Hyperkalemic Periodic Paralysis (HYPP) is a genetic disorder affecting the skeletal muscles of horses, characterized by episodes of muscle weakness or paralysis. It is caused by a mutation in the gene responsible for encoding a sodium channel in muscle cells, which leads to abnormal muscle cell membrane excitability. This condition is predominantly observed in certain lines of Quarter Horses and related breeds. Clinical signs of HYPP can range from mild muscle twitching to severe paralysis, and episodes can be triggered by factors such as stress or dietary changes. This page compiles peer-reviewed research studies and scholarly articles that explore the genetic basis, pathophysiology, clinical presentation, and management strategies for Hyperkalemic Periodic Paralysis in horses.
Quarter horses (QH), a prominent athletic breed in Brazil, are affected by muscular genetic disorders such as myosin-heavy chain myopathy (MYHM), polysaccharide storage myopathy (PSSM1), hyperkalemic periodic paralysis (HyPP), and malignant hyperthermia (MH). Bull-catching (vaquejada), primarily involving QH, is a significant equestrian sport in Brazil. Since the allele frequencies (AF) of MYHM, PSSM1, HyPP, and MH in vaquejada QH remain unknown, this study evaluated the AF in 129 QH vaquejada athletes, specifically from the Brazilian Northeast. These variants were exclusively observed in hete...
Aleman M, Scalco R, Malvick J, Grahn RA, True A, Bellone RR.Deleterious genetic variants are an important cause of skeletal muscle disease. Immunohistochemical evaluation of muscle biopsies is standard for the diagnosis of muscle disorders. The prevalence of alleles causing hyperkalemic periodic paralysis (HYPP), malignant hyperthermia (MH), polysaccharide storage myopathy 1 (PSSM1), glycogen branching enzyme deficiency (GBED), myotonia congenita (MC), and myosin heavy chain myopathy (MYHM) in horses with muscle disease is unknown. Archived slides processed for immunohistochemical analysis from 296 horses with muscle disease were reviewed blinded and c...
Ryan A, Gurney M, Steinbacher R.A 10-year-old 466 kg mustang gelding presented to an equine referral hospital for surgical repair of nasal, frontal and lacrimal bone fractures from an unknown trauma. Surgical repair was performed under general anaesthesia, including a right-sided maxillary regional anaesthetic block with mepivacaine hydrochloride. Progressive hyperkalaemia was documented perianaesthetically (T-3 mins; 134 mins after induction; potassium 6.4 mmol/L (ref 3.5-5.1 mmol/L). Perianaesthetic bradycardia was attributed to alpha -2 agonist infusion administration, and other characteristic ECG changes (flattened ...
Choi YH, Penedo MC, Daftari P, Velez IC, Hinrichs K.Preimplantation genetic diagnosis has great potential in the horse, but information on evaluation of equine embryo biopsy samples is limited. Blastocysts were biopsied using a Piezo drill and methods for whole-genome amplification (WGA) investigated. Results for 33 genetic loci were then compared between biopsy samples from in vitro-produced (IVP) and in vivo-recovered (VIV) blastocysts. Under the experimental conditions described, WGA using the Qiagen Repli-g Midi kit was more accurate than that using the Illustra Genomiphi V2 kit (98.2% vs 25.8%, respectively). Using WGA with the Qiagen kit,...
Pang DS, Panizzi L, Paterson JM.A 3-year-old, 400 kg, gelding Quarter Horse was presented for investigation of epistaxis. Methods: The horse was bright, alert and responsive with rectal temperature, heart rate and respiration rate within normal limits. Results: During a second general anaesthetic for surgical treatment of guttural pouch mycosis by balloon-tipped catheter occlusion of the right major palatine artery and ligation of the right external carotid artery, signs consistent with hyperkalaemic periodic paralysis (HYPP) were exhibited. These included concurrent hyperkalaemia, hypercapnoea, sinus tachycardia, and muscle...
