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Biomedical subjects

H Karppanen

Publications and source records attributed to H Karppanen.

At least 73 records · Page 4Linked to original sources
PubMed1982

Analeptic effect of centrally administered histamine H2-receptor agonist dimaprit but not impromidine in urethane-anesthetized rats.

Intracerebroventricularly administered dimaprit decreased the depth of urethane anaesthesia. Ventilatory stimulation, positive corneal reflex and increased susceptibility to pain were observed. Furthermore, dimaprit decreased the lethal effect of large doses of urethane. The analeptic property of dimaprit was not shared by the potent H2-receptor agonist, impromidine, Histamine increased ventilatory tidal volume but no other stimulatory effects were observed. These findings suggest that the analeptic effects of dimaprit were not mediated by H2-receptors. Among the analeptic effects of dimaprit, only the protection against urethane toxicity was antagonized by metiamide. However, this phenomenon appeared to be due to the nonspecific interaction between the three bradypnoeic drugs metiamide, dimaprit and urethane. The histamine-induced increase in ventilatory tidal volume was not antagonized by diphenhydramine or metiamide, suggesting the existence of a novel histaminergic mechanism in the central nervous system.

Anesthesia↗
PubMed1982

Control of circulation by cerebral catecholaminergic and histaminergic mechanisms.

Catecholamines are formed, released and metabolized in the cerebral regions known to regulate the cardiovascular system. The release of catecholamines in these brain areas is associated with changes in cardiovascular function. Injections of exogenous catecholamines into certain brain regions induce cardiovascular changes and mimic the effects of the release of endogenous catecholamines in the same regions. In addition, drugs with selective effects on cerebral catecholamine functions also induce cardiovascular changes. Changes in cerebral catecholamines have also been found in arterial hypertension. Taken together, these observations provide strong evidence that cerebral catecholaminergic mechanisms have a crucial role in both the normal and pathological control of circulation. Cerebral catecholaminergic mechanisms also mediate, at least in part, the therapeutic effects of clonidine, alpha-methyldopa and some other antihypertensive drugs. Recent findings suggest that histaminergic mechanisms in the brain may also be important in the control of circulation and in the mediation of drug effects. Since the cerebral mono-aminergic systems are necessary for the physiological control of circulation, it is likely that the cerebral catecholaminergic and possibly histaminergic pathways are also involved in the mediation of the effects of psychological stress factors on the cardiovascular system.

Blood Circulation↗
PubMed1982

Cardiovascular and ventilatory effects of taurine and homotaurine in anaesthetized rats.

The cardiovascular and ventilatory effects of intravenous (i.v.) or intracerebroventricular (i.c.v.) injections of the aminosulphonic acids, taurine and homotaurine, were studied in urethane-anaesthetized rats. Taurine induced dose-dependent falls in blood pressure, heart rate and ventilatory tidal volume on i.c.v. but not on i.v. administration. Homotaurine induced dose-dependent hypotension and bradycardia when given i.v. and i.c.v. It was, however, more effective when injected i.c.v., and the decrease in ventilatory tidal volume occurred after i.c.v. administration of homotaurine only. Pretreatment of the rats with reserpine attenuated both the hypotensive and bradycardic responses to taurine and homotaurine. Atenolol and atropine both partly inhibited, and in combination totally abolished, the bradycardic effects of taurine and homotaurine without changing the hypotensive responses to these compounds. The ventilatory responses were not significantly changed by any of the pretreatments. The results suggest that the central cardiovascular effects of taurine and homotaurine are mediated both by a decrease in sympathetic tone and an increase in the parasympathetic tone.

Animals↗
PubMed1981

A community-based intervention study on the feasibility and effects of the reduction of salt intake in North Karelia, Finland.

A community-based programme to reduce salt consumption to lower general blood pressure levels has been started in North Karelia, a county eastern Finland with high hypertension and CVD rates. The programme is based on the previous activity in the community to control CVD risk factors (the North Karelia Project). Previously, however, salt reduction was not included among the objectives. The aim of the study is to evaluate the feasibility and effects of this new community programme to reduce salt intake. The study period is from spring 1979 to spring 1982. At the outset and at the end cross-sectional random population samples, ages 14 to 65, are examined both in North Karelia and a matched reference community. The surveys include among other measurements 24-hour urine collection (for Na, K and creatinine excretion) and blood pressure. The effect evaluation is concerned whether the programme reduced the general salt intake and whether this was associated with reduction in blood pressure levels among the population. Principles and methods of intervention are presented. Preliminary results from the baseline survey confirmed the high salt intake of the population: the mean 24-hour urinary Na excretion was 215-218 mmol among men and 171-173 mmol among women. The respective K excretion values were 89-91 mmol and 72-72 mmol, and Na/K ratios 2.5-2.6 and 2.4-2.5.

Adolescent↗
PubMed1981

Epidemiological studies on the relationship between magnesium intake and cardiovascular diseases.

