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

Chaudry, I. H.; Sayeed, M. M.; Baue, A. E.

doi:10.1152/ajpregu.1977.233.3.r83

Cited by 14 publications

(8 citation statements)

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“…All the chemical ingre dients necessary for FR generation, in fact, are available. During the ischemic stage, there is an increase in renal concentrations of catabolites derived from the anoxic degradation of adenine nucleotides, adenosine, inosine and hypoxanthine [37,55,56], The kidney contains xan thine dehydrogenase [57], which is converted to xanthine oxidase within 30 min of ischemia [36]. Peroxidation of the membrane lipids, furthermore, occurs during reper fusion only, since the production of malonyldialdehyde (the main product of such peroxidation) is not increased at the end of ischemia, but only after reperfusion [38].…”

Section: Hypothesis: the Case For Oxygen Free Radicals In Ischeinic-pmentioning

confidence: 99%

The Case for Oxygen Free Radicals in the Pathogenesis of Ischemic Acute Renal Failure

Canavese

Stratta

Vercellone

1988

Nephron

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One of the more glaring paradoxes of ischemic acute renal failure is that such injury appears to be worse in the kidney as opposed to other organs, even thouth the kidney is the best oxygenated. An answer can be deduced from the anatomical and physiological background, together with a reappraisal of the role of medullary vascular damage and recent evidence of the importance of the postischemic component of ischemic injury, which is mediated by oxygen free radicals. As far as oxygenation is concerned, the kidney’s Achilles heel is the tubules of the outer strip of the outer medulla, which are also those that have the most metabolic activity. It is here that ischemic injury begins, and is maintained and exacerbated in the postischemic stage by the free radicals. These are produced by the kidney in large quantities, since it has all the necessary chemical ingredients available. It is therefore readily understandable why the kidney, being the best oxygenated organ, is so sensitive to an ischemic insult, since the damage caused in the postischemic stage is increased the greater the amount of oxygen brought in by reperfusion.

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Section: Hypothesis: the Case For Oxygen Free Radicals In Ischeinic-pmentioning

confidence: 99%

The Case for Oxygen Free Radicals in the Pathogenesis of Ischemic Acute Renal Failure

Canavese

Stratta

Vercellone

1988

Nephron

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“…Since oxygen content difference between arterial and mixed venous blood remained unchanged, ATP might contribute in part to the body's energy resources. Chaudry et al (1974Chaudry et al ( , 1977 stated that ATP administered exogenously entered into the cells and its beneficial effect appeared but not only through vasodilatation because more potent vasodilatory agents, such as ADP or AMP, failed to produce any beneficial effect.…”

Section: Oxygen Consumptionmentioning

confidence: 99%

“…Chaudry et al (1974Chaudry et al ( , 1977 have used ATP as an energy source for the treatment of shock. Sodium nitroprusside (SNP) has been widely used not only to produce controlled hypotension but also in the treatment of congestive heart failure (Miller et al 1976) and hypertensive crisis (Page et al 1955).…”

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confidence: 99%

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Hashimoto

Rigor

Moreno

1982

Tohoku J. Exp. Med.

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Effects of Hypotension Induced by Adenosine Triphosphate and Sodium Nitroprusside on Dogs with Denervated Hearts. Tohoku J, exp. Med., 1982, 138 (1), 27-37 Adenosine triphosphate (ATP) and sodium nitroprusside (SNP) are administered to patients to induce and control hypotension during anesthesia. SNP is authorized for clinical use in USA and UK, and ATP is clinically used in other countries such as Japan. We investigated how these two drugs act on the cardiovascular systems of 20 dogs whose hearts had been denervated by a procedure we had devised. ATP (10 dogs) or SNP (10 dogs) was administered to reduce mean arterial pressure by 30% to 70% of control. Before, during and after induced hypotension, we measured major cardiovascular parameters. Hypotension induced by ATP was accompanied by significant decreases in mean pulmonary arterial pressure (p<0.001), central venous pressure (p<0.001), left ventricular end-diastolic pressure (p<0.001), total peripheral resistance (p<0.001), rate pressure product (p <0.001), total body oxygen consumption (p <0.05), and heart rate (p<0.001); all these variables returned normal within 30 min after ATP was stopped. Cardiac output did not change. During hypotension produced by SNP similar decreases were observed in mean pulmonary arterial pressure (p<0.01), central venous pressure (p <0.001), left ventricular end-diastolic pressure (p <0.01), total peripheral resistance (p <0.001), rate pressure product (p <0.001), and oxygen content difference between arterial and mixed venous blood (p <0.05), while heart rate (p <0.001) and cardiac output (p<0.05) were increased. Recoveries of heart rate and left ventricular end-diastolic pressure were not shown within 60 min after SNP had been stopped. Both ATP and SNP should act on the pacemaker tissue of the heart. adenosine triphosphate; sodium nitroprusside; denervated heart; induced hypotension; cardiovascular effects Adenosine triphosphate (ATP) is known to produce profound changes in the cardiovascular system and has been administered intravenously for controlled

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“…When the concentration of ATP-MgCl, in the medium was increased to 2.5 mM, intracellular ATP levels in 'shock' muscles increased and showed approximately the same values as observed in control musclcs. It has becn shown that ATP can cross cell membranes of muscle (Chaudry and Gould 1970a), liver, and kidney (Chaudry et al 1975d). Thus, the reversal of insulin resistance could be due to the restoration of muscle ATP levels by external ATP (Chaudry et al.…”

Section: A4uscle a Tp Contentsmentioning

confidence: 99%

Reversal of Insulin Resistance by ATP in Hemorrhagic Shock

Chaudry¹,

Sayeed²,

Baue³

1975

Can. J. Physiol. Pharmacol.

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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.

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

Cited by 14 publications

References 0 publications

The Case for Oxygen Free Radicals in the Pathogenesis of Ischemic Acute Renal Failure

The Case for Oxygen Free Radicals in the Pathogenesis of Ischemic Acute Renal Failure

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Reversal of Insulin Resistance by ATP in Hemorrhagic Shock

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