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PubMedDate not supplied

The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat.

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.

Acetates↗
PubMed1987

The effect of maternal hyperglycemia on acid base balance and lung liquid production in the fetal sheep.

In 10 chronically catheterized fetal sheep, the effects of 100 g of glucose infused (intravenous) to the pregnant ewe on lung liquid production and acid-base status were investigated. Maternal and fetal hyperglycemia occurred within 15 min of the infusion of glucose. There was a significant increase in fetal PCO2 from 41.67 +/- 1.00 to 46.89 +/- 1.83 mm Hg and a decrease in fetal arterial pH from 7.42 +/- 0.016 to 7.33 +/- 0.026 (n = 7). This acidosis was probably the result of fetal lactacidemia. There was also a decrease in fetal PO2 (p less than 0.001) following the infusion of glucose to the ewe. This, along with the acidosis, might account for the increased risk of unexplained fetal death in the diabetic pregnancy especially near term. Following the infusion of glucose to the ewe there was an increase in maternal plasma osmolality by 16 +/- 3.35 mosmol/kg (n = 9) and in fetal plasma osmolality by 14 +/- 2.64 mosmol/kg (n = 9; p less than 0.001). Fetal lung liquid production fell from 0.195 +/- 0.04 to 0.093 +/- 0.02 ml/min (n = 6; p less than 0.001). There was no change in the excretion of osmol by the lungs. The decreased lung liquid production was probably due to a decrease in the net movement of fluid across the pulmonary epithelium.

Acid-Base Equilibrium↗
PubMed1992

[Respiratory regulation system].

In 1874, Kussmaul described "featiful terminal dyspnea" in a case of severe diabetic coma. Probably, this was the first sign of respiratory regulation for metabolic acidosis. After this first case, about 40 years has been needed to establish the theory of acid-base equiribration, namely Henderson-Hasselbalch's equation. pH = 6.1 + log [HCO3-]/[H2CO3] This equation indicates that plasma pH is determined by the ratio of HCO3 concentration and H2CO3 concentration. Because of linear relationship between H2CO3 and PaCO2, pH depend on the ratio of HCO3- and PaCO2. In the state of metabolic acidosis, increase of [H+] stimulates ventilation and decreases the PaCO2. Inversely, in the state of metabolic alkalosis, increase of PaCO2 occurs. These reactions are called "respiratory compensation" or "respiratory regulation". The respiratory regulation system will not retern pH to normal (7.4), but compensation has some limitation which is shown as "SIGNIFICANCE BAND". In this paper, physiological and clinical importance of respiratory regulation and significance band is discussed.

Acid-Base Equilibrium↗
PubMed1977

Rhinocerebral mucormycosis.

Mucormycosis is a fulminant fungal infection occurring in debilitated patients with an underlying pathologic condition. The rhinocerebral form of the disease, which comprises nearly one half of recently reported cases, is most often found in uncontrolled diabetics or profoundly dehydrated children. Infection usually begins in the nose and progresses through the paranasal sinuses, invading the orbit and CNS secondarily. Despite the known pathogenesis of this disease, the ophthalmologist is often first to consider the diagnosis, due to inadequate intranasal examination by the primary physician. The delay caused by late occurrence of orbital manifestations has resulted in poor survival rates, despite vigorous therapy. In recent years, increased physician awareness has led to earlier diagnosis of rhinocerebral mucormycosis. This report presents 13 cases with which we have delt since 1963. The long-term survival rate is 85%. Aggressive surgical therapy, with repeated debridement, in combination with intravenous amphotericin B, have led to this high rate of cure.

Acidosis↗
PubMed1978

Hyperlactatemia in diabetics with retinopathy during combined sulphonylurea and phenformin therapy.

Blood lactate concentration has been measured at intervals over a twelve hour period in four maturity-onset diabetics with retinopathy treated by sulphonylurea and phenformin therapy. Despite moderately good control of blood glucose, all four patients had markedly elevated concentrations of blood lactate (12h means of 2.1-2;4 mmol/1) with concentrations greater than 3 mmol/1 at some time during the day. Hepatic function was normal in all patients and in all four patients plasma creatinine was 80-85 mumol/1, (normal range 60-125 mumol/1) so that the usual indications for not using biguanides were absent. It is concluded that diabetics with retinopathy constitute a group of patients with an increased risk of phenformin-associated lactic acidosis, and that plasma creatinine estimation may be unreliable in assessing whether patients are suitable for phenformin therapy.

Aged↗
PubMed1977

Low-dose intravenous insulin: treatment of diabetic ketoacidosis in children (suitability for use in community hospitals).

