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M M Sayeed

Publications and source records attributed to M M Sayeed.

At least 91 records · Page 5Linked to original sources
PubMed1977

Evidence for enhanced uptake of ATP by liver and kidney in hemorrhagic shock.

It has been shown that infusion of ATP-MgCl2 proved beneficial in the treatment of shock; however, it is not known whether this effect is due to improvement in the microcirculation or direct provision of energy or a combination of the above or other effects. To elucidate the mechanism of the salutary effect of ATP-MgCl2, we have now examined the in vitro uptake of ATP by liver and kidney of animals in shock. Rats were bled to a mean arterial pressure of 40 Torr and so maintained for 2 hrs. After the rats were killed, liver and kidney were removed and slices of tissue (0.3-0.5 mm thick) were incubated for 1 h in 1.0 ml of Krebs-HCO3 buffer containing 10 mM glucose, 5 mM MgCl2, and 5 mM [8-14C]ATP or 5 mM [8-14C]ADP, or 5 mM [8-14C]AMP, or 5 mM [8-14C]adenosine in 95% O2-5% CO2 and then homogenized. Tissue and medium samples were subjected to electrophoresis to separate and measure the various nucleotides. The uptake of [14C]ATP but not that of [14C]ADP or [14C]adenosine by liver and kidney slices from animals in shock was 2.5 times greater than the corresponding uptake by control slices. Thus, the beneficial effect of ATP-MgCl2 in shock could be due to provision of energy directly to tissue in which ATP levels were lowered.

Adenosine↗
PubMed1976

Insulin resistance and its reversal by in vivo infusion of ATP in hermorrhagic shock.

Hemorrhagic shock in rats was produced by bleeding the animals to a mean arterial pressure of 40 mmHg, which was maintained for 2 h. Muscles from these animals ('shock' muscles) demonstrated basal glucose uptake values unchanged from control values but, unlike the control muscles, the "shock' muscles showed resistance to the stimulation of glucose uptake by insulin. Infusion of ATP-MgCl2, ADP-MgCl2, adenosine-MgCl2, or GTP-MgCl2 to animals following shock had no effect on basal glucose uptake; however, ATP-MgCl2 but not the other nucleotides permitted insulin to exert its stimulatory effect on such muscles. An optimal insulin effect in ATP-MgCl2 treated 'shock' muscles occurred at an insulin concentration of u.001 U/ml, which is also the concentration required to produce optimal insulin effect in control muscles. Following 1-h incubation in Krebs-HCO3 medium, intracellular ATP contents of 'shock' muscles were about 50% lower than in control muscles. Treatment with ATP-MgCl2 following shock, however, resulted in ATP contents in such muscles similar to those in control muscles. Possible mechanisms for this reversal of insulin resistance by in vivo infusion of ATP-MgCl2 in shock are discussed.

Adenosine Diphosphate↗
PubMed1976

Uptake of ATP by liver and kidney in vitro.

Rat liver and kidney slices were incubated at 37 degrees C for 1 h in 1.0 ml of Krebs-HCO3 buffer containing 10mM glucose and one of the following: 5 mM [8-14C]ATP, 5 mM [8-14C]ADP, 5 mM [8-14C]AMP, or 5 mM [8-14C]ation medium and tissue extract were subjected to electrophoretic separation and the radioactivity present in ATP, ADP, AMP, IMP, inosine, adenosine, and hypoxanthine was counted. Extensive degradation of the added nucleotide was observed in the presence of both tissues. The concentrations of 14C-labeled ATP and ADP found in the liver and kidney indicated that these compounds were present within the cells. Evidence is presented which suggests that ATP, and to a lesser extent ADP, entered the liver and kidney as such and were not synthesized within the cell from 14C-labeled adenosine.

Adenosine↗
PubMed1976

Differences in the altered energy metabolism of hemorrhagic shock and hypoxemia.

The effect of hemorrhagic shock, hypoxemia, and anoxia on the levels of adenine and pyridine nucleotides of liver and kidney was assessed. ATP levels in liver and kidney of animals in shock or animals subjected to 7 min of anoxia decreased by 85 and 73%, respectively. Under hypoxic conditions (arterial PO2 AT 18 MMHg), the decrease was only 62 and 48% in liver and kidney, respectively. Tissue NAD levels decreased and NADH levels increased during shock but were found to be essentially unaltered during experimental hypoxemia. Thus, shock produced greater alterations in adenine and pyridine nucleotides than did hypoxemia alone, indicating that stagnant hypoxemia due to shock is more deleterious to energy metabolism than is severe hypoxemia with an otherwise normal circulation. The results also suggest that if an anterial PO2 OF 18 MMHg represents the initial stages of tissue hypoxia, then tissue ATP levels are a more sensitive indicator of this than NAD levels.

