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| Year : 1981 | Volume
: 27
| Issue : 1 | Page : 20-4 |
A serial study of ECG and electrolyte changes in albino rats after bile duct ligation.
Bilgrami NL, Bilgrami GG, Kumar SS
How to cite this article:
Bilgrami N L, Bilgrami G G, Kumar S S. A serial study of ECG and electrolyte changes in albino rats after bile duct ligation. J Postgrad Med 1981;27:20 |
How to cite this URL:
Bilgrami N L, Bilgrami G G, Kumar S S. A serial study of ECG and electrolyte changes in albino rats after bile duct ligation. J Postgrad Med [serial online] 1981 [cited 2023 Oct 2];27:20. Available from: https://www.jpgmonline.com/text.asp?1981/27/1/20/5668 |
The elctrolyte metabolism of the myocardium is closely related to the function of the heart muscle. Electrolyte abnormalities influence impulse formation, conduction and repolarisation. These may result in cardiac arrythmias and ECG changes. Sodium and potassium are important ions responsible for the myocardial electromechanical activity. The major effect of potassium is on the resting membrane potential and the sodium influences the action potential.
Changes in the serum and cardiac electrolytes after bile duct ligation in albino rats have been studied by earlier authors.[7] ECG abnormalities have also been observed following biliary obstruction in patients and experimental animals.[6], [8], [10] to ECG changes were also seen in patients of infectious hepatitis and no correlation was found with serum bulirubin, SGOT, SGPT, or thymol turbidity levels[3] Changes in electrolytes in serum and myocardium and their correlation with ECG changes in biliary obstruction have, however, not been investigated thoroughly. The present study has therefore been planned to investigate serial changes in serum and cardiac electrolytes (Na & K), serum bilirubin and ECG after bile duct ligation in albino rats.
Thirty male albino rats were used for this study. They were fed on standard cube diet for rats and mice (Hindustan Lever Laboratory). The rats were equally divided in four test group and one control group. Rats in group IV were operated first and subsequently the rats in groups III, II and I were operated at the interval of four days between each group. Rats in the control group were operated with the rats in group I.
After an overnight fast, the rats were subjected to laparotomy under light ether anesthesia. Bile duct was exposed after retracting the liver. It was ligated at two places and sectioned in between in the test groups of rats and was left intact in the control group. Abdomen was closed by continuous sutures and the wound sealed with tincture benzoin. Food was allowed after 12 hours of operation.
All the thirty rats were killed by breaking the neck by sudden stretch under ether anaesthesia on the 17th day of bile duct ligation of group IV rats. Thus rats in group IV, III, II, I and control had biliary obstruction for 16, 12, 8, 4 and 4 days respectively. Thorax was opened and blood collected directly from heart for the estimations of bilirubin9 and electrolytes (Na & K).[4] Heart was taken out, weighed and then processed for estimation of cardiac sodium and postassium.[7]
Electrocardiograms were recorded on all the rats under light ether anaesthesia once before the ligation of the bile duct and then before killing them. Hypodermic needles were inserted in all the four limbs of the rats and were connected to the electrodes of the ECG machine. Lead II was recorded at 1 mV at paper speed of 50 mm/sec.
Significant ECG changes were observed in the animals subjected to bile duct ligation. Fall in the heart rate was observed in all the animals. The fall was less than 50 beats per minute in 29% rats, between 51-100 beats per minute in 540, rats and more than 100 beats per minute in 17% rats. Arrythmias (supraventricular) were observed in 25% rats and ST-T changes in 29% rats. The incidence of these changes increased with the severity of bradycardia. When the fall in the heart rate was less than 50 beats per minute, the incidence of these changes was only 38% compared to 75% when the fall in heart rate was more than 100 beats per minute.
The ECG changes increased with the duration of biliary obstruction. Decrease in the heart rate was 46 ± 10 beats after 4 days of bile duct ligation and 101 ± 17 beats after 16 days of bile duct ligation. Arrythmias and ST-T changes also increased from 17% in group I to 50% in group IV.
Changes in serum bilirubin, serum and cardiac sodium and potassium increased with the duration of bile duct ligation [Table 1]. Statistically significant changes (compared to control group) started appearing from the 1st group in serum bilirubin, serum sodium and serum potassium. Cardiac potassium decreased significantly from the 2nd group but the change in cardiac sodium was not found significant in any of the groups.
Changes in the serum bilirubin and cardiac electrolytes in the test group of rats were correlated with the ECG changes [Table 2]. There was no significant correlation of serum bilirubin level either with the severity of bradycardia or with the occurrence of arrythmias or ST-T changes. Cardiac sodium was also not related to these changes. On the other hand, the cardiac potassium decreased significantly with the severity of bradycardia and the appearance of ST-T changes.
The role of serum billirubin and cardiac potassium in the genesis of arrythmias and ST-T changes was compared with the help of critical values [Table 3]. Amongst the rats in which the cardiac potassium level decreased below the level of critical value for cardiac potassium, 63% developed arrythmias as compared to 33% amongst the rats in which the serum bilirubin level increased beyond its critical value. The incidence of ST-T changes was 88% amongst the rats having cardiac potassium below the critical value in this group as compared to 33% when the serum bilirubin was higher than its critical value [Table 3].
ECG abnormalities in biliary obstruction have been reported by earlier authors also.[6], [8], [10] Dehn et al[3] reported bradycardia in 90% cases of jaundice but found no correlation with serum levels of bilirubin, SGOT, SGPT or thymol turbidity. Varying degrees of arrhythmias, ST-T changes, P wave and P-R interval changes and Q-T' interval changes have also been described by these authors. Our findings of the ECG changes after bile duct ligation in rats generally agree with their findings. Like other authors, we could not find any significant correlation between the serum bilirubin levels and the ECG changes.
