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Biomedical subjects

J Sprung

Publications and source records attributed to J Sprung.

At least 91 records · Page 5Linked to original sources
PubMed1992

The effect of acute hypothermia and serum potassium concentration on potassium cardiotoxicity in anesthetized rats.

We examined the effects of hypothermia on serum K+ concentration and the interaction of body temperature and K+ load on cardiac toxicity in anesthetized rats. Serum K+ concentration significantly decreased to 2.61 +/- 0.13, 2.59 +/- 0.19 and 2.39 +/- 0.14 mmol/l at 31.0 degrees C, 28.0 degrees C and 25.0 degrees C, respectively, from the control value of 2.80 +/- 0.15 mmol/l at 37.0 degrees C. We used a 300% increase in baseline QRS duration as evidence of cardiac toxicity. Serum K+ concentrations of 4.95 +/- 0.12, 4.71 +/- 0.10, 4.45 +/- 0.14 and 4.07 +/- 0.14 mmol/l resulted in cardiac toxicity at 37.0 degrees C, 31.0 degrees C, 28.0 degrees C, and 25.0 degrees C, respectively. These data indicate that the level at which an elevation of serum K+ concentration causes cardiac toxicity diminishes with progressive hypothermia. We conclude that hypothermia induces hypokalemia, possibly through redistribution, and that the myocardium appears to be more sensitive to the toxic effects of K+ as hypothermia deepens.

Acidosis↗
PubMed1992

Changes in functional residual capacity and regional diaphragm lengths after upper abdominal surgery in anesthetized dogs.

The respiratory performance of the diaphragm may be altered by changes in mechanical or neural factors, or both, induced by upper abdominal surgery. We conducted this study to examine the effects of upper abdominal surgery on postoperative respiratory function. We studied resting lengths of four diaphragm regions, three in the costal and one in the crural diaphragm, with biplane video-roentgenography in six dogs immediately after upper abdominal surgery and up to 30 days postoperatively. Functional residual capacity was 16.7% smaller immediately after surgery compared with values obtained in the same animals after 30 days. Simultaneously measured resting lengths of each of the diaphragm regions immediately after surgery were longer, on average by 8.3%, than 30 days postoperatively. During the postoperative course, resting diaphragm lengths gradually and uniformly decreased as functional residual capacity increased. Phrenic nerve stimulation in four other dogs immediately after identical surgery resulted in large diaphragm shortening (from 42% to 55%), indicating that neither the diaphragm nor phrenic nerves were injured by the surgical manipulation. We hypothesize that respiratory dysfunction after upper abdominal surgery may be, at least in part, attributed to a decreased central drive for breathing caused by activation of the afferent limb of an inhibitory reflex owing to stretching of the diaphragm.

Abdomen↗
PubMed1991

Horner's syndrome and trigeminal nerve palsy following epidural anaesthesia for obstetrics.

While Horner's syndrome is a rare but occasionally reported side-effect of epidural block administered for labour, trigeminal nerve palsy has been described only once. The cases described in this report confirmed the benign nature of these neurological complications of epidurally administered anaesthetics which were not detrimental to fetal viability. The complications may be attributed to extensive cephalad spread of local anaesthetic, sometimes via unexplained routes and with surprisingly selective targeting effect (unilateral trigeminal nerve palsy). The atypical and unusually high cephalad spread of local anaesthetic in pregnant women at term is believed to be due to pregnancy-related altered anatomy and physiology of the epidural space.

Adult↗
PubMed1991

Effects of acute hypothermia and beta-adrenergic receptor blockade on serum potassium concentration in rats.

BACKGROUND AND METHODS: We hypothesized that beta-adrenergic receptor blockade would result in an increase in serum potassium concentration in hypothermic rats given a potassium load compared to non-beta-blocked, hypothermic, potassium-loaded rats. To test this hypothesis, we investigated the interaction between body temperature and beta-adrenergic receptor blockade on serum potassium concentrations in ureter-ligated rats with and without potassium loading. To achieve this goal, we performed three experiments. In the first experiment, serum potassium concentrations were determined in 16 rats as they were continuously cooled from 37 degrees C to 22 degrees C. In the second experiment, 12 ureter-ligated rats were cooled to 31 degrees C, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling and on rewarming. Twelve other ureter-ligated rats were cooled to 31 degrees C, then given a potassium load until their serum potassium concentrations returned to their baseline values, after which they were rewarmed to 37 degrees C. Serum potassium concentrations were determined before and after cooling, during the potassium infusion, and on rewarming. In the third experiment, 14 rats were pretreated with propranolol and 14 rats served as controls. Half of the rats in each of these two groups were kept at 37 degrees C and half were cooled to 25 degrees C. All rats were then given a 690-mumol potassium chloride infusion. Serum potassium concentrations were determined before and after the potassium infusion. RESULTS: The rats developed hypokalemia with cooling, which spontaneously resolved in the rats without supplementation on rewarming to 37 degrees C. The hypothermic hypokalemic rats that had their serum potassium concentrations corrected to normothermic status (2.93 +/- 0.17 mmol/L) had marked increases in serum potassium concentrations (4.22 +/- 0.15 mmol/L) on rewarming. In the normothermic rats, potassium loading after beta-adrenergic receptor blockade resulted in even higher serum potassium concentrations (5.65 +/- 0.36 mmol/L) compared with non-beta-blocked rats given equal potassium loads (4.6 +/- 0.4 mmol/L). However, in hypothermic (25 degrees C) rats given the same potassium load, there was no difference in serum potassium concentrations in beta-blocked (6.5 +/- 0.35 mmol/L) and non-beta-blocked rats (6.63 +/- 0.3 mmol/L). CONCLUSIONS: These results suggest that acute hypothermia causes a decrease in serum potassium, probably secondary to redistribution, which is reversible on rewarming. Supplementation of potassium during hypothermia can cause a significant increase in serum potassium concentration on rewarming. Blocking beta-adrenergic receptors with propranolol did not effect hypothermia-induced hypokalemia, suggesting that the beta-adrenergic mechanism may not be functional in hypothermia.

