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Biomedical subjects

M Henning

Publications and source records attributed to M Henning.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of Sarcocystis miescheriana infection on carcass quality and on the water-binding capacity of the meat of halothane-tested fattening pigs.

Ten halothane-positive pigs (stress sensitive, group A) and ten halothane-negative pigs (stress insensitive, Group C) with a mean body weight of 36 kg were each inoculated orally with 50,000 sporocysts of Sarcocystis miescheriana. Twelve halthane-positive pigs (Group B) and ten halothane-negative pigs (Group D) served as non-infected controls. Thirteen weeks post infection (p.i.) the lean: fat ratios of the pigs of the infected groups A and C were lower (A, 1:0.41 +/- 0.09; C, 1:0.50 +/- 0.10) than those of the pigs of the non-infected groups B and D (B, 1:0.50 +/- 0.08; D, 1:0.55 +/- 0.08). The back-fat thickness, the fat thickness 'A' and the fat thickness 'B' were thinner in infected pigs than in non-infected pigs. The difference in Lendenstärkespeckquotient (Loin Fat Thickness Quotient) (LSQ) between infected and non-infected pigs was not statistically significant. The values of the water-holding capacity were lower in infected pigs than in non-infected pigs, the difference being statistically significant only in the halothane-negative groups (C, 0.45 +/- 0.02; D, 0.48 +/- 0.04). The water-absorbing capacity was significantly higher in the infected groups (A, 5.92 +/- 3.99%; B, 2.26 +/- 1.08%; C, 8.96 +/- 2.90%; D, 4.97 +/- 2.51%). In conclusion, it can be said that there was a slight tendency towards a better carcass quality and a better water-binding capacity in infected pigs, although this was combined with reduced growth rates.

Absorption↗
PubMed1987

Effects of Sarcocystis miescheriana infection on carcass weight and meat quality of halothane-tested fattening pigs.

Ten halothane-positive pigs (Group A) and ten halothane-negative pigs (Group C) were each infected per os by 50,000 sporocysts of Sarcocystis miescheriana when they had reached a mean body weight of 36 kg. Twelve halothane-positive pigs (Group B) and ten halothane-negative pigs (Group D) served as non-infected controls. Thirteen weeks p.i. (post infection), the pigs were slaughtered and the carcass weights and the number of cystozoites in several muscles were determined. In addition, 11 parameters of meat quality were measured in Musculus longissimus dorsi (M.l.d.) and Musculus semimembranosus (M.s.): pH and temperature 30 min and 24 h p.m. (post mortem), electrical conductance 45 min, 60 min and 24 h p.m., colour brightness (FOP) and rigor values 30 min and 24 h p.m. Additionally, the AMP, ADP, ATP and lactate contents were determined in samples from the M.l.d. The mean carcass weights of the infected pigs (A: 79.9 +/- 6.9 kg; C: 76.3 +/- 11.6 kg) were lower than those of the pigs of the non-infected groups (B: 85.7 +/- 8.0 kg; D: 87.5 +/- 7.0 kg). The pH values at 24 h p.m. were significantly higher in the M.l.d. of infected pigs than in M.l.d. of non-infected pigs. Electrical conductance in the M.s. at 45 min p.m. was significantly higher in the halothane-negative infected pigs, but at 24 h p.m., the mean values of electrical conductance in the M.s. of the pigs of both infected groups were significantly lower than in the control groups. FOP values at 30 min p.m. were raised in the M.l.d. of the halothane-negative infected pigs, but at 24 h p.m., differences between infected and non-infected pigs could no longer be found. Mean rigor values were higher in the pigs of the infected groups at 24 h p.m., but the difference from the non-infected groups was not statistically significant. AMP was reduced only in the meat of halothane-positive infected pigs, while lactate was reduced in both infected groups. Using conventional methods for the determination of meat quality, the hypothesis of impaired meat quality in Sarcocystis-infected pigs could not be confirmed. The meat quality parameters investigated were, in part, better in infected pigs than in non-infected controls.

Adenosine Diphosphate↗
PubMed1985

Chronic serotonergic blockade with ketanserin in the spontaneously hypertensive rat.

Spontaneously hypertensive rats were fed ketanserin-enriched (17 mg/100 g) or control chow for 6 weeks. After 6 weeks the blood pressure was reduced (16%). Pressor responses to phenylephrine were not different from control responses, which indicates that at this time the antihypertensive effect was not directly related to an alpha-adrenoceptor blockade. Cardiovascular responses to stress (jet air), baroreceptor sensitivity (bradycardia to phenylephrine), and central catecholamine turnover were unchanged, which supported the view that central mechanisms probably do not contribute to the antihypertensive effects of ketanserin.