A regimen is described to simplify current methods of ketoacidosis therapy by using only standard intravenous equipment and without requiring albumin administration. After an initial intravenous insulin bolus of 2 units, a dose of up to 3 units per hour was sufficient to bring patients out of ketoacidosis. No hypoglycemia, significant hypokalemia, or rapid fall in serum osmolality was detected. Patients showed steady increases in endogenous bicarbonate and were out of metabolic acidosis in 8.4 hours. This modified regimen appears to be a safe and easy method of treating diabetic ketoacidosis in children and is suited for use in community hospitals. Since the method is described for children over the age of three or those not in severe coma, consultation should be sought for any infant and for any child in severe coma or with a significant complication, such as severe infection.

Child↗
PubMed1976

Pathogenesis, diagnosis and treatment of diabetic ketoacidosis.

The diagnosis of diabetic ketoacidosis must be suspected and the initiation of treatment should be prompt to provide a satisfactory outcome in the treatment of diabetic ketoacidosis. Corrections of fluid and electrolyte deficiencies should be made slowly; rapid "push"injections or large infusions of sodium bicarbonate should avoided and ample amounts of potassium should be given early. Precautions should be taken so that blood glucose concentrations do not fall rapidly, and so that blood glucose levels of 250-300 mg/100 ml are maintained by the administration of 5-10% glucose solutions. Bicarbonate therapy is indicated only in severe acidosis (pH less than or equal to 7.1). Physicians who are trained in the care of diabetes mellitus should supervise the treatment. In our hospital the same staff physicians and fellows attend all patients with diabetes. In addition the efforts of our house staff and nurses have contributed significantly to the care of these patients.

Adult↗
PubMed1985

Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats.

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.

Animals↗
PubMed1989

Change of serum inorganic phosphate complexes in diabetic ketoacidosis.

The concentrations of serum inorganic phosphate complexes (HPO4(2-), H2PO4-, NaHPO4-, KHPO4-, CaHPO4 and MgHPO4) were studied during diabetic ketoacidosis. On admission to hospital the H2PO4- concentration was significantly increased, in comparison with well-controlled diabetics. After 12-24 h the concentration of all phosphate complexes decreased. At 72 h only the MgHPO4 concentration was decreased. These changes are related to acidosis, insulin therapy and tubular dysfunction.

Adolescent↗
PubMed1997

A guide for predicting arterial CO2 tension in metabolic acidosis.

This presentation examines the relation of arterial CO2 tension to the severity of acidemia in three large groups of cases of diabetic ketoacidosis, totalling 405 episodes. In particular, it evaluates the previously reported anecdotal observation that PaCO2 (in torr) in such patients is usually numerically close to the two-digit number to the right of the pH decimal point, down to a pH of 7.10-7.15. The relations between measured arterial CO2 tension levels and calculated plasma bicarbonate concentration in the three groups were very similar to those previously reported by others and us, the regression equations approximating PaCO2 = 1.5 x [HCO3-] + 8. Further, in the 262 episodes with blood pH 7.10-7.37, down to a pH of 7.10-7.15, the average PaCO2 in torr often did approximate the two-digit number to the right of the decimal point in the pH value. This relation provides a quick and easily remembered alternative guide for predicting the approximate expected PaCO2 in patients with metabolic acidosis. The basis for this apparently fortuitous relation between PaCO2 and blood pH may be the closely similar correlation between PaCO2 and 1/cH+ (i.e., 10PH), which in turn derives from the physiologically significant relation of alveolar ventilation to blood pH, and the inverse relation between PaCO2 and alveolar ventilation.

Adult↗
PubMed2007

Recent metformin ingestion does not increase in-hospital morbidity or mortality after cardiac surgery.

BACKGROUND: Perioperative treatment of type 2 diabetes with metformin, an oral hypoglycemic drug, is thought to increase the risk of life-threatening postoperative lactic acidosis. In contrast, metformin improves serum glucose control and has beneficial cardiovascular effects, which may decrease the risk of adverse outcomes. In this investigation we sought to determine the influence of metformin treatment on mortality and morbidity compared with treatment with other oral hypoglycemic drugs in diabetic patients undergoing cardiac surgery. METHODS: In this retrospective investigation, 1284 diabetic patients, with recent oral hypoglycemic ingestion (presumed to be 8-24 h preoperatively), underwent cardiac surgery from 1994-2004. Propensity scores were calculated from a logistic model which included baseline characteristics and perioperative variables. Four-hundred-forty-three (85%) of the metformin-treated patients were matched on nearest propensity score using greedy matching techniques with 443 nonmetformin-treated patients. Postoperative outcomes were compared between matched metformin- and nonmetformin-treated patients. RESULTS: In-hospital mortality, cardiac, renal, and neurologic morbidities were similar between groups. Metformin-treated patients had less postoperative prolonged tracheal intubation [OR (95% CI), 0.3 (0.1, 0.7), P = 0.003], infection [0.2 (0.1, 0.7), P = 0.007] and overall morbidities [0.4 (0.2, 0.8), P = 0.005]. CONCLUSIONS: These data suggest that recent metformin ingestion is not associated with increased risk of adverse outcome in cardiac surgical patients. Alternatively, metformin treatment may have beneficial effects.