Animals↗
PubMed1991

Amniotic fluid embolism during epidural anesthesia for cesarean section.

A survivor of a clinically severe presentation of amniotic fluid embolism during cesarean section performed under epidural anesthesia is presented. Some general pathophysiologic features of amniotic fluid embolism are discussed in the context of presented case: seizures as a first sign of amniotic fluid embolism, heart failure and coagulopathy. In addition we discuss the management of the epidural catheter in coagulopathy in the presented case.

Adult↗
PubMed1990

Determinants of transdiaphragmatic pressure in dogs.

We measured the transdiaphragmatic pressure (Pdi) during bilateral phrenic nerve stimulation and evaluated the determinants of its change with lung volume, chest wall geometry, and respiratory system impedance in supine dogs. Four rows of radiopaque markers were sewn onto muscle bundles of the costal and crural diaphragm between their origin on the central tendon and their insertion on the rib cage and spine. The length of the diaphragm (L) was determined from the projection images of marker rows using biplane fluoroscopy. Measurements were made at lung volumes between total lung capacity and functional residual capacity before and after the infusion of Ringer lactate solution into the abdominal cavity. In contrast to relaxation, during tetanic stimulation the active lengths of the muscle bundles were similar at all volumes, but the diaphragm assumed different shapes. Although the small differences in active muscle length with volume and liquid loads are consistent with only small changes in muscle force output, Pdi varied by a factor of greater than or equal to 5. There was no single L/Pdi curve that fitted all data during 50-Hz stimulations. We conclude that under these experimental conditions Pdi is not a unique measure of the force produced by the diaphragm and that lung volume, chest wall geometry, and respiratory system impedance are important determinants of the mechanical efficiency of the diaphragm as a pressure generator.

Action Potentials↗
PubMed1990

Effect of body position on regional diaphragm function in dogs.

The in situ lengths of muscle bundles of the crural and three regions of the costal diaphragm between origin and insertion were determined with a video roentgenographic technique in dogs. At total lung capacity (TLC) in both the prone and supine positions, the length of the diaphragm is not significantly different from the unstressed excised length, suggesting that the diaphragm is not under tension at TLC and that there is a hydrostatic gradient of pleural pressure on the diaphragmatic surface. Except for the ventral region of the costal diaphragm, which does not change length at lung volumes greater than 70% TLC, all other regions are stretched during passive deflations from TLC. Therefore below TLC the diaphragm is under passive tension and supports a transdiaphragmatic pressure (Pdi). The length of the diaphragm relative to its unstressed length is not uniform at functional residual capacity (FRC) and does not follow a strict vertical gradient that reverses when the animal is changed from the supine to the prone position. By inference, the length of muscle bundles is determined by factors other than the vertical gradient of Pdi. During mechanical ventilation, regional shortening is identical to the passive deflation length-volume relationship near FRC. Prone and supine FRC is the same, but the diaphragm is slightly shorter in the prone position. In both positions, during spontaneous ventilation there are no consistent differences in regional fractional shortening, despite regional differences in initial length relative to unstressed length.

Animals↗
PubMed1989

In vivo regional diaphragm function in dogs.

A biplane videofluorographic system was used to track the position of metallic markers affixed to the abdominal surface of the left hemidiaphragm in supine anesthetized dogs. Regional shortening was determined from intermarker distances of rows of markers placed along muscle bundles in the ventral, middle, and dorsal regions of the costal diaphragm and of one row on the crural diaphragm. Considerable variability of regional shortening was seen in a given row, which was reproducible on repeat study in individual dogs but which differed between mechanical ventilation and spontaneous breathing. There were no consistent patterns among dogs. Regional shortening obtained from the change in length of rows extending from chest wall to central tendon showed no consistent differences among dogs during spontaneous breathing. At equal tidal volumes, all regions (except the ventral costal diaphragm) shortened more during spontaneous breathing than during mechanical ventilation.

Animals↗