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Biomedical subjects

J D Blachley

Publications and source records attributed to J D Blachley.

17 recordsLinked to original sources

The cervical wound of General James Longstreet.

BACKGROUND: Lieutenant General James Longstreet was arguably the finest corps commander on either side during the Civil War. He was severely wounded at the Battle of the Wilderness in Virginia on May 6, 1864, after a successful flank attack that nearly routed the Union army. DESIGN: A thorough review of the firsthand accounts of the events leading up to and following Longstreet's wounding was made. In addition, all articles listed in the medical literature describing Longstreet's care and numerous recent texts and articles about Longstreet have been researched. RESULTS: After being wounded on May 6, Longstreet received appropriate care by John Syng Dorsey Cullen, MD. Cullen controlled the hemorrhage from Longstreet's wound, helped evacuate him from the battlefield, and diligently cared for him during his convalescence. CONCLUSIONS: Longstreet was wounded by "friendly fire." The bullet's trajectory and the location of the gunshot wound suggest a posterior wound of entry rather than an anterior one as has been previously assumed.

Famous Persons↗

Effect of magnesium salt anions on potassium balance in normal and magnesium-depleted rats.

Potassium depletion often accompanies clinically significant magnesium depletion, and magnesium replacement is most frequently undertaken with magnesium sulfate. However, inorganic sulfate acts as a nonreabsorbable anion in the distal nephron, an effect that could potentially interfere with the correction of any associated potassium deficiency. We have investigated the effect of a variety of magnesium salts, including sulfate and nonsulfate forms, on cation balance and skeletal muscle ion composition in normal and magnesium-depleted rats. Even modest amounts of dietary sulfate increased the urinary excretion of potassium in both normal and magnesium-depleted rats. During a 7-day feeding period, diets containing MgSO4 or MgO with an equivalent amount of Na2SO4 resulted in significantly greater urinary excretion of potassium than diets without sulfate. In normal animals, this kaliuresis did not produce hypokalemia or muscle potassium depletion. Magnesium-deficient feeding produced magnesium depletion, kaliuresis, and a decline in both plasma and muscle potassium content. When magnesium was restored to the diet without sulfate, urinary potassium excretion decreased, and both magnesium and potassium deficits were corrected. However, when magnesium refeeding included sulfate salts, magnesium stores returned to normal, whereas the kaliuresis and potassium depletion persisted. When accompanied by a high sodium intake, the kaliuretic effect of sulfate was increased.

Animals↗

Extrarenal potassium adaptation: role of skeletal muscle.

Following the ingestion of a high-potassium-content diet for only a few days, the plasma potassium of rats rises only modestly in response to a previously lethal dose of potassium salts. This acquired tolerance, termed potassium adaptation, is principally the result of increased capacity to excrete potassium into the urine. However, a substantial portion of the acute potassium dose is not immediately excreted and is apparently translocated into cells. Previous studies have failed to show an increase in the content of potassium of a variety of tissues from such animals. Using 86Rb as a potassium analogue, we have shown that the skeletal muscle of potassium-adapted rats takes up significantly greater amounts of potassium in vivo in response to an acute challenge than does that of control animals. Furthermore, the same animals exhibit greater efflux of 86Rb following the termination of the acute infusion. We have also shown that the Na+-K+-ATPase activity and ouabain-binding capacity of skeletal muscle microsomes are increased by the process of potassium adaptation. We conclude that skeletal muscle is an important participant in potassium adaptation and acts to temporarily buffer acute increases in the extracellular concentration of potassium.

Adaptation, Physiological↗

Uremic pruritus: skin divalent ion content and response to ultraviolet phototherapy.

Pruritus is a frequent and troublesome consequence of end-stage renal disease. We have surveyed 155 chronic dialysis patients and found pruritus to be a significant problem in approximately 70%. Seventeen patients reporting severe pruritus were treated thrice weekly with total body exposure to either UVA or UVB light. UVB light resulted in resolution of pruritus in all cases. UVA light was without significant effect. Skin biopsies obtained before and after UV phototherapy revealed elevated contents of calcium, magnesium, and phosphorus in all pruritic patients. The resolution of pruritus following UVB treatment was associated with a reduction of skin phosphorus to values comparable with nonpruritic uremics or healthy volunteers. Uremic pruritus may be due to increased skin divalent ion content resulting in microprecipitation of calcium or magnesium phosphate.