Animals↗
PubMed1984

Antihypertensive effects of chronic 5-hydroxytryptamine (5-HT2) receptor blockade with ketanserin in the spontaneously hypertensive rat.

The effects of chronic oral treatment with the 5-hydroxytryptamine (serotonin) receptor blocking agent ketanserin (17 mg/100 g dry food) on blood pressure, heart weight, peripheral vascular reactivity, baroreceptor sensitivity, central cardiovascular reactivity and central catecholamine turnover were investigated in the spontaneously hypertensive rat. Blood pressure measurements were performed in conscious rats 24 h after insertion of catheters. After 6 weeks treatment basal blood pressure was reduced (16%) compared to control rats (given identical food, except for ketanserin). Both heart weight and body weight were reduced (both to 93% of control values) leaving heart weight/body weight ratio unchanged. Pressor responses to phenylephrine and depressor responses to isoprenaline (after pretreatment with reserpine and atropin) were not different while the blood pressure increase to 5-hydroxytryptamine was inhibited, indicating that after 6 weeks treatment the blood pressure reduction is not directly related to alpha-adrenoceptor blockade. Cardiovascular response to stress (jet air), baroreceptor sensitivity (bradycardia to phenylephrine) and central catecholamine synthesis rates (accumulation of 5-hydroxytryptophan and dihydroxyphenylalanine after synthesis inhibition) were unchanged supporting earlier evidence that central mechanisms probably do not contribute to the hypotensive effects of ketanserin.

Animals↗
PubMed1983

Mediation and mechanisms of the hypotensive effect of L-dopa in the sea-gull: Larus argentatus.

We have investigated the mediation of the hypotensive action of L-DOPA after peripheral DOPA decarboxylase (DC) inhibition in the sea-gull, Larus argentatus. Vagotomy prevented the bradycardia and hypotension occurring after L-DOPA in birds pretreated with an inhibitor of peripheral DC. L-DOPA alone, given to intact birds, resulted in a slight increase in blood pressure (BP), accompanied by a tendency to bradycardia. Spinal transection in combination with vagotomy reversed the bradycardia and reinforced the increase in BP seen in intact birds after L-DOPA. The dopamine receptor antagonist spiroperidol did not alter the hypotension and bradycardia after L-DOPA in birds pretreated with a peripherally acting DC inhibitor. Yohimbine antagonized the effects of L-DOPA, restoring the BP to near basal values within 5 min after i.v. injections, while prazosin had no such effect. The heart rate returned towards basal values after both yohimbine and prazosin. We conclude that L-DOPA elicits its hypotensive action in the sea-gull via activation of central alpha-adrenoceptors, which may belong to the alpha 2-subtype. The bradycardia may involve central activation of adrenoceptors of both the alpha 1- and alpha 2-types. The hypotension and bradycardia are mediated via vagal activation and probably also inhibition of sympathetic nervous output. The functional significance of sympathetic fibres running along with the vagus nerve is suggested.

Animals↗
PubMed1983

Cardiovascular and biochemical effects of L-DOPA in the sea-gull, Larus argentatus.

We have investigated the effects of L-DOPA alone and in combination with three different inhibitors of L-aromatic aminoacid decarboxylase (DC), carbidopa, benserazid and alpha-monofluoromethyldopa (MFMD) on blood pressure (BP) and catecholamine content in conscious or anaesthetized sea-gulls, Larus argentatus. The results show that L-DOPA, given i.p., is taken up and decarboxylated to dopamine (DA) in brain and heart. Carbidopa inhibits the peripheral synthesis of DA from exogenous L-DOPA while central decarboxylation is enhanced when compared to the effects of L-DOPA alone. Benserazid and MFMD inhibit both central and peripheral formation of DA after L-DOPA injections. L-DOPA given alone leads to a slight increase in BP, while heart rate (HR) decreases somewhat. After peripheral inhibition of DC using carbidopa, L-DOPA elicits a reduction in BP both in conscious and anaesthetized birds. HR is significantly reduced in anaesthetized birds. Pretreatment with benserazid or MFMD abolishes the cardiovascular effects of L-DOPA. It is concluded that L-DOPA lowers the BP via activation of central mechanisms.

Animals↗
PubMed1982

Alpha-Monofluoromethyldopa (MFMD) in combination with L-DOPA Effects on tissue catecholamines and blood pressure in rats.