Adenine Nucleotides↗
PubMed1976

Alterations in high-energy phosphates in hemorrhagic shock as related to tissue and organ function.

Hemorrhagic shock was produced in conscious rats by cannulating the subclavian arteries and bleeding the animals to a mean arterial pressure of 40 mm. Hg, which was maintained for one hour (early shock) or 2 hours (late shock). Analysis of diaphragm (working muscle) showed that there was a significant decrease in adenosine triphosphate (ATP), adenosine diphosphate (ADP), and creatine phosphate levels beginning with early shock, whereas in soleus muscle (resting muscle) these changes were not observed until late shock. Decreases in adenine nucleotides of diaphragm were less than in working organs such as liver and kidney in early shock. This suggests that the extent of decrease in adenine nucleotides during shock may be related to the metabolic activity of the organ.

Adenine Nucleotides↗
PubMed1975

Effect of hydrocortisone and dexamethasone on xylose uptake by isolated rat soleus muscle.

To determine the effects of glucocorticoids on sugar uptake, xylose uptake by isolated rat soleus muscle of bilaterally adrenalectomized animals was studied. The results indicate that in vitro addition of 10-4 M hydrocortisone, dexamethasone or hydrocortisone sodium succinate had no inhibitory effect on basal xylose uptake. In the presence of both low and high medium insulin, the above steroids failed to inhibit insulin-stimulated uptake. When the concentration of hydrocortisone sodium succinate was increased to 10-2 M, insulinstimulated uptake was decreased. The results thus indicate that glucocorticoids at concentrations observed under physiological or pathological conditions do not inhibit basal or insulin-stimulated sugar uptake.

Animals↗
PubMed1975

The effect of insulin on glucose uptake in soleus muscle during hemorrhagic shock.

Hemorrhagic shock was produced by bleeding conscious rats to a mean arterial pressure of 40 mm Hg, which was maintained for 2 h. Basal glucose uptake by isolated soleus muscle from normal rats and rats subjected to hemorrhagic shock ('shock' muscles) increased with the increase ib medium glucose concentration. Uptake values were similar in both groups of muscles. This indicates that there were no alterations in the basal glucose carrier mechanism during shock. Whereas insulin (0.1 U/ml) stimulated glucose uptake in control muscles under aerobic as well as under anaerobic conditions, it had no stimulatory effect in 'shock' muscles under either environment. Maximal stimulation of glucose uptake in 'shock' muscles was observed at an insulin concentration of 0.2 U/ml. The ability of muscle to bind insulin was not altered during shock. The present experiments indicate that insulin responsiveness to tissues is altered in shock. This could be due to alterations in the insulin sensitivity of the glucose carrier mechanism during shock.

Anaerobiosis↗
PubMed1975

Reversal of insulin resistance by ATP in hemorrhagic shock.

Hemorrhagic shock was produced by bleeding rats to a mean arterial pressure of 40 mm Hg (1 mm Hg = 133 N/m2), which was maintained for 2 h. Muscles from these animals ('shock' muscles) showed resistance to the stimulation of glucose uptake by insulin. Addition of 1 mM ATP-MgCl2 to the medium had no effect on basal glucose uptake in either group of muscles, but it permitted insulin to exert its stimulatory effect in 'shock' muscles. An optimal insulin effect on glucose uptake in 'shock' muscles incubated without ATP was observed at an insulin concentration of 0.2 Unit/ml. When 1 mM ATP-MgCl2 was added to the medium, optimal insulin effect in 'shock' muscles was observed at an insulin concentration of 0.007 Unit/ml. Increasing the concentration of ATP-MgCl2 to 2.5 mM in the medium resulted in an optimal insulin effect at an insulin concentration of ATP-MgCl2 to 2.5 mM in the medium resulted in an optimal insulin effect at an insulin concentration of 0.001 Unit/ml in 'shock' muscles. Following 1 h cubation in Krebs-HCO3 medium, intracellular ATP contents of 'shock' muscles were approximately 50% lower than in control muscles. Addition of 1 mM ATP-MgCl2 to the incubation medium had no effect on the intracellular ATP contents of either group of muscles following incubation; however, 2.5 mM ATP-MgCl2 elevated intracellular ATP contents of 'shock' muscles but had no effect in control muscles. Possible mechanisms for this reversal of insulin resistance by ATP-MgCl2 in shock are discussed.

Adenosine Triphosphate↗
PubMed1975

Characteristics of sodium and potassium transport in the lung.