Biopsy↗

The harmful effects of ethanol on ion transport and cellular respiration.

The deleterious effects of ethanol on a variety of tissues may result largely from altered ion permeabilities and transport. Clinically relevant ethanol concentrations in blood increase the sodium permeability of the plasma membrane and depress active sodium transport by suppressing Na, K-ATPase activity. As a result, intracellular sodium concentration increases. The total tissue content of calcium increases. Important transport mechanisms deranged by ethanol probably include those regulating calcium-sodium and hydrogen-sodium exchange at the plasma membrane and calcium uptake by the sarcoplasmic reticulum. A modest decline in magnesium content of muscle occurs after chronic exposure to ethanol. This also has been associated with accumulation of calcium. After days to weeks of sustained ethanol intake, sodium pump activity, active sodium transport and tissue oxygen consumption increase. The cell membrane potential, initially lowered by alcohol, increases to supraphysiological levels. This is likely an electrogenic effect of increased sodium transport in response to a sodium leak. Eventually the earlier derangements in tissue composition, including retention of sodium, chloride, and calcium, and reductions in magnesium, potassium, and phosphate, slowly undergo correction. This biphasic response of injury and adaptation appears to depend upon adequate nutrition and the absence of other factors that can adversely affect cell function. That the Na, K-ATPase activity and oxygen consumption remain elevated suggests an ongoing sodium leak of the sarcolemmal membrane. Chronic ethanol-induced cell necrosis may be related to the increased intracellular calcium that accompanies the increase in sodium permeability. Conceivably, critically elevated concentrations of calcium in the cytoplasm may activate autolytic enzymes that in turn may be responsible for structural damage to the cell.

Animals↗

Muscle cell electrical hyperpolarization and reduced exercise hyperkalemia in physically conditioned dogs.

Contracting muscle cells release K ions into their surrounding interstitial fluid, and some of these ions, in turn, enter venous plasma. Thereby, intense or exhaustive exercise may result in hyperkalemia and potentially dangerous cardiotoxicity. Training not only reduces hyperkalemia produced by exercise but in addition, highly conditioned, long-distance runners may show resting hypokalemia that is not caused by K deficiency. To examine the factors underlying these changes, dogs were studied before and after 6 wk of training induced by running on the treadmill. Resting serum [K] fell from 4.2 +/- 0.2 to 3.9 +/- 0.3 meq/liter (P less than 0.001), muscle intracellular [K] rose from 139 +/- 7 to 148 +/- 14 meq/liter (P less than 0.001), and directly measured muscle cell membrane potential (Em) in vivo rose from -92 +/- 5 to -103 +/- 5 mV (P less than 0.001). Before training, resting Em of isolated intercostal muscle in vitro was -87 +/- 5 mV, and after incubation in 10(-4) M ouabain, Em fell to -78 +/- 5 mV. After training, resting Em of intercostal muscle rose to -95 +/- 4, but fell to -62 +/- 4 mV during incubation in 10(-4) M ouabain. The measured value for the Em was not completely explained by the increased ratio of intracellular to extracellular [K] or by the potassium diffusion potential. Skeletal muscle sarcolemmal Na,K-ATPase activity (microM inorganic phosphate mg-1 protein h-1) increased from 0.189 +/- 0.028 to 0.500 +/- 0.076 (P less than 0.05) after training, whereas activities of Mg2+ -dependent ATPase and 5'nucleotidase did not change. In untrained dogs, exercise to the point of exhaustion elevated serum [K] from 4.4 +/- 0.5 to 6.0 +/- 1.0 meq/liter (P less than 0.05). In trained dogs, exhaustive exercise was associated with elevation of serum [K] from 3.8 +/- 0.3 to 4.2 +/- 0.4 (NS). The different response of serum [K] to exercise after training was not explainable by blood pH. Basal insulin levels rose from 7.0 +/- 0.7 microU/ml in the untrained dogs to 9.9 +/- 1.0 microU/ml (P less than 0.05) after training. Although insulin might have played a role in the acquired electrical hyperpolarization, the reduced exercise-produced hyperkalemia after training was not reversed by blockade of insulin release with somatostatin. Although the fundamental mechanisms underlying the cellular hyperpolarization were not resolved, our observations suggest that increased Na-K exchange across the sarcolemmal membrane, the increase of Na,K-ATPase activity and possibly increased electrogenicity of the sodium pump may all play a role in the changes induced by training.

