Hyperkalemic periodic paralysis in horses

Eleven horses (3 mares, 7 stallions, 1 gelding) with clinical and biochemical evidence of hyperkalemic periodic paralysis were studied. Each horse had history of episodic weakness, muscular tremors, or collapse, which lasted for periods of a few minutes to hours. Diagnosis was based on hyperkalemia in association with a spontaneous episode of paralysis or by precipitation of an episode by oral administration of potassium chloride. Clinical and biochemical events were documented during spontaneous and induced episodes of muscular weakness. During episodes, electrocardiographic findings were consistent with hyperkalemia. Electromyography performed between episodes revealed fibrillation potentials and positive sharp waves, complex repetitive discharges, and myotonic discharges. Histologic changes in muscle biopsy specimens varied from no overt changes in some horses to vacuolation in type-2B fibers with mild degenerative changes in other horses. Electron microscopy of myofibers revealed dilatations of the sarcoplasmic reticulum. Analysis of blood samples taken serially during induced attacks in 5 horses revealed marked hyperkalemia (5.5 to 9.0 mEq/L), with normal acid-base status, hemoconcentration, and modest changes in muscle-derived enzymes. Close correlation (r2 = 0.882) between total plasma protein and plasma potassium concentrations was observed and indicated a shift of fluid out of the extracellular fluid compartment. Treatment of either spontaneous or induced episodes by IV administration of calcium, glucose, or bicarbonate resulted in rapid recovery. Dietary management or daily administration of acetazolamide effectively controlled episodes. An affected mare was bred to an affected stallion, and 3 affected offspring were produced by embryo transfer. Blood samples from another extended family of affected horses were analyzed for identification of a genetic marker.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of high intensity exercise on the plasma concentration of lactate, potassium and other electrolytes

To study the effect of short term high intensity exercise on plasma lactate, potassium, sodium and chloride concentrations, five Thoroughbred horses were galloped on a treadmill at a 5 degree incline. Following a standardised warm-up period, they were galloped at 8, 10, or 12 metres/sec for 2 mins. One horse also galloped at 14 metres/sec for 1.5 mins. Sequential arterial and/or venous blood samples were collected during exercise and recovery. At 12 metres/sec, the effect of different recovery modes, ie, standing, walking or trotting, on the electrolytes was also examined. There was a progressive rise in plasma potassium concentration during galloping, with peak values occurring at the end of the exercise bout. In some cases, values above 10 mmol/litre were recorded at the highest workloads. Plasma lactate concentrations peaked during early recovery, with values up to 32 mmol/litre. A high correlation existed between peak potassium and lactate concentrations (venous r = 0.923, and arterial r = 0.989). Following exercise there was a rapid return to baseline plasma potassium concentrations, but by 12 mins recovery there was still an elevated lactate concentration, the extent depending on the intensity of the exercise bout and the recovery mode. There was a small rise in plasma sodium but no significant change in plasma chloride concentrations during exercise. However, when adjusted for the decrease in plasma volume, as determined from total plasma protein concentration, there was a decrease in circulating amounts of both electrolytes.     

Hyperkalaemic periodic paralysis in Australian Quarter Horses

SUMMARY Three Quarter Horse stallions and 5 of their 11 tested progeny were diagnosed as affected with the inherited autosomal dominant defect hyperkalaemic periodic paralysis in Victoria in 1992. The diagnoses were based on the appearance of clinical signs and associated increased plasma potassium concentrations in response to oral potassium loading. All affected horses were descendants of the American Quarter Horse Impressive. Indirect evidence indicates that at least 3 other affected Quarter Horse stallions have stood or are standing at stud in Australia. The clinical details of the affected horses are described and the size of the affected population in Australia is discussed.     

Equine hyperkalemic periodic paralysis: review and implications.

The purpose of this review is to present an up-to-date summary of the signs, diagnosis, treatment, and implications of equine hyperkalemic periodic paralysis. The review encompasses all original articles published between 1986 and early 1993. Hyperkalemic periodic paralysis is the result of a genetic mutation in the skeletal muscle sodium channel gene. It is inherited as an autosomal dominant trait; most affected horses are heterozygotes. The classical signs are muscle fasciculation, spasm, and weakness associated with hyperkalemia. However, these signs are only rarely observed in affected horses. Potential sequelae to attacks are abrasions and involuntary recumbency; these problems are not specific for hyperkalemic periodic paralysis, but they occur more frequently in hyperkalemic periodic paralysis-affected horses. It is also likely that hyperkalemic periodic paralysis results in greater muscle mass. There are suggestions that homozygotes may be more severely affected and show signs of upper respiratory obstruction as foals. The practitioner needs to be aware of the tests for hyperkalemic periodic paralysis, and their limitations, so that he can properly diagnose this condition. The industry has the difficult problem of deciding whether or not testing should be mandatory and the fate of positive horses.     