Freshly prepared lung slices were incubated in an oxygenated Krebs-Ringer bicarbonate medium for 90 min at 0.5 degrees C (chilling) followed by 60 min at 38 degrees C (rewarming). Fresh tissue cation contents (mean +/- SE) in mmol/kg dry wt were: sodium, 431 +/- 7; potassium, 416 +/- 10. After chilling, tissue sodium increased to 757 +/- 11 and potassium decreased to 113 +/- 6. Upon rewarming there was a net increase in tissue potassium of about 150 (mmol/kg dry wt) and a net decrease in tissue sodium of about 130. Tissue extrusion of sodium and reaccumulation of potassium observed at 37 degrees C were abolished when 1 mM ouabain, dinitrophenol, or iodoacetamide was added to the incubation medium. Similar results were obtained when the medium contained no potassium or when medium Na was replaced by choline. The data indicate the presence of active Na+-K+ transport in lung cells somewhat similar to that found in other mammalian tissue.

Animals↗
PubMed1975

Na+ minus K+ transport and adenosine nucleotides in the lung in hemorrhagic shock.

This study was undertaken to determine the effects of hemorrhagic shock on cellular energy production and utilization in the lung. Energy-dependent Na+ minus K+ transport was measured by quantitating tissue cation changes during a cold (0.5 degrees C.) and a subsequent warm (37 degrees C.) incubation of lung slices from rats in late hemorrhagic shock and from unbled control rats. Active Na+ extrusion and K+ reaccumulation by the tissue were observed upon rewarming of lung slices from shock animals. Whereas K+ reaccumulation was not altered with shock, the rate of Na+ extrusion was approximately 40 percent higher. The measurement of the intracellular water content with cold and warm incubations showed no alterations with shock. Extracellular water increased with chilling in shock tissue but not in normal tissue. Lung tissue contents of adenosine triphosphate, adenosine disphosphate, or adenosine monophosphate were likewise unaltered. Thus cellular energy utilization or production in the lung was not damaged by hemorrhagic shock but a tendency toward increased interstitial water seemed to be present.

Adenine Nucleotides↗
PubMed1975

Degradation of adenine nucleotides by the soleus muscle in hemorrhagic shock.

Our previous studies have shown a salutary effect of adenosine triphosphate-magnesium chloride (ATP-MgCl2) administered to animals in shock. The presence of adenine nucleotide converting enzymes on cell surfaces and the ability of nucleotides to act at the cell surface have been recognized also. To investigate the fate of administered or externally applied ATP and to determine whether it would be subjected to increased degradation with shock, the soteus muscles from rats subjected to hemorrhagic shock and from control animals were incubated in the presence of ATP, adenosine diphosphate (ADP), or adenosine monophosphate (AMP) with MgCl2. Comparable degradation of the added nucleotides was observed with both control muscles and those from bled animals. Adenylate kinase activity was detected to the same extent in the medium after incubation with both groups of muscles, but other enzymes were not, suggesting that the latter enzymes were located on the exterior surface of the muscle cell. Thus with shock there was no increase in the breakdown of the nucleotides by the enzymes on the muscle surface (ATPase, AMPdeaminase) or the cellular enzyme, adenylate kinase.

Adenine Nucleotides↗
PubMed1975

Evidence for enhanced uptake of adenosine triphosphate by muscle of animals in shock.

Although it has been shown that infusion of adenosine triphosphate (ATP)-magnesium chloride (MgCl2) proved beneficial in the treatment of shock, it is not known whether this effect is due to improvement in the microcirculation or to direct provision of energy. In searching for the mechanism of this, we have now examined the in vitro uptake of ATP by soleus muscle of animals in shock. Rats were bled to a mean arterial pressure of 40 mm. Hg and so maintained for 2 hours. Following death the two soleus muscles from each animal were removed and incubated in Krebs-HCO3 buffer containing 10 mM. of glucose, 5 mM. (8--14C) of ATP, 5 mM. (8--14C) of ADP, or 0.5 mM. (8--14C) of adenosine, and 5 mM. of MgCl2 for 1 hour under an atmosphere of 95 percent O2 to 5 percent CO2. Following homogenization and centrifugation, samples of the muscle extract and the medium were subjected to electrophoresis to separate the various nucleotides. The concentrations of the several nucleotides in medium and muscle were calculated from the radioactivity observed in each fraction. The uptake of 14-C-ATP by muscles from animals in shock was three times greater than was the uptake by control muscles. This leads us to conclude that the beneficial effect of ATP-MgCl2 to animals in shock could be due to provision of energy directly to tissues in which ATP levels were lowered.

Achilles Tendon↗