We have investigated the interaction of alpha-monofluoromethyldopa (MFMD) with the effects of i.p. injected L-DOPA (200 mg.kg-1) on blood pressure and tissue catecholamines in normal and spontaneously hypertensive rats (SHR). MFMD 10 mg.kg-1 (i.p.) effectively antagonizes the L-DOPA induced increase in heart dopamine (DA). This action is also seen after 15 or 50 mg.kg-1. The accumulation of DA in the brain is very much reduced by MFMD 50 mg.kg-1 while after 15 or, especially, 10 mg.kg-1 more DA is formed in the brain than after L-DOPA alone, probably due to the peripheral decarboxylase inhibition which presents more L-DOPA to the brain. We conclude that MFMD 10 mg.kg-1 gives a relatively selective peripheral inhibition of the decarboxylation of L-DOPA and this dose combination was accordingly found to result in a reduction of blood pressure in conscious animals. This hypotensive response to L-DOPA was attenuated after MFMD 15 mg.kg-1 and was absent after MFMD 50 mg.kg-1. Interestingly, the hypotensive effect of L-DOPA after MFMD 10 or 15 mg.kg-1 was more pronounced in SHR.

Animals↗
PubMed1982

Dihydralazine inhibits tyrosine hydroxylase in vivo in the rat.

The effect of dihydralazine on monoamine metabolism in the rat was investigated. Dihydralazine, 5 mg/kg i.v., reduced noradrenaline (NA) in the heart. After pretreatment with phenoxybenzamine an NA depletion was evident also in the brain. Dihydralazine did not affect the utilization of NA or dopamine in the brain as judged by the disappearance rates of these amines following synthesis inhibition by alpha-methyl-p-tyrosine. However, dihydralazine reduced the synthesis of monoamines as evidenced by a decreased accumulation of the monamine precursor dihydroxyphenylalanine (and 5-hydroxytryptamine) subsequent to treatment with NSD 1015. It is concluded that dihydralazine inhibits central tyrosine hydroxylase (and tryptophan hydroxylase) in the rat.

Animals↗
PubMed1982

Cardiovascular effects in the rat of ketanserin, a novel 5-hydroxytryptamine receptor blocking agent.

Following intravenous administration of ketanserin (0.3-10 mg kg-1) to conscious or anaesthetized normotensive and spontaneously hypertensive rats there were dose-dependent blood pressure reductions but no compensatory tachycardia. Intracerebroventricular administration of ketanserin (25-500 microgram) had inconsistent and largely insignificant cardiovascular effects. In a dose range where it produces hypotension ketanserin antagonized the pressor responses to adrenaline and noradrenaline as well as to 5-hydroxytryptamine in monoamine depleted and spinalized rats. It is suggested that the hypotensive action of ketanserin in the rat does not involve a central mechanism but a peripheral alpha-adrenolytic action is implicated.

Animals↗
PubMed1982

Hormonal pattern during development of hypertension in spontaneously hypertensive rats (SHR).

Urinary excretion of sodium, noradrenaline, dopamine, aldosterone, prostaglandin E2 and plasma renin activity were determined in 7 and 16 weeks old spontaneously hypertensive rats (SHR) and in two normotensive control strains, ordinary Wistar control rats (NCR) and Wistar-Kyoto normotensive rats (WKR). Each group consisted of 10-11 rats. The animals were kept in metabolic cages. Experiments were performed on standard diet (5-8 mmol Na+/100 g food) and with an increased (15.6 and 56.0 mmol Na+/100 g food) salt intake. At 7 weeks of age, when SHR are in a borderline phase of hypertension, they exhibited a decreased urinary sodium excretion, and an increased urinary noradrenaline excretion compared to controls. The latter might reflect an increased overall activity of the sympathetic nervous system. Urinary dopamine excretion was also increased probably mirroring a higher activity in a renal natriuretic dopamine system. Plasma renin activity and urinary aldosterone excretion were depressed. At 16 weeks of age, when SHR are in an early establishment phase of hypertension, urinary sodium excretion was still lower in SHR, while urinary noradrenaline and dopamine excretions had become normal compared to controls. Plasma renin activity and urinary aldosterone excretion remained depressed. Urinary PGE2 excretion, only determined in this age group, was significantly higher in SHR.

Aldosterone↗
PubMed1981

Cardiovascular effects of clonidine in an avian species, Larus argentatus.

