Uterine blood flow and oxygen consumption in rhesus monkeys with retained placentas.
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A significant percentage of cows (11%) fail to release the placenta within 12 h postpartum. Failure of collagen breakdown seems to be related to the retention of placentas. Sections of placentomes incubated with bacterial collagenase caused an increase in placentome proteolysis (6.6-fold) and placentome collagenolysis (94-fold) within 4 h in a dose-related fashion (r = 0.94). Injections of collagenase (825 U/cc) into the placentomes, via umbilical vessels, decreased the cotyledon-caruncle binding force (determined by manometry) to 30 +/- 5 mm Hg from 97 +/- 2 mm Hg, and increased proteolysis by 42% within 8 h (r = -0.95). Hyaluronidase at various concentrations (400-8 250 U/cc) and at various incubation times (up to 8 h) was not effective. Hyaluronidase (825 U/cc) and collagenase (825 U/cc) were not synergistic in loosening cotyledon-caruncle attachment. A single 15-min collagenase pulse, given prior to perfusion with collagenase-free blood, was as effective in loosening cotyledon attachment as was a sustained 2-h perfusion of blood with collagenase added. It was concluded that collagenase caused collagenolysis and loosening of cotyledon from caruncle, but collagenolysis and cotyledon-caruncle separation were not facilitated by the presence of hyaluronidase.
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In the dairy cow, a statistical association between milk fever (MF) and placental retention (PR) has been observed in epidemiological studies. In order to prevent both diseases, an understanding of their common aetiological mechanism is necessary. In this paper, a new causal hypothesis concerning the nutrition-induced association between PR and MF has been put forward. This hypothesis integrates the aetiological concepts arising from the studies carried out by the authors of this paper, and those reviewed from the literature. The aetiological pathway leading to associated MF and PR in the dairy cow appears to include 3 main interrelated mechanisms: 1), decreased synthesis of cyclooxygenase products (mainly PgF2 alpha) via precalving linolenic acid-rich diets; 2), lack of calcium availability at calving via calcium-rich diets before calving; 3), intensive lipomobilization around calving due to a lack of energy supply. The risk for both MF and PR appears to be maximum with old cows fed diets rich in green fodder (fresh or ensiled) and in calcium, and poor in cereals in the prepartum period.
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