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Biomedical subjects

J A Reynoldson

Publications and source records attributed to J A Reynoldson.

At least 55 records · Page 3Linked to original sources
PubMed1988

Cortisol concentrations in blood and urine of horses.

A survey of the concentrations of cortisol in blood and urine samples taken from thoroughbred and standardbred horses after racing is presented. Statistical analysis showed the only significant difference between thoroughbred and standardbred horses was a higher cortisol concentration in thoroughbred urine. Urine volume and pH had no significant influence on the urinary cortisol concentration, however 9.5% of the urinary cortisol variation could be explained due to the influence of plasma cortisol concentration. The results of cortisol and ACTH administrations are also shown and compared with the survey results.

Adrenocorticotropic Hormone↗
PubMed1987

Cardiovascular and respiratory effects of the acaricide amitraz.

Amitraz is a formamidine compound used as a topical acaricide mainly in dogs and cattle. In an initial attempt to explain some of its side-effects, the actions of amitraz were studied on the cardiovascular and respiratory systems in thiopentone/methoxyflurane-anaesthetized dogs. In separate experiments, amitraz, at doses of 1, 2 and 5 mg/kg i.v., dissolved in DMSO, increased blood pressure for 1 hour. Heart rate decreased initially then showed a dose-related return towards control values. Tidal volume, respiratory rate and respiratory minute volume all showed initial transient depression. Hyperventilation was a feature after high doses of amitraz. Cumulative doses of amitraz of 0.5, 1, 2, 5 and 10 mg/kg i.v., at intervals of 5 min, increased blood pressure. Heart rate decreased at lower doses but increased slightly after higher doses. Five minutes after injection, cardiac index had returned to control values while total peripheral resistance showed a dose-related increase. The mechanism of action of amitraz in dogs cannot be determined from these results; however, other reports have described an alpha 2-adrenoceptor agonist action of this formamidine compound.

Analysis of Variance↗
PubMed1987

Venoconstriction causes different effects in the hindquarters venous compartment of cats and dogs.

1. A study was made of venoconstrictor mechanisms in the hindquarters region of cats and dogs by the use of autoperfused hindquarter preparations, together with the measurement of vena cava blood flow (VCBF). 2. Noradrenaline, adrenaline and angiotensin II (AII) were all administered intraarterially and their ability to alter perfusion pressure and VCBF was examined. 3. All three drugs increased perfusion pressure in both cats and dogs as a result of increases in arterial resistance. At the same time, noradrenaline and adrenaline increased VCBF in cats, while AII had a variable effect. In contrast, all three drugs decreased VCBF in dogs. 4. These differences in the venoconstrictor responses obtained in cats and dogs may be explained by an action of the drugs at different loci within the venous compartment of the two species.

Angiotensin II↗
PubMed1987

Radioimmunoassay of thromboxane B2 in horse plasma.

A radioimmunoassay for thromboxane B2 (TXB2) in unextracted horse plasma was evaluated. Sensitivity of the assay was 14.0 (SD 5.6) pg ml-1 of plasma. Interassay and intra-assay variation were 21.3 per cent and 4.3 per cent, respectively. The percentage of tracer bound in unextracted plasma in the absence of TXB2 was often higher than that in buffer. Therefore standard curves were obtained using standards diluted in plasma from horses treated with aspirin or in charcoal treated TXB2-free plasma. Standard curves determined in plasma and buffer were parallel. This assay was used to determine the half-life of exogenous TXB2 in horses. The mean value of 20.7 minutes (n = 3) is similar to that determined in other species. Storage of plasma samples at -20 degrees C for four months was found to alter the TXB2 levels in an unpredictable manner. Mean recovery was 102.4 per cent (SD 44.1). Effect of variability in sample collection and handling was assessed, but no consistent source of artifactual generation of TXB2 was found.

Animals↗
PubMed1986

Lack of production of thromboxane A2 by the sheep heart following coronary occlusion.

Blood pressure, heart rate and ECG were monitored continuously and coronary venous blood samples assayed for thromboxane B2. Arterio-coronary venous lactic acid differences were estimated. In anaesthetized sheep, 60 sec occlusions of the left circumflex coronary artery caused hypotension with little change in heart rate. Five minute occlusions produced similar changes accompanied by cardiac arrhythmias and a larger fall in blood pressure. In conscious sheep heart rate rose and blood pressure was maintained. ECG and lactic acid changes indicated severe myocardial ischaemia but not change in thromboxane release was detected. The apparent lack of involvement of thromboxane may reflect a relative inability of sheep platelets to produce this substance or a failure to provide an adequate stimulus for synthesis.