Mählmann Ch, Steiger A.Persons involved in equine breeding, namely veterinarians, horse breeders and breeding association judges, often lack of an apropriate consciousness about the relevance of heritability or supposed heritability of common horses diseases, which might play a distinctive role in the aetiology of numerous of these diseases. Executing animal welfare rights in equine breeding, the major concern should focus on an objective evaluation of pain, suffering and damages caused by different hereditary diseases. The basis of assessment for hygienic breeding has to be defi ned according to the actual animal w...
Finno CJ, Spier SJ, Valberg SJ.The recent development of equine genome maps by the equine genome community and the complete sequencing of the horse genome performed at the Broad Institute have accelerated the pace of genetic discovery. This review focuses on genetic diseases in the horse for which a mutation is currently known, including hyperkalemic periodic paralysis, severe combined immunodeficiency, overo lethal white syndrome, junctional epidermolysis bullosa, glycogen branching enzyme deficiency, malignant hyperthermia, hereditary equine regional dermal asthenia, and polysaccharide storage myopathy. Emphasis is placed...
Aleman M.Muscle disorders are a common cause of disability in horses. For many years, clinical manifestations such as muscle pain, exercise intolerance, weakness, and stiffness were believed to be caused by a single syndrome. However, in the past years a broad spectrum of muscle disorders have been recognized including glycogen and polysaccharide storage myopathies, malignant hyperthermia, mitochondrial myopathy, hyperkalemic periodic paralysis and others. For some, a specific mutation has been identified. Recognition of the myopathic clinical phenotype and thorough clinical, electrodiagnostic, and his...
O'Rourke BA, Dennis JA, Healy PJ.Improvements to restriction fragment length polymorphism (RFLP)-based genotyping assays currently used for detection of mutations responsible for bovine ferrochelatase and myophosphorylase deficiencies, and equine hyperkalemic periodic paralysis (HYPP) are described. Reports of sporadic inhibition of restriction enzyme activity suggest a critical factor in RFLP-based genotyping assays should be assurance that restriction enzymes perform to specification with every sample. The RFLP genotyping assays that use either a mismatched recognition sequence in one or both of the oligonucleotides, or inc...
Sosa Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, Rose RJ.The second day of a 3-day event is the most physically demanding of the 3 days. If this is performed under hot and humid environmental conditions, detrimental effects on cardiovascular and thermoregulatory function and, therefore, on exercise capacity, may occur due to exercise-induced dehydration. We hypothesised that the administration of fluid equivalent to 6% of the horse's bodyweight prior to a simulated second day of a 3-day event would increase plasma volume and limit increases in core temperature. Seven Standardbred geldings underwent a training protocol prior to the study. A standardi...
Duggan VE, MacAllister CG, Davis MS.An 18-month-old Quarter Horse filly was evaluated because of dorsal displacement of the soft palate associated with epiglottic dysfunction that caused exercise intolerance and an abnormal respiratory noise. The abnormality of the epiglottis was corrected by use of a sedative dose of xylazine hydrochloride. There was no familial predisposition to hyperkalemic periodic paralysis, which may cause similar laryngopharyngeal signs, and the horse did not respond to administration of acetazolamide. There was no known history of trauma that could have caused neuritis, which has also been suggested as a...
Alberts MK, Clarke CR, MacAllister CG, Homer LM.To determine the pharmacokinetics of acetazolamide administered IV and orally to horses. Methods: 6 clinically normal adult horses. Methods: Horses received 2 doses of acetazolamide (4 mg/kg of body weight, IV; 8 mg/kg, PO), and blood samples were collected at regular intervals before and after administration. Samples were assayed for acetazolamide concentration by high-performance liquid chromatography, and concentration-time data were analyzed. Results: After IV administration of acetazolamide, data analysis revealed a median mean residence time of 1.71 +/- 0.90 hours and median total body c...
Kollias-Baker C.Therapeutic medications play a crucial role in the successful therapy of many musculoskeletal diseases that occur in horses. For example, appropriate antibiotic therapy is extremely important in the treatment of diseases caused by infections with microorganisms such as botulism, tetanus, osteomyelitis, and muscle abscesses. In addition, numerous prescription medications and nutritional supplements are available for the treatment of osteoarthritis in horses. Many of these agents currently on the market fall into a new class of drugs called SADMO agents. Unfortunately, the efficacy and mechanism...