Similar ECG changes have also been reported following parenteral administration of bile salts and bile pigments in various experimental animals. [14] Bile salts and bile pigments also increase in obstructive jaundice. Both are cardiac depressants. Bile pigments act by uncoupling the oxidative phosphorylation and bile salts by depressing the sympathetic nerve endings, stimulating the vagal endings and by direct depression of the myocardium.[11], [14]
The pattern of changes in serum and cardiac electrolytes observed in this study is similar to the observations of Hass et al (1942),[7] in albino rats following bile duct ligation. Their study was, however, not serial and the electrolyte changes were not correlated with ECG changes. The electrolyte changes are perhaps secondary to liver damage after bile duct ligation. The damaged liver cannot metabolise aldosterone properly. leading to its accumulation in blood which, in turn, acts on the kidneys to preserve sodium and to increase urinary potassium loss.[13] In the present study cardiac sodium did not increase significantly in spite of a significant rise in serum sodium. However, with decrease in serum potassium, the cardiac potassium showed significant decrease [Table 1]. The serum K: Na ratio is about 1:35; therefore even a slight change in serum potassium is likely to affect cardiac potassium significantly. A slight change in serum sodium is unlikely to affect cardiac sodium. Perhaps this is the reason why cardiac potassium decreased significantly but not cardiac sodium.
Significant correlation between the ECG changes and the cardiac potassium levels has been observed in the present study. Relationship between potassium content of heart and the functional status of mitochondria and myocardium has been shown.[7] The high potassium content within the cell acts as energy utilizing mechanism (K battery) which initiates the source of energy for muscle contraction. The ECG abnormalities of hypokalaemia are due to functional abnormalities of the myocardium rather than the structural changes. The myocardial action potential is increased and the repolarisation wave shifts from systole to diastole.[12] ST abnormalities, decrease in amplitude of T wave, prolongation of QT but not QTc (corrected QT) and P wave abnormalities are found. Hypokalaemia also facilitates supraventricular and ventricular ectopics and arrythmias and these are attributed to the prolonged duration of repolarisation, which is not yet completed when the myocardium is no longer refractory. At this time the membrane potential is closer to the threshold potential than at rest hence the ectopic foci elicit an action potential more readily.[5]
Coni (1969)[2] and Christy and Clements 1978)[1] could not find any correlation between serum potassium levels and ECG changes of hypokalaemia, and suggested that the ECG alterations reflect cardiac potassium content. The present study completely supports their statement in that ECG changes correlate with the cardiac potassium contents but not with the serum potassium levels.
| 1. | Christy, J. H. and Clements, S. D.: Endocrine and metabolic disorders. In, "The Heart, Arteries and Veins." Ed.: Hurst, J. W., Logue, R. B., Schlant, R. C. and Wenger, N. K., McGraw-Hill Book Co., New York, 1978, pp. 1749-1751.  |
| 2. | Coni, N. K.: The myocardium of periodic paralysis. Postgrad. Med. J., 45: 691-694, 1969. |
| 3. | Dehn, H., Feil, H. and Rinderknecht, R. E.: Electrocardiographic changes in cases of infectious hepatitis; Study of 11 cases occurring in epidemics. Amer. Heart J., 31: 183-190, 1945. |
| 4. | Domingo, W. R. and Klyne, W,: Photoelectric flamephotometer. Biochem. J., 45: 400-408, 1949. |
| 5. | Friedberg, C. K.: "Diseases of the Heart." W. B. Saunders Co., Philadelphia and London, 1966, p. 1654. |
| 6. | Gulstein, W. H.: Ultrastructural changes of coronary artery endothelium associated with biliary obstruction in rats. Amer. J. Path., 71: 49-60, 1973. |
| 7. | Haas, W. and Elster, K.: Electrolyte determination and morphological studies on the rat heart in cholestasis; A contribution to the problem of metabolic hypodynamic heart insufficiency. Z. Kreislauflorsch, 51: 763-774, 1962. |
| 8. | Havranek. J. and Kral, V.: Coronary disease of heart and diseases of gall bladder and bile duct. Casopis Lekaru Ceshych., 100: 47-55, 1961. |
| 9. | Malloy, H. T. and Evelyn, K. A.: The oxidative determination of bilirubin in bile with the photo-electric method. J. Biol. Chem., 119: 481-490, 1937 and 122: 597-603, 1938. |
| 10. | Marburger, P. I.: Paroxysmal tachycardia in diseases of biliary system. Med. Elin. Stadt. Krankenanst. Karlsyke. Med. Welt. (Stuttg.). 30: 1708-1710, 1976. |
| 11. | Rozdilsky, B.: Toxicity of bilirubin on adult animals. Arch. Path., 72: 8-17, 1961. |
| 12. | Suravics, B.: Relationship between electrocardiogram and electrolytes. Amer. Heart. J., 73: 814-834, 1967. |
| 13. | Thorn, G. W., Adams, R. D., Braunwald. E., Isselbacher, K. J. and Petersdorf, R. G.: "Harrison's Principles of Internal Medicine". McGraw-Hill Kogakusha Ltd., Tokyo, 1977, p. 272. |
| 14. | Wakim, K. G., Essex, H. E. and Mann, F. C.: Effect of whole bile and bile salts on the innervated and denervated heart. Amer. Heart J., 20: 486-491, 1940. |
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