Cardiovascular and endocrine responses to haemorrhage in the pig

Heart rate (HR), mean arterial pressure (MAP), indices of sympathetic and parasympathetic activity (plasma concentrations of adrenaline, noradrenaline and pancreatic polypeptide, PP), vasopressin (VP) and aldosterone (ALDO) were measured in six pigs during continuous bleeding resulting in hypovolaemic shock, from which five survived. Three stages of haemorrhage could be defined. Stage I. Resting MAP was 85 ± 6 mmHg and increased to 96 ± 5 mmHg with a blood loss of 275 (range 250–300) (10 (9–12)% of the estimated blood volume) concomitant with an increase in HR from 105 ± 5 to 113 ± 6 beats min^-1 (P < 0.05). Stage II. After a blood loss of 375 (300–500) ml (15 (13–16)%) MAP fell to 62 ± 9 mmHg and HR to 95 ± 5 beats min^-1 (P < 0.05). Stage III. A blood loss of 1113 (825–1450) ml (44 (30–52)%) resulted in a MAP of 50 ± 4 mmHg and an increase in HR to 206 ± 3 beats min^-1 (P < 0.05). Adrenaline increased from 0.3 ± 0.1 to 0.8 ± 0.3 (stage II) and 3.6 ± 1.1 nmol l^-1 (stage III) (P < 0.05); noradrenaline from 0.4 ± 0.1 to 1.5 ± 0.4 (stage II) and 5.9 ± 1.7 nmol l^-1 (stage III) (P < 0.05); PP from 6.2 ± 1.6 to 13.3 ± 2.3 (stage II) and 20.9 ± 7.8 pmol l^-1 (stage III) (P < 0.05). VP changed only marginally, but ALDO increased from 496 ± 54 to 623 ± 76 pmol l^-1 (stage III) (P < 0.05). The results suggest that a high HR and intense sympathetic activity is seen during severe haemorrhage in the pig while vagal slowing of the heart and moderate hypotension are prominent when bleeding amounts to approximately 15% of the estimated blood volume.     

The effect of exercise on postprandial lipidemia in type 2 diabetic patients

To elucidate if postprandial exercise can reduce the exaggerated lipidemia seen in type 2 diabetic patients after a high-fat meal. Two mornings eight type 2 diabetic patients (males) (58 ± 1.2 years, BMI 28.0 ± 0.9 kg m⁻²) and seven non-diabetic controls ate a high-fat breakfast (680 kcal m⁻², 84% fat). On one morning, 90 min later subjects cycled 60 min at 57% . Biopsies from quadriceps muscle and abdominal subcutaneous adipose tissue were sampled after exercise or equivalent period of rest and arterialized blood for 615 min. Postprandial increases in serum total-triglyceride (TG) (incremental AUC: 1,702 ± 576 vs. 341 ± 117 mmol l⁻¹ 600 min), chylomicron-TG (incremental AUC: 1,331 ± 495 vs. 184 ± 55 mmol l⁻¹ 600 min) and VLDL-TG as well as in insulin (incremental AUC: 33,946 ± 7,414 vs. 13,670 ± 3,250 pmol l⁻¹ 600 min), C-peptide and glucose were higher in diabetic patients than in non-diabetic controls (P < 0.05). In diabetic patients these variables were reduced (P < 0.05) by exercise (total-TG incremental AUC being 1,110 ± 444, chylomicron-TG incremental AUC 1,043 ± 474 mmol l⁻¹ 600 min and insulin incremental AUC 18,668 ± 4,412 pmol l⁻¹ 600 min). Lipoprotein lipase activity in muscle (11.0 ± 2.0 vs. 24.1 ± 3.4 mU g per wet weight, P < 0.05) and post-heparin plasma at 615 min were lower in diabetic patients than in non-diabetic controls, but did not differ in adipose tissue and did not change with exercise. In diabetic patients, 210 min after exercise oxygen uptake (P < 0.05) and fat oxidation (P < 0.1) were still higher than on non-exercise days. In type 2 diabetic patients, after a high-fat meal exercise reduces the plasma concentrations of triglyceride contained in both chylomicrons and VLDL as well as insulin secretion. This suggests protection against progression of atherosclerosis and diabetes.     

