The results are based on the Norwegian Cattle Health Recording System, which has been in place for the entire country since 1975. The dairy breeds in Norway consist of 94% Norwegian Red and 4% crossbreeds with Norwegian Red. No other breed consists of more than 0.5% of the total population. During the past 30 yr, there have been 11,563,692 dairy cows within the recording system, corresponding to 8,633,532 cow-years and 8,632,516 calvings. This population consisted of 3,038,675 first-calving cows. Altogether, 8,435,704 different diagnoses were recorded from 4,444,485 different cows each year. The general trend for all recordings was an increase in the incidence rate of all cases from 0.74 per 365 d at risk (cow-year) in 1976 to 1.36 in 1990, and then a decrease to 0.62 in 2002. The corresponding figures for cows treated per cow-year were 0.44 up to a maximum of 0.82, and then a decrease to 0.46 per cow-year in 2002. The most common diseases were acute (severe to moderate) clinical mastitis, chronic (mild) clinical mastitis, ketosis, milk fever, teat injuries, retained placenta, silent heat or anestrous, indigestion, cystic ovaries, and metritis. Clinical mastitis increased from 0.15 cows treated per cow-year in 1975 to 0.44 in 1994, and then decreased to 0.23 in 2002. Ketosis began at 0.10 in 1975, increased to 0.24 in 1985, and then decreased to 0.05 in 2005. For several of the most common diseases, there was a reduction of more than 50% from the 1990s to the years after 2000. Validation processes confirmed that this fluctuation reflected the general trend in the population. The disease recording system also reflected the known outbreaks of bovine respiratory syncytial virus during 1976, 1989 to 1990, and 1995. A marked increase in malformation diagnoses could be seen in 1986 and in 1989 and 1990. These could be related to the Chernobyl nuclear power plant accident in April 1986. The diagnosis that showed the most stability throughout these 30 yr was retained placenta. The 3 main reasons for the large fluctuation for many of the diseases could be the following: a breeding effect, an effect of preventive work, and an effect of changing the therapeutic attitude. Many of the actions taken to bring about improvements would not have been possible without a functioning and practical recording system. Our experience is that an organ-related diagnosis system with up to 60 or 70 different diagnoses will meet the needs of the dairy industry.

IntroductionWe developed a minimally invasive, closed chest pig model with the main aim to describe hemodynamic function during surface cooling, steady state severe hypothermia (one hour at 25°C) and surface rewarming.MethodsTwelve anesthetized juvenile pigs were acutely catheterized for measurement of left ventricular (LV) pressure-volume loops (conductance catheter), cardiac output (Swan-Ganz), and for vena cava inferior occlusion. Eight animals were surface cooled to 25°C, while four animals were kept as normothermic time-matched controls.ResultsDuring progressive cooling and steady state severe hypothermia (25°C) cardiac output (CO), stroke volume (SV), mean arterial pressure (MAP), maximal deceleration of pressure in the cardiac cycle (dP/dtmin), indexes of LV contractility (preload recruitable stroke work, PRSW, and maximal acceleration of pressure in the cardiac cycle, dP/dtmax) and LV end diastolic and systolic volumes (EDV and ESV) were significantly reduced. Systemic vascular resistance (SVR), isovolumetric relaxation time (Tau), and oxygen content in arterial and mixed venous blood increased significantly. LV end diastolic pressure (EDP) remained constant. After rewarming all the above mentioned hemodynamic variables that were depressed during 25°C remained reduced, except for CO that returned to pre-hypothermic values due to an increase in heart rate. Likewise, SVR and EDP were significantly reduced after rewarming, while Tau, EDV, ESV and blood oxygen content normalized. Serum levels of cardiac troponin T (TnT) and tumor necrosis factor-alpha (TNF-α) were significantly increased.ConclusionsProgressive cooling to 25°C followed by rewarming resulted in a reduced systolic, but not diastolic left ventricular function. The post-hypothermic increase in heart rate and the reduced systemic vascular resistance are interpreted as adaptive measures by the organism to compensate for a hypothermia-induced mild left ventricular cardiac failure. A post-hypothermic increase in TnT indicates that hypothermia/rewarming may cause degradation of cardiac tissue. There were no signs of inadequate global oxygenation throughout the experiments.

Pharmacodynamic effects and pharmacokinetics of dopamine are maintained during the rewarming phase at moderate hypothermia. However, at 25 °C dopamine pharmacokinetics were seriously altered and dopamine failed to increase cardiac index since stroke index was reduced with incrementing dosages. Properties of the low-flow, high-viscosity circulatory state, combined with altered pharmacokinetics of dopamine, may explain lack of beneficial--and potentially harmful--effects from dopamine administration at 25 °C.