remain unclear. Cyclic AMP (cAMP) regulates sodium reabsorption in the proximal nephron. This study investigates the role of cAMP metabolism in renal dysfunction in cirrhosis. METHODS: Renal function was studied by the clearance technique in anesthetized control and cirrhotic rats with or without ascites. cAMP phosphodiesterase (PDE) activity was measured in the renal cortex in vitro. Moroever, the effects on renal function of the intravenous administration of cAMP and rolipram, a powerful and specific cAMP-PDE4 inhibitor, were evaluated. RESULTS: In control and in non-ascitic cirrhotic rats, cAMP administration significantly increased sodium and phosphate excretions, but did not change these excretions in cirrhotic rats with ascites. cAMP-PDE activity was higher in ascitic than in control rats (P < 0.05). Rolipram infusion significantly increased sodium and phosphate excretion only in cirrhotic rats with ascites. CONCLUSION: These results suggest that increased renal cAMP-PDE activity is responsible for resistance to the natriuretic effects of cAMP in cirrhosis and plays a role in the development of ascites.

Analysis of Variance↗

PubMed2003

Insulin resistance and endothelial dysfunction.

Insulin has multiple metabolic actions, including effects on blood vessels. Insulin normally increases blood flow by a mechanism which involves generation of nitric oxide (NO) via the arginine-NO pathway. Although insulin itself is a weak and physiologically unimportant vasodilatator, it appears to markedly potentiate endothelium-dependent vasodilatation. Therefore, anything that impairs insulin action in endothelial cells can be expected to be associated with endothelial dysfunction, i.e. loss of NO bioactivity in the vessel wall. Consistent with the idea that insulin resistance and endothelial dysfunction frequently coexist, all insulin-resistant conditions examined to date have been associated with endothelial dysfunction. However, the latter can also be caused by factors other than insulin resistance-such as a high concentration of low-density lipoprotein (LDL) cholesterol. Therapies which reverse insulin resistance-such as exercise, insulin and inhibitors of the renin-angiotensin-aldosterone (RAA) axis-also reverse endothelial dysfunction, which may thus be an inherent feature of insulin resistance.

Cardiovascular Diseases↗

PubMed1976

Drug metabolism in thyroid disease.

Thyroid dysfunction can influence the physiological disposition of drugs. Depending on the pharmacokinetic properties of the individual drug, changes in the rate of metabolism ranging from profound to moderate or negligible have been observed. Since renal function is also influenced by thyroid disease, changes in renal elimination of drugs which are excreted in the urine mainly as unchanged drugs have to be considered as another reason for altered drugs disposition in thyroid disease. In patients with thyrotoxicosis lower, and in patients with myxoedema, higher, digitalis plasma levels have been observed. The altered disposition of cardiac glycosides in thyroid dysfunction can be attributed to changes in renal elimination and metabolism. These findings may be the kinetic correlate for the clinical observation that larger than the usual dose of digitalis is required in thyrotoxic patients and lower in hypothyroid patients. Antipyrene half-lives are very much shortened during hyperthyroidism and prolonged appreciably during hypothyroidism. The alterations in the disposition of these drugs seen during thyroid dysfunction can be ascribed to changes in its rate of metabolism which is controlled by the levels of circulating thyroid hormones. N-demethylation of aminopyrine is depressed both in hyper- and hypothyroid patients as compared with euthyroid subjects. Changes in the half-life of this drug were observed only during hypothyroidism. The physiological disposition of the antithyroid drug propylthiouracil is not changed during thyrotoxicosis. A decrease in plasma half-life of methimazole is however, observed during hyperthyroidism, whereas in hypothyroid patients half-life is increased. The few data available so far do not allow general prediction of how thyroid disease could alter drug metabolism in man.

Administration, Oral↗

PubMed1989

Differential sensitivity to beta-cell secretagogues in cultured rat pancreatic islets exposed to human interleukin-1 beta.