Naylor JM, Nickel DD, Trimino G, Card C, Lightfoot K, Adams G.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 matu...
Sloet van Oldruitenborgh-Oosterbaan MM.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 HYP...
Yudkowsky ML, Beech J, Fletcher JE.In equine hyperkalemic periodic paralysis (HyperPP), there is evidence suggesting that the primary defect in the sodium channel is associated with a secondary alteration in triacylglycerol-associated fatty acid metabolism (TAFAM) in skeletal muscle. Furthermore, TAFAM may be involved in the therapeutic action of phenytoin. The effects of phenytoin treatment on the transcript levels of three key proteins in TAFAM, hormone sensitive lipase (HSL), carnitine palmitoyltransferase (CPT), and fatty acid binding protein (FABP), were examined. These transcripts were quantitated by competitive reverse t...
Sah RL, Tsushima RG, Backx PH.We examined the ability of local anesthetics to correct altered inactivation properties of rat skeletal muscle Na+ channels containing the equine hyperkalemic periodic paralysis (eqHPP) mutation when expressed in Xenopus oocytes. Increased time constants of current decay in eqHPP channels compared with wild-type channels were restored by 1 mM benzocaine but were not altered by lidocaine or mexiletine. Inactivation curves, which were determined by measuring the dependence of the relative peak current amplitude after depolarization to -10 mV on conditioning prepulse voltages, could be shifted in...
Maxson-Sage A, Parente EJ, Beech J, Lindborg S, May LL, Teleis DC.To determine the effect of exercise on arterial blood gas tensions and upper airway and cardiac function in clinically normal Quarter Horses and horses heterozygous and homozygous for hyperkalemic periodic paralysis (HYPP). ANIMALS AND PROCEDURE: 5 clinically normal Quarter Horses, and 5 heterozygous and 2 homozygous HYPP-affected horses were examined before, during, and after exercise on a high-speed treadmill. Arterial blood gas tensions, ECG, and echocardiogram were obtained prior to exercise. Upper airway endoscopy, collection of arterial blood samples, and continuous electrocardiography w...
Toribio RE, Bain FT, Mrad DR, Messer NT, Sellers RS, Hinchcliff KW.Three weak, recumbent neonatal foals with skin lesions, including a thin wooly coat, were born to mares being treated for equine protozoal myeloencephalitis. Mares received sulfadiazine or sulfamethoxazole-trimethoprim, pyrimethamine, folic acid, and vitamin E orally. Foals were anemic, leukopenic, azotemic, hyponatremic, and hyperkalemic. Serum folate concentrations in the 3 foals and 2 mares were lower than those reported in the literature for clinically normal brood mares. Treatment was unsuccessful. For each foal, necropsy revealed lobulated kidneys with thin cortices and a pale medulla, a...
Naylor JM.Hyperkalemic periodic paralysis is an autosomal codominant genetic disease of horses who are descendants of the quarter horse sire Impressive. It produces a muscular phenotype that has been selected by show judges, which has resulted in the rapid dissemination of this disease. Clinical attacks are characterized by muscle fasciculation and spasm, and they respond to treatments for the concurrent hyperkalemia.
The Journal of physiologyDecember 1, 1996
Volume 497 ( Pt 2), Issue Pt 2 349-364 doi: 10.1113/jphysiol.1996.sp021773
Hanna WJ, Tsushima RG, Sah R, McCutcheon LJ, Marban E, Backx PH.1. The Na+ channel mutation associated with equine hyperkalaemic periodic paralysis (HPP) affects a highly conserved phenylalanine residue in an unexplored region of the alpha-subunit. This mutation was introduced into the rat skeletal muscle Na+ channel gene at the corresponding location (i.e. F1412L) for functional expression and characterization in Xenopus oocytes. 2. In comparison with wild-type (WT) channels, equine HPP channels showed clear evidence for disruption of inactivation: increased time-to-peak current, slowed rates of whole-cell current decay, significant increases in sustained...
