Salivation

One of the earliest cattle problems involved widespread poisoning of cattle by arsenic at the turn of the century. Abnormal intake of arsenic results in severe colic (salivation, thirst, vomiting), diarrhea, bloody feces, and a garliclike odor on the breath cirrhosis of the liver and spleen as well as reproductive effects may be noted. Arsenic trioxide in the feed must be approximately 10 mg/kg body weight for these effects to occur. 

Pharmacology. Lycorine was first examined by Morishima wl found it relatively non-toxic to mammals. Given per os or subcutaneous, to the dog or cat, it causes, in small doses, salivation and in large dos vomiting and diarrhoea. It has no special effect on the blood pressure death seems to be due to a generalised collapse. Post mortem —hyper m and ecchymoses in the stomach, intestine, pulmonary pleura and end... 

Saline. /. salt works, saline, saltern. Salinenwasser, n. saline water, salinisch, a. saline, sahsch, a. Petrog.) salic. salivieren, v.t. salivate. 

Speichel-fluss, to. flow of sahva salivation, -fliissigkeit, /. sahva. -kasten, to. sahva chamber (as in a blowpipe) moisture cham ber. -mittel, n. sialagog. -saft, to. sahva. -stoflf, TO. ptyalin. 

Vagal effects, salivation/A blood pressure, dry mouth/4- ocular accommodation Vagal effects, salivation adrenergic/A blood pressure/facilitates D1 stim Hyperreactivity/facilitates a-activation... 

The act of vomiting is a complex process accompanied by several events apart from activation of the motor nerves and various voluntary muscles involved in the increase of intragastric pressure and evacuation of the stomach contents. Vomiting is preceded by a deep inspiration, closure of the glottis and raising of the soft palate to prevent vomitus entering the trachea and nasopharynx, respectively. There is also increased heart rate, pallor, salivation, sweating and lacrimation. 

DIARRHEA. When these dragp are used orally they occasionally result in excessive salivation, abdominal cramping, flatus, and sometimes diarrhea The patient is informed that these reactions will continue until tolerance develops, usually within a few weeks. Until tolerance develops, the nurse ensures that proper facilities, such as a bedside commode, bedpan, or bathroom, are readily available. The patient is encouraged to ambulate to assist the passing of flatus. If needed, a rectal tube may be used to assist in the passing of flatus. The nurse keeps a record of the fluid intake and output and tlie number, consistency, and frequency of stools if diarrhea is present. The primary health care provider is informed if diarrhea is excessive because this may be an indication of toxicity. 

Local irritation and headache may occur at tlie beginning of therapy. The patient is instructed to notify the primary health care provider if abdominal cramping, diarrhea, or excessive salivation occurs. 

Lichtman et al. 2001 Tzavaraet al. 2000). A dog model of precipitated cannabinoid withdrawal, which includes increased salivation, vomiting, diarrhea, restless behavior, and trembling, has also been described (Lichtman et al. 1998). 

Neurological effects related to cholinesterase depression occurred in seven children acutely exposed to methyl parathion by inhalation as well as orally and dermally (Dean et al. 1984). The children were admitted to a local hospital with signs and symptoms of lethargy, increased salivation, increased respiratory secretions, and miosis. Two of the children were in respiratory arrest. Two children died within several days of each other. All of the children had depressed plasma and erythrocyte cholinesterase levels (Table 3-2). These effects are similar to those occurring in methyl parathion intoxication by other routes (see Sections 3.2.2.4 and 3.2.3.4). Three adults exposed in the same incident had normal plasma (apart from one female) and red blood cell cholinesterase, and urinary levels of 4-nitrophenol (0.46-12.7 ppm) as high as some of the ill children. 

Male rats exposed to 264 mg/m of methyl parathion by inhalation had 59% (range 53-61%) inhibition of blood (a combination of erythrocyte and plasma) cholinesterase 1 hour after exposure (EPA 1978e). These animals had typical cholinergic signs of toxicity salivation, exophthalmos, laerimation, spontaneous defecation and urination, and muscle fasciculation. Values for controls were not provided. Death was not correlated to the degree of eholinesterase inhibition in whole blood. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

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