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Biomedical subjects

J Hrdlicka

Publications and source records attributed to J Hrdlicka.

29 records · Page 2Linked to original sources
PubMed1978

The toxicity of myoporum tetrandrum (Boobialla) and myoporaceous furanoid essential oils for ruminants.

Boobialla (Myoporum tetrandrum)leaf contains from 0.25 to 0.5% wet weight of furanoid sesquiterpene essential oils of which the main component is dehydrongaione. The plant was toxic when dosed to calves at equivalent dose rates of oils of from 50 to 134 mg/kg, causing mainly extensive haemorrhagic centrillobular necrosis; and to sheep at equivalent dose rates of oil of from 55 to 66 mg/kg, causing either centrilobular or periportal liver lesions with or without acute pulmonary oedema. An essential oil mixture of similar composition derived from Myoporum deserti produced similar syndromes. In addition, treatment of calves with phenobarbitone or Melaleuca linariifolia essential oils prior to dosing with the Myoporum oils caused periportal hepatic necrosis rather than the centrilobular lesion which occurred usually in this species. The liver lesions found in the experimental calves and sheep respectively, were thus similar to those reported in suspected field cases of Boobialla poisoning in cattle and goats in Western Australia. The liver injury that may be expected in intoxication of livestock by myoporaceous plants containing this type of essential oils can thus be either periportal, midzonal or centrilobular necrosis, depending, probably, on the nutritional regime of the animal immediately prior to consumption of the toxic plant.

Animals↗
PubMed1977

Comparison of analgesia by intravenous butorphanol and meperidine in patients with post-operative pain.

Intravenous doses of butorphanol tartrate (0.5 mg, 1.0 mg and 2.0 mg) and meperidine hydrochloride (20 mg and 40 mg) were compared under controlled conditions employing a double blind study design. Informed consent was obtained from all post-operative patients suffering from moderate to severe pain who participated in this study. Approximately 25 patients were included in each group. The data from 125 patients were subjected to statistical analysis. The results indicated that butorphanol is approximately 40 to 50 times more potent than meperidine. In addition, at most of the time intervals, there were no statistically significant differences between the responses to butorphanol 0.5 mg and 1 mg and meperidine 20 mg and 40 mg; but the response to butorphanol 2 mg was significantly (p less than 0.05) better than the low dose of each agent. The low doses of butorphanol (0.5 mg) and meperidine (20 mg) appear to have an effective duration of action of less than two hours. The larger doses (butorphanol 1.0 mg and 2.0 mg and meperidine 40 mg) appeared to produce a two- to four-hour duration of action. The largest butorphanol dose (2.0 mg) appeared to produce the longest duration of action. A comparison of the test groups with respect to the incidence and type of side effects showed that butorphanol 2.0 mg produced a greater incidence of drowsiness (39 per cent). The overall incidence of drowsiness for patients receiving either the 0.5 mg or 1.0 mg dose of butorphanol was 12 per cent, as compared with an 8 per cent overall incidence in the meperidine group. The incidence of other side effects was relatively low in all test groups. No significant differences were noted among the groups with regard to the onset (usually less than or equal to 30 minutes post-therapy) or the duration (usually less than or equal to 2 hours) of side effects. Butorphanol appears to be a safe and effective analgesic for the relief of moderate to severe post-operative pain.

Adult↗
PubMed1977

The oral toxicity for sheep of triterpene acids isolated from Lantana camara.

Toxic Lantana camara taxa growing in Queensland all contain the triterpene acids lantadene A, reduced lantadene A and lantadene B. These when dosed as pure compounds orally to sheep were similarly toxic at 65 to 75, 42 to 80 and 200 to 300 mg/kg body weight respectively, causing jaundice, photosensitisation, kidney and liver lesions typical of natural and experimental lantana poisoning. Because of its comparative toxicity and abundance lantadene A is the most significant toxic principle in the plant. Reduced lantadene A because of its low concentration in the leaves (5% of lantadene A) and lantadene B because of its significantly lower toxicity are thus unlikely to be of much importance in the poisoning of ruminants following consumption of the plant. In addition, the structural features of both lantadene A and B molecules given to sheep by the oral route do not conform to the chemical structures previously reported to be required for liver damaging action of the verbenaceous triterpenes administered to rabbits by the intraperitoneal route.

Animals↗
PubMed1976

The hepatotoxicity of O,O-diethyl, O-phenyl phosphorothionate (SV1) for the rat.

The parathion analogue O, O-diethyl, O-phenyl phosphorothionate (SV1) is hepatotoxic when given in large intraperitoneal doses (400 mg/kg body weight) to male rats that have been treated previously with phenobarbitone. The lesion produced at 24 h after dosing is a periacinar hydropic degeneration which appears identical to that caused by carbon disulphide (CS2) in similarly pretreated rats. Both lesions are characterized by a marked depression in hepatic microsomal cytochrome P-450 levels, no change in the concentrations of Na+, K+ and Ca++ in liver water, in contrast to the periacinar necrogenic lesion caused by tccl4 in which Na+ and Ca++ levels markedly increase while that of K+ decreases. The similarity of the SV1 and CS2 induced liver changes, the fact that both chemicals undergo a similar oxidative desulphuration in the liver microsomes and that prior induction of the latter enzymes is necessary in order to produce the injury suggest a similar mechanism for both lesions. A reactive form of sulphur released from the metabolism of CS2 and phosphorothionates in the liver may become covalently bound to constituents of the endoplasmic reticulum of the liver cell and in this way initiate the toxic liver changes. Drugs and chemicals which contain P=S or C=S bonds and which undergo oxidative desulphuration in the liver could thus be similarly hepatotoxic.

Animals↗