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Biomedical subjects

O V Sjaastad

Publications and source records attributed to O V Sjaastad.

14 recordsLinked to original sources
PubMed1992

Etiology of acetonemia in Norwegian cattle. 1. Effect of ketogenic silage, season, energy level, and genetic factors.

Plasma acetoacetate concentration in the 1st mo of lactation and its relation to BW change, milk yield, DMI, and BW postpartum were studied in 361 first lactation cows during 6 yr. The cows were fed concentrate at 6 and 3 kg/d. Calvings took place from August to December. Single observations for all cows were fitted by a multitrait animal model that accounted for all genetic relationships. Heritability for acetoacetate was .11 with a genetic correlation of .87 for milk yield, -.65 for weight change, and -.13 for BW postpartum. Acetoacetate was higher at 3 kg/d of concentrate than at 6 kg/d, and calving after 3 to 4 mo of indoor feeding was related to higher acetoacetate than was calving shortly after the pasture season. Acetoacetate was related to weight loss postpartum, but at a different degree in different years. In some years, compounds of the silage caused strongly elevated plasma concentrations of acetoacetate after feeding. Experiments were performed to compare hay with silages of different qualities. Rumen concentration of different amines 3 h postfeeding was taken as an index of the amine load of the cow. The concentration of several amines in rumen fluid were high after feeding ketogenic silage.

Acetoacetates↗
PubMed1990

Adenine nucleotides, serotonin, and aggregation properties of platelets of blue foxes (Alopex lagopus) with the Chediak-Higashi syndrome.

Bleeding times, concentrations of serotonin in whole blood, and concentrations of adenine nucleotides as well as aggregation properties of platelets were examined in 18 blue foxes with Chediak-Higashi-like syndrome (CHS) and 16 controls. A claw of each ketamine-sedated fox was cut until bleeding started and the bleeding time was recorded as the time from the first to the last drop. The bleeding time was greatly increased in CHS foxes. Platelet counts of CHS foxes were normal, but aggregation induced by adenosine diphosphate (ADP), serotonin, collagen, and arachidonate was impaired. Adrenaline and serotonin was impaired. Adrenaline and serotonin potentiated the aggregatory effect of ADP on control as well as on CHS platelets. The mean concentration of ADP in CHS platelets was about one-third that in controls, whereas adenosine triphosphate (ATP) was approximately one-half that in controls. Serotonin could not, in most cases, be detected in blood of CHS foxes. These findings suggest that the prolonged bleeding time in the CHS foxes is, at least partly, due to a storage pool deficiency. The drastically reduced, and in some cases absent, aggregation of CHS platelets in response to arachidonate suggests that defective arachidonate metabolism contributes to the impaired hemostasis.

Adenine Nucleotides↗
PubMed1990

Plasma progesterone in reindeer in relation to ovariectomy and hysterectomy.

Four semi-domesticated reindeer were ovariectomized and 3 both ovariectomized and hysterectomized, 30-70 days before expected parturition. Anaesthesia with etorphine/propyonylphenthiazine was followed by an increase in the plasma concentration of progesterone of peripheral blood. The concentration of progesterone returned to pre-anaesthetic values before ovariectomy. Ovariectomy did not result in any substantial change in the plasma progesterone concentration within an observation period of 35-120 min. Hysterectomy was followed by a marked decrease in peripheral plasma progesterone within 60 min. The progesterone concentration in ovarian venous blood was slightly higher than the jugular venous blood in 1 animal and 150 and 400 times higher in the 2 other animals examined. Thus, despite lack of marked changes of progesterone in jugular venous blood upon ovariectomy, it is concluded that the ovaries are a major production site of progesterone in pregnant reindeer. The progesterone in uterine venous blood was close to that in the jugular vein in 1 animal, and slightly higher in 2 others. This observation, and the maintenance of pregnancy in spite of ovariectomy in 2 out of 4 animals, point to the foeto-placental unit as an additional source of progesterone production.

Animals↗
PubMed1977

Urinary histamine excretion in migraine and cluster headache. Further observations.

