Page 266 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Cardiovascular Toxicity Chapter | 14 233

VetBooks.ir which is common in southern Arizona, contain oxalates heart’s conduction system and favoring cardiac arrhyth-
21
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that may induce Ca
mia (Mordukhovich et al., 2009; el Bahri and Ben
deficiency. Oxalates bind Ca
in
Romdane, 1991).
the gastrointestinal tract, e.g., in horses, and lead to a
change in the Ca 21 level of the blood along with a subse- Large doses of arsenic lower blood pressure and slow
21
quent effect on the muscular system. The Ca to oxalate down the pulse rate. In frogs the heart stops in diastole
ratio in the diet greater than 0.5:1 is considered safe. due to the paralysis of the motor ganglia. Since it is quick
The formation of calcium oxalates also leads to acting, cardiovascular collapse is to be expected. The
hypocalcemia, which interferes with electrical activity of lethal dose for arsenic trioxide for horses is 10 45 g/kg
the heart, as it inhibits the Ca 21 pump active in the gener- b.w. and LD 50 of sodium arsenite in goats is 125 mg/kg b.w.
ation of the action potential, resulting in the relaxation of (EFSA, 2005). Treatment is symptomatic and supportive.
the muscles. The reduced activity of the heart can
culminate in cardiac arrest. The LD 50 of oxalic acid is IONOPHORES (ANTIBIOTICS)
375 mg/kg b.w. for rats.
Only limited data on cardiac manifestation of oxalosis Ionophores are carboxylic polyether antibiotics that are
in animals are available. Ingestion of sodium oxalate given as feed additives to cattle. Ionophores alter the flow
(VonBurg, 1994) results in weak and irregular pulse, of cations across cell membranes and reduce Gram-
hypotension, necrosis of the myocardium, and eventually positive bacteria responsible for bloat. Since ionophores
cardiovascular collapse. have a narrow range of safety, feed mixing errors facilitate
Recommended treatment includes oral dosing with poisoning. In horses, this leads to cardiac muscle damage;
calcium lactate followed by an emetic, i.e., binding the in cattle, this leads to both skeletal and cardiac muscle
unabsorbed oxalates to calcium and then removing them. damage.
The cardiac signature of the poisoning in horses
manifests itself by prolongation of atrial and ventricular
NITRATE-CONTAINING PLANTS
depolarization and repolarization (Hall, 2006). Also,
Sorghum, corn, wheat, Johnson grass, pigweed, and alfalfa depression of the ST segment, absence of the P-wave,
are a few of the plants that accumulate nitrate. The level of ventricular tachycardia, AV-block and atrial fibrillation
accumulation depends on a number of variables including are noted. Cardiac lesions and heart failure occur. In
the type of soil, environmental conditions, such as fertiliza- cattle, QT and QRS prolongation, first degree heart
tion and climatic conditions, soil moisture, and tempera- block, and T-wave amplitude increases are typical.
ture. Plants with more than 0.4% nitrate dry weight or Cardiac lesions and heart failure are also possible.
ingestion of as little as 0.05% of the animal’s weight of Analogous effects have been noted in sheep. The LD 50
such plants may be lethal to livestock (Yong et al., 1990). of monensin is 2 3 mg/kg b.w. in horses; 20 34 mg/
In the gastrointestinal tract, nitrates are converted to kg b.w. in cattle, and 10 12 mg/kg b.w in sheep
nitrite, which leads to the formation of methemoglobin (Doonan et al., 1989).
that cannot carry oxygen to tissues. Animals thus suffo- Beside the growth-promoting function of ionophores
cate. Clinical symptoms include rapid breathing through in ruminants, it is used as a coccidiostat in poultry.
the mouth in livestock and an elevated heart rate. With a Cardiac effects of infested poultry include reduced lipid
methemoglobin concentration greater than 35%, cardiac levels, reduced heart weight, low heart rates, and low
dysrhythmia is observed. Tissue changes are few, but blood pressure. Monensin has a narrow therapeutic win-
hemorrhages particularly on the heart are noted. Acutely dow, and intoxication causes muscle necrosis and myo-
poisoned animals are usually treated with methylene blue globinuria. Targets include cardiac muscles. It causes
(10 mg/kg, i.v). In view of the vasodilation caused by inotropism, tachycardia, cardiomyopathy, and cardiac fail-
nitrate, vasoconstrictor drugs may also be used. ure. Horses are especially vulnerable. There is no antidote
available for monensin poisoning.

METAL-INDUCED CARDIAC TOXICITY
FERTILIZERS
Arsenic
Accidental ingestion of fertilizer can cause serious poi-
Although considerable native vegetation contains arsenic, soning in the affected animals (Villar et al., 2003).
the sources of intoxication usually are sprays or ingestion Predominantly, though not exclusively, nitrates cause the
of feed contaminated by arsenic (Selby et al., 1977). damage. Rabbits exposed to ammonium sulfate fertilizer
Arsenic in drinking water also poses an additional risk of suffer cardiac arrest (Sato et al., 1999). In another
cardiovascular effect including hypertension, prolongation case with fertilizer containing nitrogen, phosphoric
of the QT portion of the ECG, indicating a disorder of the acid, and potassium, the rabbits suffered hyperkalemia,