Plasma oxytocin,prolactin, insulin and LH after 24 h of fasting and after refeeding in lactating sows

The effects of 24 h of fasting and refeeding on the release of oxytocin, prolactin, insulin and LH in three lactating sows were investigated. The sows were starved, but supplied with water ad libitum, from 09.00 h on day 27 of lactation until 15.00 h on day 28 of lactation, when they were refed. Blood samples were collected continuously, using an automatic collection system, at a rate of 1 ml min^-1 from 09.00 to 21.00 h on day 28 (P1 = 6 h period after the 24 h fast, P2 = 6 h period after refeeding). For both P1 and P2 the mean number of nursings was 7.0 ± 1.0. Plasma insulin and glucose decreased to very low levels during fasting and increased (P < 0.001) after refeeding (insulin, 2.5 ± 0.7 vs. 28.9 ± 0.7 mU 1^-1; glucose, 2.6 ± 0.3 vs. 6.4 ± 0.3 mmol 1^-1). Following fasting, levels of prolactin were low (2.8 ± 0.1 μg 1^-1), and sucking did not induce significant release of prolactin. However, prolactin increased rapidly after refeeding (5.4 ± 0.1 μg 1^-1, P < 0.001). Neither the 24 h fast nor refeeding had a marked effect on basal levels of oxytocin, the percentage of sucklings with an oxytocin peak or the size of oxytocin peak. LH release (average and basal levels and number of pulses/6 h) during fasting was similar to that measured after refeeding. Plasma CCK increased significantly after feeding. The results indicate that the release of prolactin is also regulated by feed intake. Consequently the 24 h fast in lactating sows may alter milk production via an inhibition of prolactin release. Neither a stimulatory effect of insulin nor an inhibitory effect of prolactin on LH release was observed.     

Atrial natriuretic peptide attenuates pressor but enhances natriuretic responses to angiotensin II in pregnant conscious goats

This study was designed to examine the actions of ANP in acute, ANGII-mediated hypertension during pregnancy. Effects on blood pressure, blood volume, and renal Na and K excretion were evaluated in conscious goats (n= 6). ANP (2 μrg min^-1), ANGII (0.5 μg min^-1), or ANGII + ANP (doses the same as for each peptide alone) was infused intravenously for 60 min. The pressor response to ANGII was reduced in pregnant goats. This reduction was seen in systolic, but not in diastolic pressure. ANP decreased pressure by 5–10 mmHg both in pregnancy and in non-pregnancy. When ANGII + ANP was infused, blood pressure initially rose as with ANGII but then declined. ANP suppressed only the elevated systolic pressure. Plasma protein concentration and haematocrit was reduced by ANGII but increased by ANP alone or together with ANGII, thereby implying fluid shift into the vasculature by ANGII and opposite movement by ANP. ANGII increased renal Na excretion to 1500 μmol min^-1in non-pregnancy, but only to half of that in pregnancy. ANP alone caused small natriuresis, but enhanced ANGII-induced natriuresis to near 3000 μmol min^-1in both non-pregnant and pregnant goats. In summary, ANP further attenuated the blunted blood-pressure rise due to ANGII in pregnant goats, and reduced plasma volume, but enhanced renal Na excretion as in non-pregnant goats. This implies that with the present combination ANP and ANGII caused a near maximal natriuretic response that was not modified by the systemic cardiovascular changes occurring in pregnant goats.     

The preference for warm drinking water induces hyperhydration in heat-stressed lactating goats

The aim of this study was to determine whether lactating goats regulate their water intake when given a choice between warm (35 °C) and cold (15 °C) water. Six lactating goats were kept individually in pens. At 07.00 h one bucket was filled with warm water and another with cold water. Water consumption was measured at intervals until 18.00 h. Water temperature was not controlled at night. Two experiments were made, one at normal room temperature (18–19 °C) and the other at 39–40 °C from 10.45 to 17.00 h. At normal room temperature the goats drank 6.0±1.4 L of the warm water but only 1.7±1.3 L of the cold water (P<0.001). The total water consumption, including the following night, was 9.2±1.6 L. This differed from control days, when only cold water was available (5.9±0.4 L; P<0.05). Neither the plasma Na concentration nor the osmolality changed, which indicate that the goats regulated their fluid balance. In the experiments involving heat stress the goats drank 11.5±1.7 L of the warm water but only 2.0±1.0 L of the cold water (P<0.001). In total, including the following night, they drank 16.2±2.6 L (P<0.001 vs. control days). Goats drank repeatedly despite falling plasma Na and osmolality, proving that their thirst was not induced by water losses. Their abdomens became distended, indicating that water was stored in the reticulo-rumen and explaining why their body weights increased. The goats appeared distressed. It is concluded that goats prefer to drink warm water. Nevertheless, our results suggest that, if possible, warm drinking water should not be given to lactating goats under hot ambient conditions.     