Carr EA, Spier SJ, Kortz GD, Hoffman EP.Evaluate histories, clinical signs, and laboratory data of 69 horses homozygous by DNA testing for hyperkalemic periodic paralysis (HPP). Methods: Cohort study. Methods: 69 of 189 horses testing homozygous for HPP between October 1992 and November 1994. Methods: Questionnaires addressing signalment, training regimes, medical history, and current status of affected horses were sent to owners, trainers, or attending veterinarians. Data from completed questionnaires were tabulated and evaluated, using descriptive statistics. Results: Sixty-nine (37%) of 189 questionnaires were completed and retur...
Bowling AT, Byrns G, Spier S.The pedigree origin of a base pair substitution in the horse muscle sodium channel gene that confers susceptibility to the muscle disease hyperkalemic periodic paralysis (HYPP) was investigated with a set of 978 Quarter Horses. The horses were chosen at random, based on a collection of blood samples taken between 1989 and 1991 to meet parentage testing requirements, primarily but not exclusively from breeding stallions. The frequency of Quarter Horses positive for the base pair substitution, all heterozygotes, was 4.4%, which corresponds to an allelic frequency of 0.02. All horses positive for...
Guglick MA, MacAllister CG, Breazile JE.An 18-month-old Quarter Horse gelding was examined because of weight loss and dysphagia of 1 month's duration. Clinical signs included lethargy, dehydration, ptyalism, and probable aspiration pneumonia. Severe dyspnea and cyanosis were evident after mild exercise. Endoscopy revealed laryngospasm and pharyngospasm. Because clinical signs and endoscopic findings were suggestive of hyperkalemic periodic paralysis (HPP), acetazolamide treatment was instituted. Marked improvement was observed within 48 hours. The horse was determined to be homozygous for HPP. It is likely that this horse's dysphagi...
Bailey JE, Pablo L, Hubbell JA.A 7-month-old Quarter Horse filly was admitted for surgical repair of a right olecranon fracture. Anesthesia was achieved with xylazine hydrochloride, guaifenesin, ketamine hydrochloride, and halothane. Two and a half hours after induction of anesthesia, myotonia, muscle fasciculations, and sweating, concurrent with high serum potassium concentration and associated electrocardiographic changes consistent with hyperkalemic periodic paralysis, were observed. Treatment included intermittent positive-pressure ventilation, changing intravenous administration of fluids from lactated Ringer's solutio...
Rudolph JA, Spier SJ, Byrns G, Rojas CV, Bernoco D, Hoffman EP.We recently reported on a linkage study within a Quarter Horse lineage segregating hyperkalaemic periodic paralysis (HYPP), an autosomal dominant condition showing potassium-induced attacks of skeletal muscle paralysis. HYPP co-segregated with the equine adult skeletal muscle sodium channel alpha subunit gene, the same gene that causes human HYPP. We now describe the Phe to Leu mutation in transmembrane domain IVS3 which courses the horse disease. This represents the first application of molecular genetics to an important horse disease, and the data will provide an opportunity for control or e...
Cannon SC, Hayward LJ, Beech J, Brown RH.1. Equine hyperkalemic periodic paralysis (E-HPP) is a dominantly inherited disorder of muscle that causes recurrent episodes of stiffness (myotonia) and weakness in association with elevated serum K+. Affected horses carry a mutant allele of the skeletal muscle isoform of the Na channel alpha-subunit. To understand how this mutation may cause the disease phenotype, the functional defect in Na channel behavior was defined physiologically by recording unitary currents from cell-attached patches on normal and affected equine myotubes. 2. The presence of the mutation was confirmed in our cell lin...
Aleman M.Muscle disorders are a common cause of disability in horses. For many years, clinical manifestations such as muscle pain, exercise intolerance, weakness, and stiffness were believed to be caused by a single syndrome. However, in the past years a broad spectrum of muscle disorders have been recognized including glycogen and polysaccharide storage myopathies, malignant hyperthermia, mitochondrial myopathy, hyperkalemic periodic paralysis and others. For some, a specific mutation has been identified. Recognition of the myopathic clinical phenotype and thorough clinical, electrodiagnostic, and his...
