Endothelium-derived relaxing factor (nitric oxide) has a tonic vasodilating action on coronary collateral vessels.

OBJECTIVES: We sought to determine whether endothelium-derived relaxing factor (nitric oxide) exerts a tonic vasodilating effect on coronary collateral channels developed in response to myocardial ischemia. BACKGROUND: Although the coronary collateral circulation is known to react to several vasoactive agents, the role of endogenously produced nitric oxide is unclear. METHODS: Coronary collateral channels were induced in the left circumflex artery bed of 12 chronically instrumented dogs by either ameroid implantation or repeated occlusion of the left circumflex coronary artery. With the native circumflex artery occluded, aortic and circumflex pressures and microsphere flows were measured before and after systemic administration of NG-nitro-L-arginine methyl ester, an arginine analogue known to block the synthesis of nitric oxide. RESULTS: NG-nitro-L-arginine methyl ester increased mean aortic pressure from a mean +/- SEM of 92 +/- 4 to 114 +/- 4 mm Hg, whereas pressure in the occluded circumflex artery decreased from 61 +/- 4 to 55 +/- 4 mm Hg. The increase in aortic-circumflex pressure gradient (from 31 +/- 4 to 59 +/- 5 mm Hg) was accompanied by a decrease in flow in the circumflex bed (from 1.31 to +/- 0.14 to 1.09 +/- 0.15 ml/min per g), resulting in an increase in coronary collateral resistance averaging 173 +/- 37% (from 26 +/- 4 to 64 +/- 9 mm Hg/ml per min per g, p < 0.01). The increase in collateral resistance could be partially reversed by administration of L-arginine. CONCLUSIONS: We conclude that nitric oxide normally exerts a substantial tonic dilating effect in coronary collateral vessels. Disease-induced alterations in endothelial function may limit collateral perfusion importantly.

Rapeseed products from double-low cultivars as feed for dairy cows: effects of long-term feeding on thyroid function, fertility and animal health.

Eighty-five dairy cows of the Swedish Red and White Breed (SRB) were included in a long-term experiment during 3 consecutive lactations. The cows were divided into 3 different dietary groups that received no rapeseed (NR), up to 1.2 kg dry matter (DM) 00-rapeseed meal plus 0.2 kg DM full-fat 00-rapeseed (MR), and up to 2.5 kg DM 00-rapeseed meal plus 0.9 kg DM full-fat 00-rapeseed (HR) per day. No significant differences in culling rates or disease rates were found between the feeding groups at any time during the experiment. The interval from calving to conception among the primiparous cows was longer for the HR-group (125 days) than for the NR-group (100 days). The response to a thyrotroph releasing hormone around 90 days postpartum during the first lactation was significantly higher for the HR-group (86.7 mu/L/h) than for the NR-group (55.2 micrograms/L/h). This indicates that at the highest level of rapeseed feeding, glucosinolates had a very mild, suppressive influence on thyroid hormone release, apparently compensated for by an increased activity along the hypothalamic-pituitary-thyroid axis. No significant differences in fertility or thyroid function were found among the pluriparous cows. During 2nd lactation the concentration of serum urea was higher in the NR-group (7.31 mmol/L) than in the HR-group (6.83 mol/L). The effects of independent environmental factors influenced fertility and thyroid function to a much greater extent than the rapeseed feeding. It was concluded that the feeding of rapeseed products from certified double low varieties of B. napus to adult dairy cows in amounts up to 3 kg rapeseed meal per cow and day would not have any negative effects on animal health or fertility.

The effect of mastitis on milk progesterone concentration in dairy cows.

A within cow comparison was made between milk progesterone levels in healthy and mastitic quarters. Material was collected from cows with mastitis induced by bacterial inoculation, or by inoculation with bacterial endotoxin. Furthermore material from cows with spontaneous subclinical mastitis was used. Milk progesterone levels were lowered due to mastitis. However, the decrease was not large enough to cause misinterpretation of where in the oestrous cycle (luteal phase or non-luteal phase) the samples were taken.

Profiles of progesterone in milk and clinical ovarian findings in postpartum cows with ovarian dysfunctions.

Milk progesterone profiles, based on twice or once weekly sampling, were constructed for postpartum dairy cows. The cows were simultaneously examined by rectal palpation and clinical ovarian findings were related to the progesterone profiles. The combination of progesterone analysis and clinical examination may be used to optimize diagnostic accuracy and a number of practical recommendations are given on the basis of the results from this study.

Blockade of nitric oxide synthesis reduces myocardial oxygen consumption in vivo.

BACKGROUND: Although cardiac myocytes and coronary vascular endothelium are known to express a constitutive form of NO synthase, the in vivo effects of tonic endogenous production of NO on myocardial O2 consumption and contractile performance remain unclear. METHODS AND RESULTS: The effects of blockade of NO synthase were determined in intact dogs. Myocardial O2 consumption decreased systematically over a wide range of hemodynamic demand after the systemic administration of N omega-nitro-L-arginine methyl ester (L-NAME) or N omega-nitro-L-arginine. Decreases after doses of 1 and 10 mg/kg L-NAME averaged 23 +/- 3.8% and 34 +/- 7.2% at a heart rate of 90 bpm in open-chest animals. Similar reductions occurred after the administration of L-NAME and N omega-nitro-L-arginine in chronically instrumented animals and were unaffected by beta-adrenergic blockade. Intracoronary infusion of L-NAME in chronically instrumented animals reduced both myocardial O2 consumption and regional segment shortening, even at a dose that did not increase systemic arterial pressure. CONCLUSIONS: The blockade of NO synthesis reduces myocardial O2 consumption in vivo. The decrease in O2 consumption is accompanied by a decrease in segment shortening. It involves a direct myocardial action of NO, is unaffected by beta-blockade, and is consistent with in vitro studies indicating that low levels of NO augment contractile performance by inhibition of a cGMP-dependent phosphodiesterase.