The early stages of insulin-dependent diabetes mellitus are characterized by a selective inability to secrete insulin in response to glucose, coupled to a better response to nonnutrient secretagogues. The deficient glucose response may be a result of the autoimmune process directed toward the beta-cells. Interleukin-1 (IL-1) has been suggested to be one possible mediator of immunological damage of the beta-cells. In the present study we characterized the sensitivity of beta-cells to different secretagogues after human recombinant IL-1 beta (rIL-1 beta) exposure. Furthermore, experiments were performed to clarify the biochemical mechanisms behind the defective insulin response observed in these islets. Rat pancreatic islets were isolated and kept in tissue culture (medium RPMI-1640 plus 10% calf serum) for 5 days. The islets were subsequently exposed to 60 pM human recombinant IL-1 beta during 48 h in the same culture conditions as above and examined immediately after IL-1 exposure. The rIL-1 beta-treated islets showed a marked reduction of glucose-stimulated insulin release. Stimulation with arginine plus different glucose concentrations, and leucine plus glutamine partially counteracted the rIL-1 beta-induced reduction of insulin release. The activities of the glycolytic enzymes hexokinase, glucokinase, and glyceraldehyde 3-phosphate dehydrogenase, were similar in control and IL-1-exposed islets. Treatment with IL-1 also did not impair the activities of NADH+- and NADPH+-dependent glutamate dehydrogenase, glutamate-aspartate transaminase, glutamate-alanine transaminase, citrate synthase, and NAD+-linked isocitrate dehydrogenase. The oxidation of D-[6-14C]glucose and L-[U-14C]leucine were decreased by 50% in IL-1-treated islets. Furthermore, there was a significant decrease in the ratios of [2-14C]pyruvate oxidation/[1-14C]pyruvate decarboxylation and L-[U-14C]leucine oxidation/L-[1-14C]leucine decarboxylation, indicating that IL-1 decreases the proportion of generated acetyl-coenzyme-A residues undergoing oxidation. However, in the presence of IL-1 there was a significant increase in L-[U-14C]glutamate oxidation. These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism. This mitochondrial dysfunction seems to reflect an impairment in proximal steps of the Krebs cycle. It is conceivable that the IL-1-induced suppression and shift in islet metabolism can be an explanation for the beta-cell insensitivity to glucose observed in the early phases of human and experimental insulin-dependent diabetes mellitus.

Animals↗

PubMed2005

Intestinal glutathione: determinant of mucosal peroxide transport, metabolism, and oxidative susceptibility.

The intestine is a primary site of nutrient absorption and a critical defense barrier against dietary-derived mutagens, carcinogens, and oxidants. Accumulation of oxidants like peroxidized lipids in the gut lumen can contribute to impairment of mucosal metabolic pathways, enterocyte dysfunction independent of cell injury, and development of gut pathologies, such as inflammation and cancer. Despite this recognition, we know little of the pathways of intestinal transport, metabolism, and luminal disposition of dietary peroxides in vivo or of the underlying mechanisms of lipid peroxide-induced genesis of intestinal disease processes. This chapter summarizes our current understanding of the determinants of intestinal absorption and metabolism of peroxidized lipids. I will review experimental evidence from our laboratory and others (Table 1) supporting the pivotal role that glutathione (GSH) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) play in mucosal transport and metabolism of lipid hydroperoxides and how reductant availability can be compromised under chronic stress such as hypoxia, and the influence of GSH on oxidative susceptibility, and redox contribution to genesis of gut disorders. The discussion is pertinent to understanding dietary lipid peroxides and GSH redox balance in intestinal physiology and pathophysiology and the significance of luminal GSH in preserving the integrity of the intestinal epithelium.

Glutathione↗

PubMed1994

[Fibrinolytic system in patients with myocardial infarction and other coronary disease risk factors].