Anesthesia↗
PubMed1986

Myocardial ischaemia following electrical stimulation of the left circumflex coronary artery in sheep: a role for thromboxane A2?

The electrical stimulation model of thrombus formation was tested on rabbit carotid artery and adapted to sheep left circumflex coronary artery (LCCA). LCCA blood flow, mean arterial pressure (MAP), heart rate (HR) and ECG were monitored continuously and arterial and coronary venous blood samples were taken for radioimmunoassay of thromboxane B2. Stimulation of the LCCA mimicked acute myocardial infarction; reduction in LCCA blood flow preceded a fall in MAP and appearance of ECG abnormalities. Thromboxane B2 levels rose by 126% 35 min after stimulation. These findings support the proposal by other authors that thromboxane plays an important role in the pathogenesis of acute myocardial infarction.

Anesthesia↗
PubMed1986

The effects of certain vasodilating prostaglandins on the coronary and hindlimb vascular beds of the conscious sheep.

Vasodilating prostaglandins were injected, in bolus doses, into the lower abdominal aorta or left circumflex coronary artery (LCCA) of conscious sheep. Local blood flow, mean arterial pressure (MAP), heart rate (HR) and ECG were monitored continuously. 6-Keto PGF1 alpha had no effect on either vascular bed in doses up to 100 micrograms. PGE2 was more potent than PGI2 in dilating hindlimb vasculature and PGE2 induced a more persistent hyperaemia whereas PGD2 elicited a biphasic response (constriction-dilation). PGE1, PGE2, PGD2 and PGI2 all produced dose-dependent vasodilation, the order of potency being PGD2 greater than PGI2 greater than PGE1 greater than or equal to PGE2. The effect of PGI2 was more transient and PGE1 and PGD2 caused small but consistent decreases in MAP and HR, respectively.

Animals↗
PubMed1986

The effects of vasoconstricting prostanoids on the coronary and hindlimb vascular beds of the conscious sheep.

Vasoconstricting prostaglandins were injected, in bolus doses, into the lower abdominal aorta on the left circumflex coronary artery (LCCA) of conscious sheep. Local blood flow, mean arterial pressure (MAP), heart rate (HR) and ECG were continuously monitored. Thromboxane B2 had no effect on either vascular bed in doses up to 100 micrograms. PGF2 alpha produced mild vasoconstriction in both vascular beds with no systemic response. The endoperoxide analogues, U-44069 and U-46619, produced complex responses in both vascular beds. Initial vasodilation was followed rapidly by prolonged vasoconstriction. In the coronary circulation, vasoconstriction was temporarily masked by a hyperaemic phase. The U-compounds also affected MAP, possibly as a result of pulmonary and systemic vasoconstriction.

Animals↗
PubMed1986

The cardiac effects of amitraz in the guinea-pig in vivo and in vitro.

Intravenous amitraz caused significant hypotension and bradycardia in pentobarbitone anaesthetized guinea-pigs. Depression of blood pressure reached a plateau with a dose of 10 mg/kg but heart rate continued to fall in a dose-dependent manner, up to a fall of 90 beats per minute after a total of 160 mg/kg/min. Amitraz was then tested on spontaneously beating guinea-pig isolated atria. The maximum bath concentration approximated a blood concentration produced by 5 mg/kg amitraz in the guinea-pig (2.3 X 10(-4) M). Amitraz did not significantly shift the dose-response curve to isoprenaline or acetylcholine but antagonized histamine rate responses competitively in the presence of propranolol (2 X 10(-6) M). Propranolol unmasked a dose-dependent depressant effect of amitraz on atrial rate, an effect abolished with atropine (1 X 10(-5) M). Amitraz increased atrial force of contraction, an effect which was not seen when propranolol was present in the bath solution. Amitraz also depressed atrial rate directly, but this effect was minor in comparison to bradycardia seen in the guinea-pig. It is likely that the cardiovascular depression seen in the guinea-pig following amitraz i.v. is caused by an alteration in autonomic drive rather than a significant direct cardiac effect.

Acetylcholine↗
PubMed1986

Praziquantel adversely affects protoscoleces of Echinococcus granulosus in vitro.

Praziquantel was shown to have adverse effects on protoscoleces of Echinococcus granulosus in vitro. Exposure to one dose of praziquantel at a concentration of 10 micrograms/ml caused protoscoleces to die within 12 to 15 days. Protoscolecidal effects were more marked when cultures were exposed to the drug continuously by the addition of multiple doses. On the basis of these observations, there is a need to reappraise the metacestocidal potential of praziquantel, particularly with regard to the development of new drug regimes employing multiple dose or sustained release schedules. Possible reasons for the reduced susceptibility of protoscoleces and juvenile worms to praziquantel observed in this study are discussed.