Animals↗

The role of dietary protein in the progression and symptomatology of chronic renal failure.

Dietary factors may have substantial impact on the clinical manifestations and even the progression of chronic renal failure. Proper dietary management can prevent certain uremic complications, decrease azotemia, and may even prevent the loss of residual renal function. Recent studies indicate that dietary protein may accelerate the normal age-related deterioration of renal function in rats. The extensive ablation of functional renal mass in rats leads to hyperemia and hyperfiltration in remnant nephrons. Continued hyperfiltration theoretically results in glomerular damage, proteinuria, and ultimately glomerular sclerosis. Dietary protein restriction reduces the remnant nephron hyperfiltration and reduces the rate of glomerular sclerosis, at least in the rat. The role of dietary protein in the pathogenesis of human nephrosclerosis remains controversial. Though dietary factors may or may not affect the rate of progression of renal insufficiency, there is no doubt that proper dietary management can limit or forestall uremic symptoms and the need for dialysis. Diets containing about 0.5 gm protein/kg body weight/day usually maintain a neutral or slightly positive nitrogen balance, while lesser amounts usually result in malnutrition. When protein intake exceeds 0.5 gm/kg/day azotemia increases dramatically. The use of nitrogen-free keto- or hydroxy-analogues of amino acids promotes positive nitrogen balance while reducing azotemia in patients with near-end-stage renal disease.

Amino Acids↗

Derangements of muscle composition, ion transport, and oxygen consumption in chronically alcoholic dogs.

Muscle ion composition, Na-K-ATPase activity, tissue respiration, and transmembrane potential differences were measured after 28 and 56 days of ethanol consumption (6.2 g X kg-1 X day-1) or an isocaloric amount of glucose in 12 and 4 dogs, respectively. Ethanol and glucose were given as supplements to an otherwise nutritious diet. After 28 and 56 days of alcohol consumption, skeletal muscle contents of phosphorus, magnesium, and potassium were significantly reduced as compared with either the control values or those in glucose-fed animals. In alcohol-fed animals, muscle sodium chloride, and calcium were significantly elevated. Ethanol consumption also resulted in hyperpolarization of the resting transmembrane potential of skeletal muscle fibers and a significant increase in Na-K-ATPase activity. No change was noted in Mg-ATPase activity. The increase in Na-K-ATPase activity was accompanied by increased sodium transport-dependent respiration. These results indicate that a subclinical myopathy may be induced by alcohol in the dog. Malnutrition did not appear to be a factor in this study, and thus the changes observed are believed to be due to ethanol per se. The magnitude and direction of these changes are similar to those observed in the skeletal muscle of chronically alcoholic humans. The changes in Na-K-ATPase activity and sodium transport-dependent respiration may represent adaptive responses of the muscle cell to ion transport or membrane disorders induced by ethanol.

Adenosine Triphosphatases↗

Renal and electrolyte disturbances associated with cisplatin.

Cisplatin is a coordinate metal complex with significant antineoplastic activity and various effects, including acute anc chronic renal insufficiency and renal magnesium wasting. Nephrotoxicity may occur in as many as 50% to 75% of patients receiving the drug, and is apparently due to renal tubular injury. Although controlled, prospective clinical trials are lacking, the available data indicate that the frequency and severity of cisplatin nephrotoxicity may be reduced by slow infusion rates; hydration before, during, and immediately after administration of cisplatin; and concomitant administration of mannitol. Preliminary animal studies indicate that chloride-containing vehicles such as 0.9% sodium chloride may prevent the aquation or hydroxylation of cisplatin and reduce its toxicity. No information is available on th prevention of cisplatin associated renal magnesium wasting. However, frequent measurement of serum cations and appropriate replacement are recommended.

