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Biomedical subjects

C Burvenich

Publications and source records attributed to C Burvenich.

At least 109 records · Page 6Linked to original sources
PubMed1985

Effect of serotonin on the motility of smooth muscles in teats of lactating cows.

The effects of serotonin, injected into one udder artery, on teat smooth muscle function were investigated in four lactating cows. Motility of longitudinal smooth muscles was recorded by a plethysmographic technique, and sphincter function by measuring milk leakage from the full udder. Serotonin (40, 120 and 360 micrograms) activated teat muscle tonicity and reduced the volume of milk leakage. The effects on longitudinal smooth muscles were reduced by mianserin and ketanserin (0.375, 1.5 and 6 mg) and by methysergide (1.5 mg). These blocking substances were also effective (0.2, 0.6 and 1.8 mg respectively) in antagonizing the inhibiting action of serotonin on milk leakage. It is suggested that serotonin effects are mediated by receptors of the S2-type.

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PubMed1984

Effect of prazosin on the function of the teat sphincter in lactating cows.

Oxytocin was infused for 60 min into the jugular vein of 8 lactating cows with full udders before milking. Under these circumstances milk loss occurred spontaneously in 3 cows and was evoked in 5 cows by reducing pressure around one teat (-30 cm water) using a plethysmographic chamber. Milk loss was measured continuously. The postsynaptic alpha-blocking agent prazosin ( PRZS ) injected either into the udder artery (2 or 5 mg) or into the jugular vein (200 mg) consistently induced a significant increase in milk leakage. It is suggested that PRZS effectively inhibits alpha-adrenoceptors in the teat sphincter muscles and thus promotes the action of beta-adrenoceptors, in this way inducing relaxation of the teat sphincter.

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PubMed1984

Action of epinephrine on the function of the teat sphincter in the lactating cow.

Under continuous IV infusion of oxytocin, milk leakage was elicited in 6 lactating cows with full udders by induction of a vacuum (-30 cm of water) around 1 mammary papilla (teat) with a plethysmographic apparatus. The volumes of milk loss were measured every minute. Epinephrine injected either into the jugular vein (20, 100, and 500 micrograms) or into the external pudic artery (1.5, 7.5, and 37.5 micrograms) induced an increase in milk leakage in 5 cows. This effect could be antagonized by the beta-blocking agent sotalol hydrochloride (0.5 to 4 mg) injected into the external pudic artery. In 1 cow, however, epinephrine given intra-arterially exerted a biphasic effect, small doses inducing stimulation, and large doses evoking inhibition of milk loss. The stimulating effects were blocked by sotalol (2 mg). The inhibiting effects were antagonized by the alpha-blocking agent prazosin (2 mg).

Animals↗
PubMed1982

Effect of prostaglandin synthetase inhibitors on mammary blood flow during experimentally induced mastitis in lactating goats.

Mammary blood flow (MBF) was recorded chronically in lactating goats by means of an electromagnetic flow probe. Experimental mastitis was induced by intramammary injection of E. coli lipopolysaccharides. Control mastitis experiments were accompanied by a significant increase in MBF characterized by 2 conspicuous peaks, by fever, increased heart rate, swelling, heat and pain of the gland, and increased chloride in milk. The non-steroidal anti-inflammatory drugs suprofen, indomethacine and flurbiprofen were potent antipyretics during mastitis but had only little effect on the biphasic MBF pattern. Indomethacine induced a strong and long lasting vasoconstriction in the udder. MBF peak I was quantitatively unaffected although flurbiprofen was able to delay its appearance. All drugs partially suppressed MBF peak II, this being most significantly with flurbiprofen. None of them prevented either swelling of the gland or high milk chloride but all inhibited pain in the gland. MBF peak II may be partially induced by the decrement stage of fever. Locally formed prostaglandins play little or no role in the genesis of MBF peak I but may be involved in MBF peak II.

Animals↗
PubMed1982

Effect of experimentally induced fever on mammary blood flow in lactating goats.

The effect of artificially induced fever on normal mammary blood flow (MBF) was studied in conscious lactating goats in a thermoneutral environment. Fever was induced either by intravenous (i.v.) injection of LPS or by intracerebroventricular (i.c.v.) infusion of PGE2. The increment stage of fever was always accompanied by a fall in MBF, shivers and miosis. There was a positive correlation between the intensity of temperature increase and MBF decrease. Once fever was established or during the decrement stage of fever, MBF returned to control levels and often increased far above pre-injection values. These specific circulatory changes observed in the lactating udder of the goat might contribute to the genesis and lysis of fever. MBF might play an important role in the pathogenesis of fever in the lactating goat. The effect of centrally induced fever was studied on the biphasic MBF pattern normally occurring during experimentally induced LPS mastitis. PGE2 was infused i.c.v. practically simultaneously with the intramammary administration of LPS. In most experiments fever occurred earlier than during control mastitis. The biphasic MBF-curve was strongly altered, MBF peak I being inhibited. Fever increment during control mastitis could be one of the factors limiting the duration of MBF peak I and fever decrement could induce peak II.

Animals↗
PubMed1981

Antidiuretic effects of intracerebroventricular infusion of adrenaline in conscious goats.

The effects of adrenaline (A) upon waterdiuresis were studied in conscious, hydrated goats, provided with a permanent cannula into the 3rd ventricle. Adrenaline induced a reduction in urinary volume and in free water clearance and a rise in the osmolality of the urine. These effects were dose-dependent and significant. A biphasic Cl-excretion pattern, consisting op of an initial fall below control level and a subsequent increase was observed. Na+ and K+ excretion rates were reduced. Central pretreatment with phentolamine completely antagonized the antidiuretic action of A. Propranolol, atropine and hexamethonium were ineffective. Alpha-adrenoceptors might be involved in vasopressin release.

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