Animals↗
PubMed1986

The effect of clonidine on venous haemodynamics in cats and dogs.

Experiments were undertaken to investigate a possible action of clonidine on venous haemodynamics, using cats and dogs with autoperfused hindquarters. This provided an arterial input to the region independent of cardiac output. Venous capacitance in the hindquarters was indicated by blood flow in the abdominal vena cava, as measured by an electromagnetic flow probe around this vessel. It was found that in both cats and dogs, clonidine given intravenously (5 micrograms kg-1 i.v.) or into the cisterna magna (1 microgram kg-1 i.c.m.) reduced mean arterial pressure and heart rate, but did not decrease hindquarter perfusion pressure. With the exception of dogs given i.v. clonidine, this drug caused a decrease in inferior vena cava (IVC) blood flow and this closely paralleled the hypotensive effect. However, when clonidine was given i.v. to dogs, the decrease in IVC blood flow preceded the hypotension. At the doses used, the reduction in IVC blood flow was larger following i.v. than i.c.m. clonidine in both species, and in all cases, it remained below control levels for at least 30 min, in spite of the constant arterial input to the region. In cats, dose-response curves were constructed to noradrenaline and adrenaline given into the perfusion circuit (i.a.) before and after clonidine. Following i.v. and i.c.m. clonidine, there was a selective depression of the venoconstrictor actions of the catecholamines, but no change in the arterial pressor action. Radiographic and latex studies in the dog and cat respectively were performed in order to visualize collateral blood flow that could account for the persistent decreases in IVC blood flow. In both species, intraspinal collateral flows were demonstrated which returned blood to the heart after ligation of the inferior vena cava below the renal veins. However, it was not possible to demonstrate radiographically any changes produced by clonidine in the collateral flow because of technical difficulties. These results suggest that clonidine causes a selective reduction in sympathetic tone to the veins that is mediated at least partly by a central action, as well as an expansion of the collateral venous routes. This, together with the selective impairment of venoconstrictor responses to both noradrenaline and adrenaline, may account for the decrease in cardiac output that is most often reported following clonidine.

Animals↗
PubMed1985

Changes in the synovia after the intra-articular injection of sodium hyaluronate into normal horse joints and after arthrotomy and experimental cartilage damage.

Sodium hyaluronate was injected into normal horse joints and joints that had undergone an arthrotomy and experimental cartilage damage. The elimination half-life for hyaluronic acid in normal joints was found to be approximately 96 h. The injection caused a non-significant increase (42%) in synovial fluid protein concentration and a fall in the intrinsic viscosity of the fluid. In the arthrotomy group the synovial fluid hyaluronic acid concentration fell after surgery but it was unaffected by the injection of sodium hyaluronate. An initial rise in the intrinsic viscosity of the synovial fluid from the arthrotomy group coincided with an increase in protein concentration. However there was no significant difference between the mean intrinsic viscosity or protein concentration in synovia from the control and treated joints at any time after surgery.

Animals↗
PubMed1984

Neuropharmacology of delta-aminolaevulinic acid--I. Effect of acute administration in rodents.

Delta-aminolaevulinic acid (ALA) is suspected of being responsible for the neuropsychiatric symptoms of acute porphyria. The object of this study was to examine the effects of ALA in vivo on a range of behavioural and physiological functions which are known to be affected in the acute porphyric attack. Aminolaevulinic acid was administered by intraperitoneal or subcutaneous injection to mice in doses up to 1000 mg/kg and effects on nociception (hot-plate and abdominal constriction tests), CNS excitability (pentobarbitone sleep-time and pentylenetetrazole-induced seizures), motor co-ordination and grip (rotating rod test) were studied. Rats were given intravenous injections or infusions of ALA of up to 24 mg and changes in blood pressure, heart rate and ED50 for noradrenaline, acetylcholine and isoprenaline examined. No statistically significant effects were noted, using buffered solutions of ALA (pH 7.0-7.4). However, unbuffered solutions of ALA caused significant bradycardia and hypotension. These results do not support the hypothesis that ALA has significant acute neuropharmacological activity in vivo when the blood-brain barrier is intact.

Aminolevulinic Acid↗
PubMed1982

Release of E prostaglandins into the cerebrospinal fluid and its inhibition by melatonin after cervical stimulation in the rabbit.