Animals↗

Role of osmolality in blood pressure stability after dialysis and ultrafiltration.

To clarify the mechanisms involved in the stability of blood pressure during ultrafiltration (UF) alone versus regular dialysis, this study systematically examined the importance of changes in serum potassium, osmolality, and plasma norepinephrine during several dialysis maneuvers. Six stable, normotensive chronic dialysis patients were subjected to a uniform 2 to 3% decrease in body weight during the 2 hours of each dialysis maneuver. Supine to upright mean blood pressure (MBP) decreased (90 to 75 mm Hg, P less than 0.05), and three patients became symptomatic after weight loss during regular dialysis, but orthostatic blood pressure was stable (89 to 86 mm Hg, NS) and the patients were asymptomatic after UF and weight loss. Isokalemic regular dialysis did not afford hemodynamic stability, as orthostatic MBP declined (85 to 56 mm Hg, P less than 0.02), and four of the patients were again asymptomatic after standing. A continuous hypertonic mannitol (25%) infusion during the 2-hour dialysis, however, kept osmolality from decreasing and was associated with a stable orthostatic MBP (89 to 83 mm Hg, NS). A continuous infusion of isotonic mannitol (5%) given in a volume of five times that of the hypertonic mannitol failed to prevent orthostatic hypotension (80 to 60 mm Hg, P less than 0.005). Plasma norepinephrine concentrations were high in these patients and increased only modestly after weight loss. These results implicate constant plasma osmolality as a critical protective factor of blood pressure during UF and further demonstrate that changes in blood pressure may be associated from changes in both serum potassium and plasma norepinephrine concentration.

Blood↗

Normal resting and exercising muscle blood flow during acute ethanol infusion.

We have examined the effect of ethanol on muscle blood flow at rest and during electrically stimulated exercise in five normal dogs using the isolated gracilis muscle preparation. Under pentobarbital anesthesia and mechanical ventilation, ethanol (15% in 0.9% NaCl) infused at 4 mL/min for 2 hr produced an arterial blood concentration of 268 +/- 10 mg/dL (X +/- SEM). Resting muscle blood flow was 6.3 +/- 0.9 mL/min/100 gm in 8 dogs infused with saline alone. During stimulated contraction using supramaximal voltage at a rate of 5 stimuli/sec, respective mean flows for ETOH and saline dogs at 1, 5, 10, and 30 min were 35.5, 19.9, 27.7, 22.2, and 22.0, 20.0, 23.6, and 19.1 mL/min/100 gm. The 1-min flow rate for ethanol infused animals was significantly greater (P < 0.05) than that observed in saline infused animals. The remainder of the values were not significantly different. Potassium release from contracting muscle was normal. These observations do not support the theory that ethanol induces vasoconstriction in the vascular bed of skeletal muscle nor do they support the postulation that muscle cell ischemia plays a role in alcoholic myopathy.

Animals↗

Low- and high-dose intravenous insulin therapy for diabetic ketoacidosis.

We compared low-dose, continuous insulin infusion with a conventional high-dose intravenous bolus method of insulin administration in 18 episodes of diabetic ketoacidosis. The average rate of reduction in serum glucose concentration was 9.5 +/- 3.8%/hr in the continuous infusion group and 10.7 +/- 4.7%/hr in the bolus group. Arterial blood pH was corrected to 7.35 by 9.9 +/- 2.6/hours in the continuous infusion group and by 10.4 +/- 3.2/hours in the bolus group. The above means are not significantly different between groups. By the time pH was corrected to 7.35, patients in the continuous infusion group had received 121 +/- 44 units of insulin, whereas those in the bolus group had received 326 +/- 152 units. The continuous low-dose insulin infusion method is as safe and efficacious as the conventional high-dose intravenous bolus method.

Blood Glucose↗