Rudolph JA, Spier SJ, Byrns G, Hoffman EP.A genetic disease observed in certain Quarter horses is hyperkalaemic periodic paralysis (HYPP). This disease causes attacks of paralysis which can be induced by ingestion of potassium. Recent studies have shown that HYPP in humans is due to single base changes within the adult skeletal muscle sodium channel gene. A large Quarter horse pedigree segregating dominant HYPP was studied to determine if mutations of the sodium channel gene are similarly responsible for HYPP in horses. We used cross-species, PCR-mediated, cDNA cloning and sequencing of the horse adult skeletal muscle sodium channel a...
Spier SJ, Carlson GP, Holliday TA, Cardinet GH, Pickar JG.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 con...
Steiss JE, Naylor JM.A three year old Quarter Horse stallion was presented with a one year history of episodes of generalized muscle tremors and stiffness, and spasm of the muscles of facial expression, lasting 10-15 minutes. Between attacks, the horse was either normal or had a localized muscle tremor in the flank region. Episodes appeared unrelated to exercise. The major abnormal findings included 1) a rise in plasma potassium from a resting level of 4.4 to 7.9 mmol/L during an attack and 2) electromyographic findings of generalized increased insertion activity and myotonic discharges. The horse was treated with...
Zhou J, Spier SJ, Beech J, Hoffman EP.It is often suggested that polygenic or environmental factors are responsible for clinical variability between patients with identical mutations. However, most dominant diseases are caused by a change-of-function alteration in the mutant allele's protein product. All patients are heterozygous and presumably express both mutant and normal proteins from the corresponding genes. Thus, a possible molecular mechanism for clinical variability could be the difference in relative levels of mutant vs. normal mRNA in different patients with the same mutation. To investigate this hypothesis, it is necess...
Alberts MK, Clarke CR, MacAllister CG, Homer LM.To determine the pharmacokinetics of acetazolamide administered IV and orally to horses. Methods: 6 clinically normal adult horses. Methods: Horses received 2 doses of acetazolamide (4 mg/kg of body weight, IV; 8 mg/kg, PO), and blood samples were collected at regular intervals before and after administration. Samples were assayed for acetazolamide concentration by high-performance liquid chromatography, and concentration-time data were analyzed. Results: After IV administration of acetazolamide, data analysis revealed a median mean residence time of 1.71 +/- 0.90 hours and median total body c...
Sah RL, Tsushima RG, Backx PH.We examined the ability of local anesthetics to correct altered inactivation properties of rat skeletal muscle Na+ channels containing the equine hyperkalemic periodic paralysis (eqHPP) mutation when expressed in Xenopus oocytes. Increased time constants of current decay in eqHPP channels compared with wild-type channels were restored by 1 mM benzocaine but were not altered by lidocaine or mexiletine. Inactivation curves, which were determined by measuring the dependence of the relative peak current amplitude after depolarization to -10 mV on conditioning prepulse voltages, could be shifted in...
Naylor JM, Robinson JA, Bertone J.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 ...
Naylor JM.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 hor...
Pickar JG, Spier SJ, Snyder JR, Carlsen RC.A recently described disorder in certain registered Quarter horses bears many clinical similarities to the muscle disease identified as hyperkalemic periodic paralysis (HPP) in humans. Pathological changes in membrane permeability or Na(+)-K+ pump activity have been proposed to produce the muscle depolarization and inexcitability that characterize the condition in humans. Biopsies of external intercostal muscle from normal and affected horses were used to determine whether alterations in either permeability and/or pump activity could be linked to the pathology in horses. Affected horse muscle ...
Glazier DB, Littledike ET, Evans RD.In 11 crossbred ponies, hyperkalemia was induced by acute intracardiac infusion of a 0.4M solution of potassium chloride. The ECG changes noticed can be assigned to 4 stages: (1) a widening and a lowering of amplitude followed by inversion and final disappearance of the P wave; (2) an increase in the amplitude of the T wave; (3) an increase in the QRS interval, with some irregularity in the ventricular rate; and (4) periods of cardiac arrest that became terminal or were followed by ventricular fibrillation. At plasma potassium values of greater than 7.5 mM/L, the T-wave amplitude and duration ...