The release of the E type of prostaglandin (PGE) into the cerebrospinal fluid of mature female rabbits was studied using an indwelling catheter in the cisterna magna. The cervix of the rabbit was stimulated 5 min after the central injection of either vehicle or melatonin solution. PGE was measured by RIA, and in unstimulated animals, the level of PGE remained steady at about 4 ng/ml. After stimulation of the cervix of control rabbits, PGE levels rose by 31 ng/ml 40--70 min after the initiation of stimulation in those animals which subsequently ovulated. PGE levels rose by only 15 ng/ml 70--115 min after stimulation in those rabbits which did not ovulate. In the melatonin-treated rabbits, PGE levels remained close to those in unstimulated controls, and ovulation did not occur. Thus, stimulation of the cervix of the rabbit produces a rise in PGE levels in cerebrospinal fluid. This endogenous PGE surge may, in turn, cause the release of LHRH and LH and induce ovulation if levels exceed a critical threshold. A weaker stimulus leads to only a smaller surge of PGE, insufficient to cause ovulation. Melatonin blocked the stimulation-induced rise in cerebrospinal fluid PGE levels and ovulation, and appears to exert its antigonadotropic activity in the rabbit by the inhibition of central PGE synthesis.

Animals↗
PubMed1981

Absorption of the toxins of Lantana camara L. from the digestive system of sheep.

When lantana was given into different regions of the alimentary tract, absorption sufficient to cause intoxication occurred from the stomachs, small intestine and large intestine, but absorption from the small intestine was quantitatively the most important. However, it was shown that the passage of ingesta into the small intestine decreased markedly a few hours after the toxin was given and it is suggested that absorption from all areas of the gastrointestinal tract is important for the progression of the disease. When bile was diverted away from the small intestine, animals were still intoxicated by lantana. This indicates that bile is not important for absorption of lantana toxins. Other experiments indicated that the lantana toxins are transported to the liver mainly in the portal blood.

Animals↗
PubMed1979

Effect of 6-hydroxydopamine on blood pressure and heart rate responses to intracisternal clonidine in conscious rabbits.

The effects of intracisternal injection (i.c.i.) of clonidine (1 microgram kg-1) on blood pressure and heart rate were studied in conscious rabbits with an implanted catheter in the cisterna magna. Each animal was studied under control conditions and 7 days after i.c.i. of 6-hydroxydopamine (6-OHDA) (1 microgram kg-1; n = 10) or ascorbic acid vehicle (n = 6). In the control experiments blood pressure and heart rate began to fall 1--2 min after i.c.i. of clonidine, with maximum falls at 10--20 min averaging 18 +/- 2 mmHg and 45 +/- 8 b/min and almost complete recovery by 90 min. After vehicle pretreatment neither response was significantly altered. After 6-OHDA the early component of the bradycardia was abolished and only a late fall in heart rate developed 30 min after i.c.i. clonidine. The magnitude of the hypotension was unaffected but the onset was slightly delayed, probably owing to the abolition of the bradycardia. The dose of 6-OHDA reduced spinal cord catecholamines to about 20% of the level observed after vehicle. Central catecholaminergic pathways are thus important in the early predominantly vagal component of the clonidine induced bradycardia, but play little role in the hypotensive response.

Animals↗
PubMed1978

Cardiovascular and behavioral effects of intracisternal 6-hydroxydopamine in the rabbit.

Acute effects of 6-hydroxydopamine (6-OHDA, 400--900 microgram kg-1 intracisternally, i.c.i.) consisted of bradycardia and hypertension, maximal 2--3 h after injection and preceded after some doses by a phase of hypotension. This pattern was obtained in completely conscious rabbits and after propanidid and sodium pentobarbitone anesthesia. After 600 microgram kg-1 i.c.i. 6-OHDA the peak rise in blood pressure (25 +/- 3.8 mm Hg) was due to a rise in peripheral resistance involving particularly renal and intestinal beds. Suprapontine mechanisms contributed to both hypertension and bradycardia. Giving pontine rabbits 6-OHDA elicited a short-latency fall in blood pressure, resembling the hypotensive phase in intact animals. Chronic effects 7 days after 600 microgram kg-1 included a rapid loss of 10% of body weight associated with reduction in food and water intake. To avoid secondary circulatory effects the rabbits were artificially fed, halving the weight loss. At 7 days blood pressure had fallen by 7.4 +/- 2.3 mm Hg probably owing to this residual weight loss. From experiments involving administration of phenotolamine and clonidine in intact rabbits and the responses of pontine animals it is likely that both descending and ascending catecholaminergic pathways have inhibitory effects on blood pressure, though some of the pathways may also be excitatory. Absence of specific chronic circulatory changes may be due to compensation through parallel pathways involving other transmitters.

Anesthesia↗