A single bout of breast milk expression does not increase resting metabolic rate

Introduction

Breastfeeding women have elevated resting metabolic rate (RMR); however, whether a single bout of lactation increases RMR is unknown. This study aimed to determine if a single bout of lactation acutely increased RMR.

Methods

Twenty-two lactating women (age: 31 ± 0.9 year, body mass index: 27.3 ± 1.2 kg/m²) were recruited. RMR was assessed at baseline and at 1- and 2-h following breast milk expression.

Results

RMR was unchanged in lactating women following a single bout of lactation (baseline: 1437 ± 39; 1 h: 1425 ± 37 2 h: 1440 ± 31 kcal/day) (p > .05). RMR was not correlated to daily milk produced (r = 0.05, p > .05), but was correlated to body mass (r = 0.74, p < .001), fat-free mass (kg) (r = 0.61, p < .01), and fat mass (kg) (r = 0.71, p < .01).

Conclusion

RMR in lactating women appears to be more related to body mass or composition in the postpartum period rather than lactation.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

It is well documented that intense exercise precipitates oxidative stress in adults. However, there is lack of related studies concerning oxidant and antioxidant status during early and late recovery periods in adolescent athletes, following endurance exercise in particular. This study investigated aspects of the serum oxidant and antioxidant status of 12 male adolescent (16.2 ± 0.6 years) trained runners during early and late recovery periods after an all-out 21-km run. Venous blood samples were taken immediately before, 2 and 4 h following (early recovery period), and 24 h following (late recovery period) the 21-km run. Samples were analyzed for serum concentrations of thiobarbituric acid-reactive substances (TBARS), uric acid (UA), reduced glutathione (GSH), and enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), and catalase (CAT). During the early recovery period, there were increases in the 4-h GSH (194.8 ± 10.4 vs. 211.8 ± 11.4 mg l⁻¹, P < 0.05), 2- and 4-h UA (307.8 ± 68.6 vs. 327.4 ± 63.8; 330.2 ± 65.1 μmol l⁻¹, P < 0.05), and 2-h CAT (2.05 ± 0.44 vs. 3.07 ± 0.51 U ml⁻¹, P < 0.05), and decreases in the 2-h XO (11.1 ± 1.5 vs. 10.3 ± 1.2 U l⁻¹, P < 0.05) compared to the corresponding pre-exercise level, respectively. No change was observed in SOD (P > 0.05). At the late recovery period, there was an increase in CAT (2.80 ± 0.49 U ml⁻¹, P < 0.05) and TBARS (2.99 ± 0.83 vs. 4.40 ± 1.38 nmol ml⁻¹, P < 0.05). These data indicate that although the antioxidant capacity of adolescent runners is augmented during the early recovery period following the 21-km run, they were not completely protected from oxidative stress during the later recovery period.     

Role of nitric oxide and adenosine in the onset of vasodilation during dynamic forearm exercise

We tested the hypothesis that nitric oxide (NO) and adenosine contribute to the onset of vasodilation during dynamic forearm exercise. Twenty-two subjects performed rhythmic forearm exercise (20 % of maximum) during control and NO synthase (NOS) inhibition (N ^G-monomethyl-l-arginine; l-NMMA) trials. A subset of subjects performed a third trial of forearm exercise during combined inhibition of NOS and adenosine (aminophylline; n = 9). Additionally, a separate group of subjects (n = 7) performed rhythmic forearm exercise during control, inhibition of adenosine alone and combined inhibition of adenosine and NOS. Forearm vascular conductance (FVC; ml min^?1 · 100 mmHg^?1) was calculated from blood flow and mean arterial pressure (mmHg). The onset of vasodilation was assessed by calculating the slope of the FVC response for every duty cycle between baseline and steady state, and the number of duty cycles (1-s contraction/2-s relaxation) to reach steady state. NOS inhibition blunted vasodilation at the onset of exercise (11.1 ± 0.8 vs. 8.5 ± 0.6 FVC units/duty cycle; P < 0.001 vs. control) and increased the time to reach steady state (25 ± 1 vs. 32 ± 1 duty cycles; P < 0.001 vs. control). Vasodilation was blunted further with combined inhibition of NOS and adenosine (7.5 ± 0.6 vs. 6.2 ± 0.8 FVC units/duty cycle; P < 0.05 vs. l-NMMA alone), but not with aminophylline alone (16.0 ± 2.2 vs. 14.7 ± 2.0 FVC units/duty cycle; P = 0.67 vs. control). Our data indicate that NO and adenosine (in the absence of NO) contribute to the onset of vasodilation during dynamic forearm exercise.     