Data are reviewed which suggest that dietary intake of magnesium may be lower than needed in the industrialized nations in the world. This low dietary intake of Mg appears to be related to the high incidence of ischemic heart disease (IHD) in these nations. Dietary supplementation of individuals in these industrialized nations with Mg is recommended to prevent risk of IHD and other cardiovascular diseases.

Cardiovascular Diseases↗
PubMed1980

Influence of analgesic antipyretics on the central cardiovascular effects of clonidine in rats.

The centrally acting antihypertensive drug clonidine has been found to stimulate the synthesis of PGF2 alpha in the brain. Centrally administered PGF2 alpha, in turn, induces rises of blood pressure and heart rate. We therefore studied the influence of inhibitors of prostaglandin (PG) synthesis on the cardiovascular effects of clonidine in urethane-anaesthetised rats. Pretreatment with indomethacin or paracetamol (100 micrograms/rat into the fourth cerebral ventricle) antagonised the central hypotensive effect of clonidine (0.125-16.0 micrograms/rat into the fourth cerebral ventricle). The bradycardic effect of centrally administered clonidine was, however, enhanced by pretreatment with paracetamol but not influenced by indomethacin pretreatment. Sodium meclofenamate (100 micrograms/rat into the fourth cerebral ventricle) did not significantly affect the clonidine-induced changes in blood pressure and heart rate. These results suggest that the clonidine-induced hypotension on one hand and bradycardia on the other hand may be mediated by partly different mechanisms. An interference of the formation of PGF2 alpha with the cardiovascular effects of clonidine cannot be completely excluded since paracetamol pretreatment potentiated the bradycardic effect of clonidine. However, inhibitors of PG synthesis did not enhance but antagonised the hypotensive effect of clonidine. Therefore it is likely that the synthesis of PGF2 alpha does not interfere with the hypotensive effect of clonidine. Moreover, the antagonism of the hypotensive effect by inhibitors of PG synthesis suggests that some hypotensive metabolite of arachidonic acid in the brain could be involved in the central hypotensive effect of clonidine.

Acetaminophen↗
PubMed1980

Metabolic effects of a low-magnesium diet in pigs.

1. Pigs were fed on semi-purified food. The magnesium content of the experimental diet was 1.0 and that of the control diet 1.9 g/kg. 2. In the low-Mg group serum triglycerides and blood lactate values were increased and base excess and standard bicarbonate values were decreased, indicating metabolic acidosis. 3. A significant positive dependence was found between blood pH and serum Mg:Ca value as well as between blood pH and serum Mg, and also between body temperature and blood lactate values in the low-Mg group. None of these dependences was significant in the control group with magesium acetate supplementation in the food. 4. No specific histopathological changes were found in heart, liver or kidney of the experimental animals. 5. The results indicate that an increase in serum triglycerides does not need to depend on the amount of quality of food fat. 6. The present study shows that, in pigs, a low-Mg diet may cause metabolic disturbances in instances with the food Mg content is distinctly higher than the normal values recommended by the (UK) Agricultural Research Council (1966) and (US) National Research Council (1968).

Animals↗
PubMed1980

Sodium and potassium excretion in a sample of normotensive and hypertensive persons in eastern Finland.

A 24-hour urine collection was carried out during a cardiovascular survey in eastern Finland. The study population comprised 148 hypertensive subjects in a random sample of the middle-aged population and 86 normotensive controls. The mean sodium excretion was 197 mmol/24h in both normotensive and hypertensive men, 179 mmol/24h in normotensive women, and 174 mmol/24h in hypertensive women. There were no significant differences in potassium excretion rate or in sodium: potassium molar ratio between the normotensive and the hypertensive among either men or women. There was no statistically significant correlation between blood pressure level and sodium or potassium excretion or sodium: potassium molar ratio. One in four of the subjects reported that they usually added salt to their food before tasting it. The results of this study show that the average level of salt intake in a Finnish population is high, and so is the sodium: potassium molar ratio. Although there was no correlation between sodium excretion and blood pressure levels, it is known that in this population the average blood pressure level is high and cardiovascular disease extremely frequent.

Adult↗
PubMed1979

Central cardiovascular and thermal effects of prostaglandin F2 alpha in rats.

Administration of PGF2 ALPHA (0.2--6.4 micrograms) into the lateral cerebral ventricle (i.c.v.) induced dose-dependent increases in blood pressure, heart rate and body temperature in urethane-anaesthetised rats, but had no effect on these parameters when the same dose range was administered intravenously. Peripheral pretreatment with sodium meclofenamate (50 mg/kg s.c.) shifted all the dose-response curves for PGF2 alpha (i.c.v.) to the left, but indomethacin (50 mg/kg s.c.) did not significantly affect those changes. Central pretreatment with sodium meclofenamate or indomethacin (1.25 mg per rat i.c.v.) failed to modify significantly the effects of centrally administered PGF2 alpha. The results support previous suggestions that PGF2 alpha may participate in the central control of the cardiovascular and thermoregulatory systems, and also suggest that there may be differences in the sites and/or modes of action between sodium meclofenamate and indomethacin.