Blood pressure and heart rate were recorded in the sea gull, Larus argentatus, under light pentibarbitone anaesthesia. Clonidine 10(-7) and 10(-8) mol . kg-1 (27 and 2.7 microgram . kg-1) i.v. produced a biphasic effect on blood pressure, a brief initial increase being followed by a prolonged hypotensive response. There was an immediate reduction in heart rate rate which persisted throughout the hypotensive phase. After spinal transection at the level of C4, clonidine administration elicited hypertension and bradycardia. Bilateral vagotomy abolished the effect of clonidine on heart rate but did not alter the blood pressure response. Vagotomy in combination with spinal transection abolished the effect of clonidine on heart rate but the hypertensive response was accentuated. Yohimbine 10(-7) or 10(-6) mol . kg-1 (0.039 or 0.39 mg . kg-1) given 5 min after clonidine 10(-7) mol.kg-1 (27 microgram . kg-1) effectively antagonized the cardiovascular effects of clonidine, while prazosin 10(-7) or 10(-6) mol . kg (0.042 or 0.42 mg . kg-1) had no such effect. We conclude that clonidine acts in the central nervous system of the sea gull to produce a lowering of blood pressure and heart rate. These effects are mediated by central inhibition of sympathetic activity and, in the case of the heart rate, mostly by central activation of vagal activity to the heart. This central action of clonidine involves activation of alpha-adrenoceptors which are blocked by yohimbine but not by prazosin and therefore may belong to the alpha 2 subtype.

Adrenergic alpha-Antagonists↗
PubMed1980

Central cardiovascular effects of gamma-hydroxybutyric acid: interactions with noradrenaline, serotonin, dopamine and acetylcholine transmission.

Gamma-hydroxybutyric acid (GHBA) increased arterial blood pressure and heart rate dose-dependently following intraperitoneal and intracerebroventricular administration to conscious rats. Cardiovascular responses to GHBA were completely prevented after pretreatment with reserpine or phenoxybenzamine and after a prehypothalamic brain transection. Intraperitoneal GHBA increased brain noradrenaline (NA) synthesis and utilization, particularly in the neocortex. Selective central NA depletion in combination with NA synthesis inhibition prevented the cardiovascular effects of GHBA. No overt interactions were observed with agents influencing 5-hydroxytryptamine (5-HT), dopamine (DA), or acetylcholine (Ach) transmission. Pentobarbitone but not diazepam or diphenylhydantoin abolished the hypertensive properties of GHBA. We conclude that the cardiovascular effects of GHBA are of central origin and that they are mediated via the peripheral sympathetic nervous system. They are dependent on an intact central NA transmission while there are few indications for a significant role of central DA-, 5-HT or Ach-mechanisms.

Acetylcholine↗
PubMed1980

Effect of GABA analogues on blood pressure and central GABA metabolism in the rat.

Gamma aminobutyric acid (GABA) and different GABA analogues were examined for their cardiovascular actions and their influence on striatal dopamine (DA) levels and GABA accumulation after aminooxyacetic acid (AOAA). Gamma hydroxybutyric acid (GHBA) and baclofen caused hypertension and tachycardia after systemic as well as intracerebroventricular administration, while the opposite was true for GABA and muscimol. The hypertension after GHBA and baclofen was not reduced by picrotoxin or bicuculline and was not influenced by varying GABA levels by 3-mercaptopropionic acid (3-MPA) or AOAA. GHBA and muscimol but not baclofen reduced GABA accumulation induced by AOAA. Picrotoxin in a subconvulsive dose increased GABA accumulation and antagonized the inhibition after GHBA or muscimol. Bicuculline and a moderate dose of picrotoxin tended to decrease GABA accumulation by themselves and if anything augmented the effects of GHBA and muscimol. GHBA and baclofen but not muscimol in combination with AOAA increased DA levels, which was not prevented by picrotoxin or bicuculline. We conclude that the cardiovascular actions of GHBA and baclofen are probably not mediated by mechanisms identical to those of muscimol or exogenous GABA. In view of the biochemical results their actions would however be compatible with a concept of different GABA receptors.

3-Mercaptopropionic Acid↗
PubMed1980

6-hydroxydopamine and the blood-brain barrier in adult conscious rats.

6-hydroxydopamine (6-OHDA), 15 or 50 mg . kg-1 given as bolus i.v. injection to adult conscious rats with aortic catheter, rapidly increased mean arterial pressure by 70-78 mmHg. The pressure returned to normal within 40-60 min. The cerebrovascular permeability in rats given 6-OHDA and sacrificed 10 or 60 min later was enhanced as indicated by extravasation of Evans blue albumin and significant increase of 125I human serum albumin content in brain tissue compared to control rats. When the increase in blood pressure was diminished by i.v. phentolamine, 6-OHDA treated rats did not differ from controls. It is concluded that the blood pressure elevation induced by i.v. 6-OHDA facilitates the entry of the drug into the brain parenchyma.

Animals↗