Pickar JG, Spier SJ, Harrold D, Carlsen RC.Ouabain, a cardiac glycoside, binds to the Na(+)-K(+)-adenosine triphosphatase (Na+ pump) and prevents active transport of Na+ and K+ across cell membranes. We used [3H]ouabain to quantify the number and affinity of Na+ pumps in skeletal muscle from Quarter Horses with the muscular disorder hyperkalemic periodic paralysis (HYPP). [3H]Ouabain-binding properties of gluteal muscle from clinically normal and affected horses were used to determine whether altered Na+ pump number or affinity could contribute to the pathologic features of muscle in affected horses. Foals and adult horses with HYPP we...
Naylor JM.Hyperkalemic periodic paralysis is an autosomal codominant genetic disease of horses who are descendants of the quarter horse sire Impressive. It produces a muscular phenotype that has been selected by show judges, which has resulted in the rapid dissemination of this disease. Clinical attacks are characterized by muscle fasciculation and spasm, and they respond to treatments for the concurrent hyperkalemia.
Naylor JM.Thirty offspring of a Quarter Horse sire, affected by hyperkalemic periodic paralysis (HPP), were examined electromyographically. On the basis of the detection of or lack of spontaneous activity with high frequency myotonic or pseudomyotonic discharges, the horses were diagnosed as being affected (14 horses) or unaffected (16 horses) with HPP. The show performance of these horses was evaluated for the first 3 to 9 years of their life by use of American Quarter Horse Association records. Horses affected with HPP performed significantly (P < 0.01) better in halter classes than did unaffected ...
Choi YH, Penedo MC, Daftari P, Velez IC, Hinrichs K.Preimplantation genetic diagnosis has great potential in the horse, but information on evaluation of equine embryo biopsy samples is limited. Blastocysts were biopsied using a Piezo drill and methods for whole-genome amplification (WGA) investigated. Results for 33 genetic loci were then compared between biopsy samples from in vitro-produced (IVP) and in vivo-recovered (VIV) blastocysts. Under the experimental conditions described, WGA using the Qiagen Repli-g Midi kit was more accurate than that using the Illustra Genomiphi V2 kit (98.2% vs 25.8%, respectively). Using WGA with the Qiagen kit,...
Ryan A, Gurney M, Steinbacher R.A 10-year-old 466 kg mustang gelding presented to an equine referral hospital for surgical repair of nasal, frontal and lacrimal bone fractures from an unknown trauma. Surgical repair was performed under general anaesthesia, including a right-sided maxillary regional anaesthetic block with mepivacaine hydrochloride. Progressive hyperkalaemia was documented perianaesthetically (T-3 mins; 134 mins after induction; potassium 6.4 mmol/L (ref 3.5-5.1 mmol/L). Perianaesthetic bradycardia was attributed to alpha -2 agonist infusion administration, and other characteristic ECG changes (flattened ...
Bowling AT, Byrns G, Spier S.The pedigree origin of a base pair substitution in the horse muscle sodium channel gene that confers susceptibility to the muscle disease hyperkalemic periodic paralysis (HYPP) was investigated with a set of 978 Quarter Horses. The horses were chosen at random, based on a collection of blood samples taken between 1989 and 1991 to meet parentage testing requirements, primarily but not exclusively from breeding stallions. The frequency of Quarter Horses positive for the base pair substitution, all heterozygotes, was 4.4%, which corresponds to an allelic frequency of 0.02. All horses positive for...
Epstein V.Hyperkalaemia affected the equine myocardium. The minimum plasma potassium concentration required to induce electrocardiographic changes was 6.2 mmol/litre and severe cardiotoxic effects were observed at levels of 8.0 to 10.1 mmol/litre in this experimental situation. The most consistent sign of hyperkalaemia was broadening and flattening of the P wave, which was generally associated with a change in T waves in the chest lead from negative to positive. The more pronounced the hyperkalaemia, the less pronounced the P wave and the more peaked positive the T wave. Severe hyperkalaemia was associa...