HYPP: hyperkalemic periodic paralysis in the horse

Hyperkalaemic periodic paralysis(HYPP) is characterized by intermittent episodes of muscular tremor, weakness, and collapse, and is probably caused by abnormal electrolyte transport in the muscle cell membrane. During an episode of HYPP, most animals are severely hyperkalaemic. HYPP is a hereditary disease and occurs only in American Quarter horses or crossbreds. Because these horses are now being imported into the Netherlands, HYPP should be included in the differential diagnosis of horses showing signs of muscle tremor, paresis, or paralysis. The present article reviews the literature on HYPP and describes a case showing typical signs of the disease.     

Growth hormone secretion in relation to plasma lactate and glucose concentrations during a maximal treadmill exercise test in horses

Veterinary Research Communications -     

Effect of ration and exercise on plasma creatine kinase activity and lactate concentration in Thoroughbred horses with recurrent exertional rhabdomyolysis

OBJECTIVE: To determine the effects of 3 rations (low grain, fat, high grain) on plasma creatine kinase (CK) activity and lactate concentration in Thoroughbred horses with recurrent exertional rhabdomyolysis (RER). ANIMALS: 5 Thoroughbreds with RER and 3 healthy Thoroughbreds (control horses). PROCEDURES: Rations were formulated to meet (low-grain and fat rations) or exceed (high-grain ration) daily energy requirements. Each ration was fed to horses in a crossover design for 3 weeks. Horses were exercised on a treadmill Monday through Friday; maximum speed on Monday and Friday was 11 m/s (6% slope), on Tuesday and Thursday was 9 m/s, and on Wednesday was 4.5 m/s. Plasma CK activity and lactate concentration were determined before and after exercise. RESULTS: Horses with RER fed the high-grain ration had significantly greater CK activity and change in CK activity 4 hours after exercise, compared with those fed the low-grain ration. Horses with RER exercised at the trot or canter had significantly greater increases in CK activity, compared with those exercised at the gallop. Plasma lactate concentrations after exercise were similar in control and affected horses. Lactate concentration and CK activity were not correlated in horses with RER. CONCLUSIONS AND CLINICAL RELEVANCE: Rations high in grain and formulated to exceed daily energy requirements may increase episodes of rhabdomyolysis in thoroughbred horses susceptible to RER.     

Familial incidence of hyperkalemic periodic paralysis in quarter horses.

The pedigrees of 17 horses with hyperkalemic paralysis were studied. All were first-, second-, or third-generation offspring of a common sire, 16 were registered Quarter Horses. Analysis indicated that it was unlikely that the concentration of hyperkalemic periodic paralysis in the offspring of this sire was attributable to chance. The familial nature of this condition should help veterinarians diagnostically. It also suggests that it is possible to reduce the incidence of this condition by breeding from non-affected lines of horses and reinforces the need for studies to determine whether the disease is genetic in origin. Although more affected horses were second-generation offspring, the proportion of horses affected was largest in the first generation and decreased progressively with each generation. This is probably because horses in the earlier generations have been observed for longer periods and thus clinical signs are more likely to have been noticed in these horses.     

Hyperkalaemic periodic paralysis in homozygous and heterozygous horses: a co-dominant genetic condition

Historical, clinical and experimental data were collected from 9 horses homozygous for HYPP (H/H). All showed episodes of respiratory stertor, described as a rattling or honking sound, usually within the first week post partum. Five horses had one or more episodes of dysphagia, in 3 horses this was accompanied by drooling and in 3 by weight loss. In comparison, only one of 35 contemporaneous half siblings (of which approximately half would be expected to be of the H/N genotype and half N/N) was observed to have respiratory stertor prior to weaning and none had problems with dysphagia. One mature homozygous stallion was infertile secondary to urospermia. Six homozygous horses died or were subjected to euthanasia; 4 age less than a year, one age 20 months and one age 5 years. The remaining 3 cases were still alive at the end of the study. A comparison of homozygous and heterozygous horses using standardised potassium chloride challenge testing indicated that during attacks homozygotes showed significantly more frequent signs of drooling, prolapse of the third eyelid, respiratory stridor and weakness than heterozygous horses. Homozygotes also had significantly more total abnormalities (including myotonic discharges, high frequency repetitive discharges, and spontaneous activity) on electromyographic examination than heterozygotes. These data imply that HYPP is inherited as a codominant genetic defect, because the homozygotes showed more severe clinical signs of disease than heterozygotes. Homozygous foals would be expected to be produced in 25% of matings in which both parents are heterozygous. Owners and veterinarians should be aware of the risks of this mating.     