Animals↗
PubMed1979

The effect of centrally administered TRH on blood pressure, heart rate and ventilation in rat.

Different doses (3, 16, 80, 400 and 2 000 ng per rat) of TRH or alternatively saline were infused into the lateral ventricle of urethane-anaesthetized rats and blood pressure, heart rate, respiration rate and tidal volume were recorded. A dose of 3 ng TRH caused a significant elevation of blood pressure and heart rate, whereas 16 ng was needed for respiration rate to be elevated. There was no change in respiratory minute volume during the experiment. We conclude that TRH has profound physiological effects and that TRH, given centrally, is a potent hypertensive, chronotropic and tachypnoeic agent.

Animals↗
PubMed1978

Effects of intravenous isoxsuprine and ritodrine, with and without concomitant dexamethasone, on fetoplacental and pituitary hormones and cyclic adenosine monophosphate during late pregnancy.

Beta sympathomimetic drugs are used to inhibit preterm labor and glucocorticoids to accelerate fetal pulmonary maturation. A study was designed to investigate the hormonal effects of intravenous infusion of isoxsuprine 150 to 200 mcg. per minute or ritodrine 100 to 150 mcg. per minute in a series of 28 women at 28 to 40 weeks' gestation, with and without concomitant dexamethasone therapy. Serial serum samples taken before and during the six hours of infusion were assayed for cyclic adenosine-3,5-monophosphate (AMP), estradiol, estriol, progesterone, human placental lactogen (hPL), thyrotropin (TSH), follicle-stimulating hormone (FSH), and human growth hormone (gGH). Ritodrine was more potent than isoxsuprine in increasing the circulating levels of cyclic AMP. The levels of placental steroid hormones decreased slightly, as did the ratio of progesterone to estradiol. Human placental lactogen and pituitary hormones showed no consistent changes. Simultaneous administration of dexamethasone did not modify these results.

Adult↗
PubMed1978

Effects of ritodrine and isoxsuprine with and without dexamethasone during late pregnancy.

beta-Adrenergic agents are used to inhibit preterm labor and glucocorticoids to accelerate fetal pulmonary maturation. A study was designed to investigate the metabolic effects of intravenous infusion of ritodrine (150 to 100 microgram/min) or isoxsuprine (200 to 150 microgram/min) in a series of 28 patients with gestations of 28 to 40 weeks, with and without concomitant dexamethasone therapy. Ritodrine was more potent than isoxsuprine in increasing the circulating levels of cyclic AMP, glucose, insulin, and triglycerides. The diabetogenic effect of both ritodrine and isoxsuprine was so slight that it did not have any clinical significance in women with normal glucose tolerance. The results were similar when these beta-adrenergic tocolytics were given to women concomitantly with intramuscular dexamethasone therapy, although dexamethasone appeared to minimally impair carbohydrate metabolism. Both ritodrine and isoxsuprine caused a significant fall in serum iron and potassium, and this effect was unaltered by dexamethasone. Serial serum potassium levels should be obtained during long-term infusion of beta-mimetics.

Adolescent↗
PubMed1978

Lack of effect of halothane on E, EA, and EAC rosette formation and cyclic AMP level of human lymphocytes.

The effect of halothane on rosette formation and cyclic adenosine monophosphate (cyclic AMP) level of human lymphocytes was investigated. A 4- or 24-hour incubation with 2% halothane had no significant effect on "early" or "late" E, EA and EAC rosette formation or intracellular cyclic AMP levels of human lymphocytes whereas cytochalasin B, which affects microfilament action, reversibly inhibited both E and EA but not EAC rosette formation. It is suggested that halothane in clinical concentrations neither disturbs the function of microfilaments, essential for E and EA rosette formation, nor affects the metabolism of cyclic AMP in unstimulated human lymphocytes.

Cells, Cultured↗
PubMed1977

Further evidence for central histamine H2-receptor involvement in the hypotensive effect of clonidine in the rat.

In urethane-anaesthetised rats, the administration of the specific histamine H2-receptor antagonist metiamide intracerebroventricularly (i.c.v.) raised the blood pressure and increased the heart rate. Metiamide (i.c.v.) antagonised the hypotensive effect of clonidine (i.c.v.) in an apparently competitive manner. 4-Methylhistamine i.c.v. did not significantly change the blood pressure. The results are consistent with the concept that the hypotensive effect of clonidine is at least partly due to a stimulation of cerebral H2-receptors. The existence of cerebral H2-receptors mediating hypotensive effects is supported by the hypertensive effect of metiamide but not by the lack of hypotensive effects of 4-methylhistamine.

Animals↗