PURPOSE: To evaluate the fibrinolytic system function in survivors of acute myocardial infarction (AMI) and to appreciate the differences between patients with history of diabetes and/or dyslipaemia and those without such history. PATIENTS AND METHODS: A series comprised of 101 patients (83 men and 18 women) surviving six months after AMI and with mean age of 61.7 +/- 8.5 years was studied. Previous history of type II diabetes mellitus was present in 22 cases, while 42 others had some type of dyslipaemia (16, hypertriglyceridaemia; 15, hypercholesterolaemia; 11 both). Of the patients with diabetes mellitus, 14 had also dyslipaemia (5, hypertriglyceridaemia; 6, hypercholesterolaemia; 3, both conditions). The rates of plasminogen-activator inhibitor (PAI-1), fibrinogen, plasminogen, and alpha-2-antiplasmin, along with the venous occlusion test to determine tissular plasminogen activator (t-PA), both functional and antigenic, before and after venous occlusion, were tested in all cases. The studies were performed at the moment of AMI and 6 months later. RESULTS: PAI-1 concentration during AMI in the patients with some concurrent lipid anomaly showed significant differences with respect to the patients without any such associated disease (p < 0.001). The patients with history of dyslipaemia had significant increase of PAI-1 (p < 0.001) with respect to those without such history. Those patients with associated diabetes showed significantly increased PAI-1 concentration with regard to those without it, both in the acute phase and 6 months later (p < 0.05); significant increase was also found when comparing the patients with diabetes and dyslipaemia with those ones with only diabetes or dyslipaemia (p < 0.05). A significant increase of PAI-1 level (p < 0.001) was found in the 6-month study in the dyslipaemia patients with respect to non-dyslipaemic, and similar findings appeared with respect to diabetics and non-diabetics (p < 0.05). The 14 patients with both disorders showed increased values when compared with those having only one associated impairment (p < 0.05). When comparing the PAI-1 rates at AMI and 6 months later in the patients with dyslipaemia or diabetes, statistically significant decrease could be noted (p < 0.05 and p < 0.01, respectively). Before venous occlusion, t-PA was significantly increased in diabetic or dyslipaemic patients (p < 0.05) and in the patients with both conditions (p < 0.01). CONCLUSIONS: Patients with AMI and abnormalities of the lipidic or glycaemic metabolism have fibrinolytic dysfunction on the basis of an increase of the main inhibitor of the fibrinolytic system and a decreased release of tissular plasminogen activator. Those patients with both metabolic abnormalities have a deeper fibrinolytic hypofunction, with higher PAI-1 concentration.

Aged↗

PubMed2002

[Diabetic cardiomyopathy: concept, heart function, and pathogenesis].

The diabetic cardiomyopathy is a disease caused by diabetes and is characterised by the presence of diastolic and/or systolic left ventricular dysfunction. Diabetes may produce metabolic alterations, interstitial fibrosis, myocellular hypertrophy, microvascular disease and autonomic dysfunction. It is thought that all of them may cause cardiomyopathy. Other abnormalities that are usually associated with diabetes such as hypertension, coronary artery disease and nephropathy should be excluded before diagnosing diabetic cardiomyopathy. There is no evidence that diabetic cardiomyopathy alone can produce heart failure. However, subclinical ventricular dysfunction has been described in young asymptomatic diabetic patients without other diseases that could affect the cardiac muscle. In these cases we should consider that diabetes is the only cause of the myocardial disease. More studies are needed to know the natural history of diabetic cardiomyopathy.

Adrenergic beta-Antagonists↗

PubMed2006

Dysfunction of cardiac ryanodine receptors in the metabolic syndrome.

This study examined the hypothesis that the prediabetic metabolic syndrome alters expression, phosphorylation state and binding affinity of cardiac RyR2. Real-time PCR and Western blot analysis were used to assess mRNA and protein expression in the left ventricle, right ventricle and right atrium from control (n=5) and chronically high-fat-fed (n=5) dogs with the metabolic syndrome. Functional integrity of RyR2 was assessed by RyR2-Ser2809 phosphorylation and the receptor's ability to bind [3H]ryanodine. We found that RyR2 phosphorylation at Ser2809 was significantly elevated in right and left ventricle from high-fat-fed dogs compared to normal control dogs. This hyperphosphorylation was associated with a decrease in RyR2 binding affinity in right and left ventricle (high-fat diet=80.2 and 90.5 fmol/mg protein vs. control=243.6 and 200.9 fmol/mg protein, respectively) and a decrease in cardiac index in exercising dogs. RyR2 phosphorylation at Ser2809 and RyR2 binding affinity were not altered in the right atria of high-fat-fed dogs. In addition, no significant differences in cardiac RyR2 mRNA or protein expression were noted between groups. These data suggest that alterations in RyR2 could be an important mechanism of early cardiac dysfunction in obesity and insulin resistance.