Administration, Oral↗
PubMed1998

Metformin and contrast media: where is the conflict?

Intravascular administration of iodinated contrast media to patients who are receiving metformin, an oral antidiabetic agent, can result in lactic acidosis. However, this rare complication occurs only if the contrast medium causes renal failure, and the patient continues to take metformin in the presence of renal failure. Because metformin is excreted primarily by the kidneys, continued intake of metformin after the onset of renal failure results in a toxic accumulation of this drug and subsequent lactic acidosis. To avoid this complication, metformin must be withheld after the administration of the contrast agent for 48 hours, during which the contrast-induced renal failure becomes clinically apparent. If renal function is normal at 48 hours, the metformin can be restarted. There is no scientific justification for withholding metformin for 48 hours before administration of the contrast medium, as currently recommended in the package insert. The authors review the pharmacology of metformin and present a departmental policy for managing patients with diabetes who receive metformin and who require intravascular administration of iodinated contrast media.

Acidosis, Lactic↗
PubMed2005

Strength-duration properties and glycemic control in human diabetic motor nerves.

OBJECTIVE: To investigate the influences of hyperglycemia on axonal excitability in human diabetic nerves. Hyperglycemia results in decreased Na+-K+ pump function, presumably leading to intra-axonal Na+ accumulation and thereby, reduced Na+ currents. METHODS: The strength-duration time constant (tau(SD)), which partly depends on persistent Na+ conductance active at the resting membrane potential, was measured in median motor axons of 79 diabetic patients. The relationship of tau(SD) with the state of glycemic control (hemoglobin A1c [HbA1c] levels) was analyzed. RESULTS: The mean tau(SD) was longer for diabetic patients than for normal controls, but the difference was not significant. Among diabetic patients, the subgroup of patients with good glycemic control (HbA1c<7%) had significantly longer tau(SD) than the patient group with poor control (HbA1c>9%; P=0.04). The mean tau(SD) was longest at the HbA1c level of 5-6%, gradually decreasing and reaching a plateau around the HbA1c level of 9%. There was an inverse relationship between HbA1c levels and tau(SD), when the HbA1c levels ranged from 5 to 9% (P=0.04). CONCLUSIONS: In diabetic nerves, tau(SD) is generally longer than normal, but hyperglycemia is associated with paradoxically shortened tau(SD), because of a decrease in axonal persistent Na+ conductance, possibly related to reduced membranous Na+ gradient, tissue acidosis, or other metabolic factors. SIGNIFICANCE: Measurements of tau(SD) could provide a new insight into changes in ionic conductance in human diabetic nerves.

Adult↗
PubMed2003

Low antioxidant content and mutation load in mitochondrial DNA A3243G mutation-related diabetes mellitus.

BACKGROUND AND PURPOSE: Diabetes mellitus (DM) is a common clinical manifestation in patients harboring mitochondrial encephalomyopathy, lactic acidosis with stroke-like episodes (MELAS)-specific A3243G mitochondrial DNA (mtDNA) mutation. However, in some MELAS family members, the presence of mtDNA mutation in the blood is not always associated with DM, and the relationship between development of DM and A3243G mtDNA mutation is not fully understood. This study evaluated the relationship between A3243G mtDNA mutation and DM in a Taiwanese family. METHODS: We analyzed the relation of genotypic and phenotypic characteristics in a 2-generation DM family associated with the A3243G mtDNA mutation. The contents of mutant mtDNA in various tissue samples of 11 family members and their serum levels of antioxidants, including protein thiols and alpha-tocopherol (vitamin E) were determined and correlated with their past history and various clinical manifestations. RESULTS: DM in 4 members of the first and second generations was associated with age and decreased serum levels of antioxidant protein thiols. In a series of studies of mutant mtDNA content in various tissues, a relatively low proportion of A3243G mutant mtDNA was noted in the elderly proband and her elderly symptomatic siblings. A low proportion of mutant mtDNA was also noted in a younger family member presenting with DM. Moreover, a significantly lower average level of protein thiols was found in the symptomatic family members compared to the asymptomatic members (2.3 +/- 0.2 vs 3.5 +/- 0.54 nmol/mg protein, p < 0.05). CONCLUSIONS: The finding of relatively lower levels of mutant mtDNA in the elderly proband and her elderly symptomatic family members indicates that DM may be a late phenotypic expression in patients harboring MELAS-specific mtDNA mutation. Decreased serum protein thiols, suggestive of increased oxidative stress, also appear to be an early sign associated with subsequent development of DM.

Adult↗