Urinary excretion of histamine, as well as histaminuria following intravenous L-histidine loading, were studied in patients with so-called vascular headache. It was found that urinary excretion of histamine was increased on one or more occasions in 7 of 22 patients with cluster headache. The excretion was significantly higher on attack days than on attack free days. With migraine, increased excretion was found in 5 of 31 patients on days of an attack, whereas the corresponding figure for headache free days was 7 of 24 patients. Three patients showed increased histamine excretion during, as well as between, attacks. The excretion on attack days was not significantly different from that on attack free days. In cluster headache patients, L-histdine administration on attack days did not indicate that an increased histamine formation took place under such circumstances. The underlying mechanism behind the increased histamine output with cluster headache may be increased formation or liberation or altered catabolism. Histamine is more likely to be a consequence than the cause of an attack of cluster headache.

Adolescent↗
PubMed1977

Histamine metabolism in cluster headache and migraine. Catabolism of 14C histamine.

Various parameters of histamine metabolism were studied in patients with migraine, cluster headache and chronic paroxysmal hemicrania. These included urinary excretion of radioactivity and of 14C histamine and its metabolites, exhaled 14CO2 and fecal radioactivity after oral as well as subcutaneous administration of radioactive histamine. No marked deviation from the normal was found except in one patient with the cluster headache variant, chronic paroxysmal hemicrania, in whom an aberration in 14C histamine degradation seemed to be present. Only minute quantities of the 14C histamine metabolite C14 imidazoleacetic acid riboside seemed to be formed during a period with severe paroxysms. During a symptom-free period no deviation from normal was observed. The most likely explanation for this finding seems to be a defect in the conversion of imidazoleacetic acid to its riboside. This defect may possibly explain the increased urinary excretion of histamine in this particular patient. The relationship of this metabolic aberration to the production of headache still remains dubious for various reasons.

Biotransformation↗
PubMed1977

Metabolism of histamine in myotonic dystrophy a dual pattern of inactivation of intestinal histamine.

The catabolism of orally and subcutaneously administered 14C histamine was studied in myotonic dystrophy patients. No definite abnormalities were observed as for subcutaneously administered histamine. The catabolism of orally administered histamine followed two distinct patterns: In patients with a relatively low endogenous urinary conjugated histamine excretion at the time of testing, small quantities of radioactivity were excreted in the stools (mean 0.25 per cent), whereas the quantity of exhaled 14CO2 was in the control range (mean 14.4 per cent), and the exhalation curve diphasic as in controls. In patients with a relatively high urinary conjugated histamine excretion, the catabolic pattern differed: There was a relatively high faecal excretion of radioactivity (mean 20.1 per cent), whereas the exhalation of 14CO2 was markedly reduced (i.e. mean 0.5 per cent, versus a mean control level of 8.9 per cent). Diphasicity of the exhalation curve was not present in these patients. It has previously been demonstrated that a patient with myotonic dystrophy may shift between being a normal and a high conjugated histamine excretor. It is thus possible that all patients with myotonic dystrophy may pass through phases with abnormal catabolism of intestinal histamine.

Administration, Oral↗
PubMed1976

Peripheral plasma levels of oestradiol-17 beta and progesterone in the bitch during the oestrous cycle, in normal pregnancy and after dexamethasone treatment.

Plasma oestradiol-17 beta concentrations in Labradors increased during pro-oestrus to an average maximal concentration of of 79-7 +/- 10-9 (S.D.) pg/ml, and then fell rapidly. In 6/7 bitches the peak occurred within 1 day of oestrus. No consistent changes in plasma oestradiol levels were observed during pregnancy and at parturition and the values were similar to those in late anoestrus. Plasma progesterone levels did not increase markedly during pro-oestrus. At oestrus, progesterone values rose and maximal concentrations, which varied from about 20 to about 55 ng/ml, were reached within a few days of the oestradiol peak. Plasma progesterone decreased in late pregnancy and in one of the three bitches studied in detail low or undetectable levels were reached 10 days before parturition. In the other two bitches an abrupt decrease in progesterone occurred just before parturition. Dexamethasone treatment (2 X 5 mg daily for 10 days) from Day 30 of pregnancy resulted in intrauterine death and resorption of the fetuses in the two bitches studied. Treatment from about Day 45 resulted in the birth of dead fetuses at Days 55 and 59 of pregnancy. The changes in plasma oestradiol levels were very small. No changes in plasma progesterone levels were seen when dexamethasone was given in late pregnancy, but an accelerated decline occurred after treatment in mid-pregnancy.

