Page 260 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

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VetBooks.ir Chapter 14

Cardiovascular Toxicity

Csaba K. Zoltani

INTRODUCTION cells. LDH-1 . LDH-2 indicates heart attack or injury. The
FABP3 gene encodes an intracellular fatty acid binding
Cardiotoxicity primarily manifests itself by the dysfunc-
protein, a marker for myocardial damage. It is released
tion of the electrophysiology of the heart, consequently
into the plasma after myocardial injury.
altering its mechanical functioning. With the blood unable
This chapter addresses the primary cardiac problems
to supply the required oxygenation to the organs, the
encountered by animals as a result of unsuitable feed or
undesirable effect of hypoxia is present. Contributing fac-
the introduction of poisons into their system by alternate
tors further include oxidative stress and the generation of
means.
reactive oxygen species (ROS) that damage cellular mem-
branes and the energy production within the cell (Kang,
2001). The inception of the electrophysiological dysfunc- PLANT-INDUCED CARDIOTOXICITY
tion in animals is primarily caused by undesirable
ingested plant ingredients, envenomation, or environmen- The primary cause of cardiotoxicity in animals is the inges-
tal toxins (Ramachandran, 2014) including insecticides, tion of plants containing phytochemicals that cause toxic-
fertilizers, herbicides, poisonous insects, vertebrates, ity. Most plants are widely distributed, though possibly
invertebrates, or fungi of the class Basidiomycete. geographically contained, and toxicity depends on various
The ingested poisonous fodder and environmental tox- factors including season, environmental conditions, particu-
ins may stimulate a wide variety of symptoms. In some lar ingredients, and part of the plant accessed.
cases, cardiotoxicity is only ancillary for the initial diag- All plants contain toxic principles that protect them
nosis, but its recognition and subsequent treatment may and deter animals and insects from ingesting them.
be of primary importance for the outcome. While these compounds may be toxic, they are essential
Cardiotoxicity is evidenced by changes in the to the plant for the formation of plant proteins and plant
electrocardiogram (ECG). Initial indicators of cardiac growth. Some grasses, such as Phalaris or Festuca arun-
injury include increase in the amplitude of the T-wave dinacea, are also poisonous. Phalaris species contain
and ST-segment elevation. In addition, biomarkers of gramine, an indole alkaloid, that in sheep causes nervous
cardiac injury give insight into the nature of the injury. system damage. Phalaris toxicity expresses itself as
These include serum levels of the two isoforms of cardiac-sudden death (Cheeke, 1995). Initially cattle,
cardiac troponin T and I, whose levels rise after ische- and to a lesser extent sheep, have their tongue nerves
mia is evident and indicate myocardial necrosis. Also affected causing swallowing paresis disabling the animal
myoglobin, released by injured myocardial cells, is from normal eating.
present. Levels of creatine kinase (CK), CK-MB (MB Gossypol, a reactive polyphenolic pigment of the cot-
designates the isoenzyme found primarily in the ton plant, when ingested, is toxic to the heart. In live-
myocardium), rise after the onset of infarction or even stock, lesions of the heart are observed leading to heart
after tachycardia. LDH-1 (lactate dehydrogenase) failure and sudden death. Pigs are similarly affected.
isoenzyme is primarily found in heart tissue, while Plant extracts containing phenolic compounds have also
LDH-2, LDH-3, LDH-4, and LDH-5 are found in many been implicated for their toxicity to animals.
other tissues. Tissue breakdown or cellular damage The effect of the toxicity varies with the genus ingest-
elevates LDH, the enzyme that catalyzes conversion of ing it. Excellent references and databases on plants exist
lactate to pyruvate and pyruvate to lactate, and its pres- (Kingsbury, 1964; Frohne and Pfander, 2005; Burrows
ence indicates hemolysis, the destruction of red blood and Tyrl, 2006; Panter et al., 2007; FDA, 2008).

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