Flow and composition of afferent mammary gland lymph.

Afferent mammary lymphatic flow was characterized in conscious lactating cows during milking and prior to, during, and after intramammary infusion of endotoxins. Lymph flow (13 to 45 ml/h) was pulsatile with monophasic and multiphasic episodes. Flow resulted from 62 to 67 episodes per h. Episodes varied from 1 to 53 s in duration. Maximum instantaneous flow ranged from 163 to 245 microliters/s. Flow did not increase consistently during milking. Lymph flow increased (5.5- to 8-fold) during endotoxin-induced mastitis. Flow rates were elevated for up to 48 h after infusion of endotoxin. Compositional comparisons between afferent mammary lymph and blood plasma showed distinct differences. Lymph contained 7, 6, and 10 times less protein, albumin, and globulin, respectively, than did plasma. Glucose concentrations were equivalent. Lymph had 17 times less cholesterol and about one-half as much triglyceride and calcium as did plasma. gamma-Glutamyl-transaminase and aspartate transaminase were substantially higher in plasma than in lymph. Afferent mammary lymph has unique compositional characteristics. The lymph ducts contained an intrinsic mechanism for lymph movement. Moreover, this mechanism was altered by inflammation. The techniques herein provide a better understanding of the mammary lymphatic system.

Endocrine responses in cows milked by hand and machine.

Plasma concentrations of oxytocin, prolactin, and cortisol were compared in five Swedish Red and White cows milked by hand versus machine. Cows were divided into two groups. One group was hand-milked; the other group was machine-milked. Treatments were switched every other day. The experiment was carried out for 6 d. Blood samples were taken prior to, during, and after milking and were assayed for hormones. More oxytocin and prolactin were released in hand-milked cows. There were no significant diurnal differences between the total amount of oxytocin released for the different treatments, but prolactin tended to be higher during hand-milking in the evening than in the morning milking. Cortisol concentrations were greater during hand-milking than during machine-milking. There were no significant treatment differences with regard to the total amount of cortisol released. During morning milking, cortisol concentrations were higher during hand-milking than during machine-milking. Our data show that hand-milking results in a pronounced and prolonged release of oxytocin and prolactin.

Effect of local stimulation of one quarter on milk production and milk components.

The existence of local udder regulatory mechanisms involved in the regulation of milk production was demonstrated. Because the four quarters of the udder are independent, yet share a common environment, the experiment was designed to give one quarter extra stimulation by hand-milking while the other quarters were machine-milked. A difference in milk production was found, proving the existence of local mechanisms. The largest differences were during evening milking with an increased production in the hand-milked quarter. The machine-milked quarters did not increase their production. The increased production was probably due to enhanced activity in the secretory cells, induced by some factor produced or activated locally in the udder.

Milking and feeding-induced release of the gastrointestinal hormones gastrin and somatostatin in dairy cows.

In monogastric animals, suckling influences the secretion of gastrointestinal hormones during lactation. The aim of the present study was to investigate whether similar effects are induced by milking in cows. Experiments were performed on four cows in midlactation. Blood samples were drawn from a chronic jugular vein catheter and gastrin, and somatostatin were determined by radioimmunoassay. Milking and feeding increased plasma gastrin. Somatostatin increased at morning milking and at feeding, but it decreased at evening milking. Atropine injected subcutaneously 30 min before milking increased resting concentrations of gastrin but decreased resting concentrations of somatostatin. Feeding-induced release of gastrin remained but the milking-induced release disappeared. The milking- and feeding-induced effect on somatostatin became more marked. We suggest that milking influences gastrin and somatostatin via activation of the vagal nerves. The gastrin release caused by milking may be mediated via a cholinergic mechanism, whereas the atropine resistant effect on gastrin caused by feeding and on somatostatin caused by both milking and feeding suggest that a noncholinergic, perhaps peptidergic, transmitter may be involved.