Animals↗
PubMed1974

Absorption and catabolism of histamine in sheep.

1. The fate of dietary histamine in sheep has been studied. When 200 mg histamine diphosphate was administered into a rumen with normal contents the average time taken for the biological activity to disappear from the rumen was about 4 hr. In sheep starved for 60 hr the activity disappeared much more slowly.2. When 0.9% NaCl solution was substituted for the normal rumen contents and the rumen was isolated in situ under anaesthesia, the disappearance of histamine was scarcely detectable. About 1% of the radioactivity introduced into such rumen preparations as [(14)C]histamine was recovered in the urine during a 6 hr period.3. When both [(14)C]histamine and 200 mg unlabelled histamine diphosphate were administered into the rumen, between 4 and 15% of the radioactivity and 2 and 11% of the biological activity reached the duodenum.4. When jejunal loops isolated between two pairs of re-entrant cannulas were perfused with 0.9% NaCl solution containing histamine a considerable fraction of the histamine was absorbed from the loops.5. When [(14)C]histamine and 200 mg histamine diphosphate were administered into the rumen an average of 9% of the radioactivity appeared in the urine. When histamine was given into the abomasum the corresponding figure in a single experiment was 25%.6. Between 11 and 34% of the radioactivity administered into the rumen as [(14)C]histamine was exhaled as (14)CO(2). Most of the (14)CO(2) seemed to stem from metabolism of [(14)C]histamine in the ruminoreticulum whereas the contribution of the intestines to (14)CO(2) was very small.7. When [(3)H]histamine was administered into the rumen most of the radioactivity in the urine a few days after administration was in the form of tritiated water. The formation of (3)H(2)O is probably a result of histamine metabolism in the fore-stomach, analogous to the formation of (14)CO(2).

Abomasum↗
PubMedDate not supplied

Effect of iron treatment on erythrocyte parameters in postnatal anemia of the pig.

The development of postnatal anemia and the preventive and curative effect of iron supplementation were examined in 34 piglets from three litters of Norwegian Landrace pigs. A prostaglandin analog was given on day 111 or 112 of pregnancy, and the piglets were removed by caesarean section. Seventeen piglets were given 180 mg iron as colloidal ferridextran subcutaneously at birth (0 = day group); the remaining 17 were given the same amount on day 13 (13-day group). The piglets had access to a milk substitute from day 1 to day 7 and pelleted food for piglets after day 13. From about 4 weeks of age the piglets ate considerable amounts of pellets. The red blood cell count (RBC) and hemoglobin concentration (Hb) at birth were 3.2 +/- 0.4 (SD) x 10(12)/L and 80.4 +/- 8.1 x 10(12) g/L, respectively. In both groups Hb, RBC, mean corpuscular volume (MCV), and particularly packed cell volume (PCV) decreased markedly the first day after birth. In the 13-day group there was a further decrease until treatment with iron on day 13. Injection with iron on day 13 led to a rapid increase in the above mentioned parameters, with statistically significant increases for Hb, PCV, and MCV four days after treatment. The calculated mass of hemoglobin was fairly constant until treatment in the 13-day group. In the group given iron at birth the data obtained indicate that the amount of iron given is insufficient to sustain a production of normal-sized erythrocytes with a normal mean corpuscular hemoglobin concentration for more than approximately 21 days. Furthermore, the present study also indicates that MCV is a sensitive indicator of iron availability in piglets.

Anemia↗