Blood lactate disappearance after maximal exercise in trained and detrained horses

The influence of training on blood lactate concentrations during treadmill exercise and a 40-minute inactive recovery period was examined in seven trained and seven detrained thorough-bred horses. Lactate concentrations were measured in venous blood collected at the end of each exercise state, and at intervals for 40 minutes afterwards. Measurements were made of maximum oxygen uptake (V̇O_2max, ml kg⁻¹ min⁻¹), VLA4 (velocity at which blood lactate concentration was 4 mmol litre⁻¹); LA8 (lactate concentration [mmol litre⁻¹] during exercise at 8 m sec⁻¹), peak lactate (highest lactate concentration after exercise), LA40 (lactate concentration 40 minutes after exercise), the time of peak lactate concentration (minutes after exercise) and the rate of disappearance of blood lactate (Rt_d). The trained horses had a significantly lower LA8 (2·1 ± 0·1 vs 6·5 ± 1 mmol litre⁻¹, P<0·01), higher VLA4 (9·8 ± 0·2 vs 5·8 ± 0·6 m sec⁻¹, P<0·01) and higher V̇0_2max (156·3 ± 3·8 vs 107·1 ± 3·9 ml kg⁻¹ min⁻¹, P<0·001). The value of Rt_d and the time of peak lactate concentration were not significantly different.     

Clenbuterol plasma concentrations after repeated oral administration and its effects on cardio-respiratory and blood lactate responses to exercise in healthy Standardbred horses

To evaluate the effects of clenbuterol on cardio-respiratory parameters and blood lactate relation to exercise tolerance, experimental horses performed standardized exercise tests on a high-speed treadmill before and after administration of the drug. Clenbuterol was administered in feed to six healthy Standardbreds at a dose rate of 0.8 micrograms/kg b.wt twice daily for 5.5 days. Each horse was tested twice, without and with a respiratory mask, during two consecutive days. One week elapsed between the baseline tests without drug and the tests with clenbuterol treatment (each horse served as its own control). The results show an unchanged heart rate response to exercise 2 h after the last clenbuterol administration. The blood lactate response and the arterial oxygen tension during exercise did not differ before and after drug treatment. The oxygen uptake as well as pulmonary ventilation relative to the work load performed was essentially unaffected. The arterial pH during exercise was significantly increased (P less than 0.05) following clenbuterol treatment. Plasma levels of clenbuterol were maximal 2 h post-administration with values between 0.45 and 0.75 ng/ml. The plasma half-life of elimination was 10.4 h (+/- 2.25 SD). In conclusion, clenbuterol did not cause any major effects on the cardio-respiratory and blood lactate parameters studied in healthy horses performing submaximal exercise tolerance tests.     

Changes in heart rate, mean arterial pressure, blood biochemistry, plasma glucose, plasma lactate and some plasma enzymes during sufentanil/halothane anaesthesia in horses

Nine horses were each anaesthetised for 40 min using SufentaniVhalothane. No surgery was performed. After premedication (detomidine 5 pgkg bwt iv) induction of anaesthesia was achieved by a combination of guaiphenesinlthiopentone. Anaesthesia was maintained by inhalation of halothane (0.8%) in oxygen. Six horses (Group 1) received 1 pgkg bwt sufentanil followed by a second injection (1 pg/kg bwt) after 20 min. Three horses (Group 2) received 2 pg/kg bwt sufentanil also followed by a second injection (2 pg/kg bwt) after 20 min. Each sufentanil injection produced a slight decrease in mean arterial blood pressure with a gradual return to the initial pressure. Bradycardia was also observed. Sufentanil injection induced apnoea needing artificial ventilation. Arterial blood was sampled for analysis during the anaesthetic procedure. At the end of anaesthesia, 1 h and 24 h after rising, venous blood was sampled to determine concentrations of lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and creatine phosphokinase (CPK). Values obtained were compared with values in blood taken before premedication. Plasma glucose and lactate concentrations just before sufentanil administration, at the end of anaesthesia and 1 h after rising were compared to control values. Plasma glucose concentration increased significantly during anaesthesia but returned to normal values 1 h after rising. All other parameters stayed within physiological ranges. In both groups spontaneous respiration returned 20–25 min after the second sufentanil injection. Recovery was uneventful.