Robinson JA, Naylor JM, Crichlow EC.The use of electromyography (EMG) as a diagnostic aid for equine hyperkalemic periodic paresis (EHPP) was investigated in seven affected and seven control horses. Affected horses were confirmed positive for EHPP either by elevated serum potassium concentration with clinical signs of myotonia, or by inducing hyperkalemia and clinical signs using oral potassium chloride challenge. All horses were asymptomatic at the time EMG was performed, using bipolar fine wire needle electrodes. The myopotentials were recorded on magnetic tape and displayed on paper charts for analysis. Insertional and restin...
Sosa Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, Rose RJ.The second day of a 3-day event is the most physically demanding of the 3 days. If this is performed under hot and humid environmental conditions, detrimental effects on cardiovascular and thermoregulatory function and, therefore, on exercise capacity, may occur due to exercise-induced dehydration. We hypothesised that the administration of fluid equivalent to 6% of the horse's bodyweight prior to a simulated second day of a 3-day event would increase plasma volume and limit increases in core temperature. Seven Standardbred geldings underwent a training protocol prior to the study. A standardi...
The Journal of physiologyDecember 1, 1996
Volume 497 ( Pt 2), Issue Pt 2 349-364 doi: 10.1113/jphysiol.1996.sp021773
Hanna WJ, Tsushima RG, Sah R, McCutcheon LJ, Marban E, Backx PH.1. The Na+ channel mutation associated with equine hyperkalaemic periodic paralysis (HPP) affects a highly conserved phenylalanine residue in an unexplored region of the alpha-subunit. This mutation was introduced into the rat skeletal muscle Na+ channel gene at the corresponding location (i.e. F1412L) for functional expression and characterization in Xenopus oocytes. 2. In comparison with wild-type (WT) channels, equine HPP channels showed clear evidence for disruption of inactivation: increased time-to-peak current, slowed rates of whole-cell current decay, significant increases in sustained...
Spier SJ, Carlson GP, Harrold D, Bowling A, Byrns G, Bernoco D.Four Quarter Horses (1 stallion, 3 mares) with hyperkalemic periodic paralysis were mated to unaffected horses to determine the genetic basis of the disease. The affected stallion was bred to 11 unaffected mares (4 Quarter Horses, 1 Arabian, 2 Standardbreds, and 4 Thoroughbreds). The 3 affected mares were bred to an unaffected Quarter Horse stallion. Of the 15 offspring obtained from these matings, 9 were affected with hyperkalemic periodic paralysis, and 6 were unaffected, consistent with an autosomal dominant mode of inheritance. Diagnosis was established by results of oral administration of...
Traub-Dargatz JL, Ingram JT, Stashak TS, Kiper ML, Tarr S, Child G, MacAllister CG.Four Quarter Horse foals ranging in age from 6 days to 2 months were determined to have upper airway stridor secondary to polymyopathy suspected to be hyperkalemic periodic paralysis. Electromyography revealed spontaneous muscle activity in all muscles examined. Electromyographic findings were similar in the dams of 3 foals (No. 1, 3 and 4). Hyperkalemia was found in foals 1 and 4. Endoscopically, the upper airway stridor in foals 1 and 3 was confirmed to be attributable to laryngeal and pharyngeal collapse or spasm. Foals 1, 2, and 3 were treated with acetazolamide. Foal 4 was not treated, at...
Datt SC, Usenik EA.Physical signs and blood changes were studied in horses with artificially produced obstructions of the duodenum and the small colon and simulated volvulus of the ileum. Horses with obstruction of the duodenum had the most violent physical signs and the shortest survival time. Blood changes were an initial rise in pH followed by acidosis, hyperkalemia and a decrease in HCO3 minus, Na+ and C1 minus. Obstruction of the small colon resulted in mild physical signs. The blood parameters recorded were normal. Simulated volvulus resulted in continuous colic. Blood changes were acidosis and hyperkalemi...