Animals↗

PubMed1989

[Alteration of prostaglandin metabolism in alcoholic liver disease: its association with platelet dysfunction after chronic alcohol ingestion].

Recently, hepatic microcirculation has been focused on as an important pathogenic factor in progression of alcoholic liver disease (ALD). Therefore, blood levels of several prostaglandins, which are associated with organ microcirculation, were determined in various liver diseases, including ALD. Blood thromboxane B2 (TXB2) level was significantly increased in ALD, when compared to other types of liver diseases, whereas both 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) and prostaglandin E were not changed. These consequences resulted in the imbalance of 6-keto PGF1 alpha to TXB2, which might promote platelet aggregation and blood vessel contraction. Indeed, the increase of beta-thromboglobulin and platelet factor 4 in blood was observed in ALD. Furthermore, in ALD, the rate of arachidonate-induced platelet aggregation was prominently enhanced, and malondialdehyde production in platelet, which was well correlated with blood TXB2 levels, significantly increased. Thus, the present study may indicate that, in ALD, hyper-aggregability of platelet is produced, because of the derangement of prostaglandin metabolism and platelet dysfunction.

Adult↗

PubMed2003

[Characteristics of metabolism and nutrition support during different periods in abdominal surgical diseases complicated by multiple organ dysfunction syndrome].

OBJECTIVE: To evaluate the characteristics of metabolism in patients with abdominal surgical diseases complicated by multiple organ dysfunction syndrome (MODS), and the effects of nutritional support in different periods. METHODS: In 32 patients out of 66 patients suffering from MODS nutritional support was given through different channels according to different disease stages. In the first period, total parenteral nutrition (TPN) should be implemented when acute stress was just over and the functions of gastro-intestinal system was still in a bad condition. During the second period, TPN and enteral nutrition(EN) could be instituted at the same time, when the state of illness was under control. In the third period, if the condition of the patients was totally controlled, and the function of stomach and intestine had completely recovered, total EN could be given after a transitional period. RESULTS: In these 32 patients, 23 patients were cured successfully and 9 patients died; the mortality was 28.12%. In those 34 patients treated with conventional methods, 19 patients were cured while 15 patients died, and the mortality was 44.11% (P<0.01). CONCLUSION: When MODS occurred, metabolism is disturbed, and the body is unable to utilize the supplied nutrients and to get rid of the catabolic products. There fore, it seemed to be necessary to give nutrition support in different manner during different periods of the disease. Otherwise, the disease might be aggravated.

Adolescent↗

PubMed2003

Paradoxical effects of pyruvate on cardiac contractile function under normal and high glucose in ventricular myocytes.

Impaired energy fuel supply and metabolism contribute to the cardiac contractile dysfunctions in diabetes. Pyruvate, a metabolic product of glycolysis and an oxidizable fuel in myocardium, has been demonstrated to enhance cardiac contractile function and alleviate hyperglycemic status. The present study was designed to examine the impact of pyruvate supplementation on cardiac mechanical function under normal glucose (NG) and high glucose (HG) conditions. Isolated adult rat ventricular myocytes were maintained in NG (5.5mM) or HG (25.5mM) medium for 24h in the absence or presence of pyruvate (5mM). Contractile indices were measured with an IonOptix edge-detection system including peak shortening (PS), maximal velocity of shortening/relengthening (+/-dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR(90)), area underneath shortening (A(con)) and relengthening (A(relax)). Myocytes maintained in HG medium displayed abnormal mechanical function simulating in vivo diabetes. These abnormalities included reduced PS, +/-dL/dt, prolonged TPS/TR(90) associated with enhanced A(con) and A(relax) compared to NG myocytes. Interestingly, these HG-induced mechanical dysfunctions were completely abolished by co-incubation of pyruvate. However, NG myocytes developed mechanical defects reminiscent of those of HG following co-incubation with pyruvate. These data suggest that pyruvate may paradoxical affect cardiac mechanical function under different glucose settings and therefore warrant caution when applying pyruvate therapeutically.

Analysis of Variance↗