Leptin and thermogenesis in humans

We examined changes in serum leptin concentrations and thermogenesis in 12 healthy men (39 ± 2 years, BMI 22.8 ± 0.3 kg m^?2) during a 4 h euglycaemic hyperinsulinaemia performed on a control day and after a day of a competitive marathon run. As compared with the control day, after the marathon, baseline FFA concentration (543 ± 0.73 vs. 955 ± 96 μmol L^?1, P < 0.05), lipid oxidation rate (0.8 ± 0.1 vs. 1.2 ± 0.1 mg kg^?1 min^?1}, P < 0.01) and energy expenditure (5.2 ± 0.1 vs. 5.5 ± 0.1 kJ min^?1}, P < 0.01) were elevated. Baseline serum leptin concentrations were similar on the control and postexercise days and increased during insulin infusion by 35–45% on both days (P ≤ 0.01). Baseline serum leptin concentration correlated directly with serum insulin ( r = 0.65, P < 0.05) and cortisol ( r = 0.64, P < 0.05), and inversely with serum growth hormone concentration ( r = ?0.66, P < 0.05). In the postexercise study, the rise in energy expenditure during insulin clamp correlated with serum leptin concentration as determined before ( r = 0.61, P < 0.05) or at the end of insulin infusion ( r = 0.55, P < 0.05). Thus, in healthy individuals with normal body weight: (1) hyperinsulinaemia increases serum leptin concentrations; (2) a rise in energy expenditure correlates with serum leptin concentration. These data suggest that leptin is involved in the regulation of energy expenditure in humans.     

The effect of acute metabolic alkalosis on bicarbonate transport along the loop of Henle. The role of active transport processes and passive paracellular backflux

The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO ₃ ⁻ via a luminal Na⁺-H⁺ exchanger and H⁺ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO ₃ ⁻ infusion, we have observed previously inhibition of LOH net HCO ₃ ⁻ reabsorption , which contributes to urinary elimination of the HCO ₃ ⁻ load and correction of the systemic alkalosis. To determine whether the activities of the Na⁺-H⁺ exchanger and/or H⁺-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH from 205.0±0.8 to 96.2±11.8 pmol · min⁻¹ (P<0.001). Luminal perfusion with bafilomycin A₁ (10⁻⁴ mol · l⁻¹) caused a further reduction in by 83% and ethylisopropylamiloride (EIPA; 5.10⁻⁴ mol · l⁻¹) completely abolished net HCO ₃ ⁻ reabsorption. The combination of bafilomycin A₁ and EIPA in the luminal perfusate was additive, resulting in net HCO ₃ ⁻ secretion (−66.6±20.8 pmol · min⁻¹;P<0.001) and abolished net fluid reabsorption (from 5.0±0.6 during AMA to 0.2±1.1 nl · min⁻¹;P<0.001). To establish whether HCO ₃ ⁻ secretion via luminal stilbenesensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2′-stilbenedisulphonate (DIDS; 10⁻⁴ mol · l⁻¹) to the perfusate. No effect was found. However, when the same LOH were exposed to luminal DIDS for more than 10 min, the direction of net HCO ₃ ⁻ movement was reversed and net HCO ₃ ⁻ secretion occurred: changed from 90.6±8.8 to −91.9±34.1 pmol · min⁻¹;P<0.01, an effect that was not observed in the control state (undisturbed acid-base balance). Thus, during AMA, neither the luminal Na⁺-H⁺ exchanger nor the H⁺-ATPase are noticeably suppressed. However, pharmacological elimination of both transporters, as well as prolonged exposure of the tubular lumen to DIDS, induced net HCO ₃ ⁻ secretion. This secretory flux may reflect paracellular backflux due to the steeper blood to lumen HCO ₃ ⁻ concentration gradient that presumably prevails in AMA.     

Effect of anaesthetizing the region of the paraventricular hypothalamic nuclei on energy metabolism during exercise in the rat

The ventromedial and posterior hypothalamic nuclei are known to influence glucoregulation during exercise. The extensive projections of the paraventricular hypothalamic nucleus (PVN) to the sympathetic nervous system suggest that the PVN also may be involved in glucoregulation during exercise. The region of the PVN was anaesthetized with bupivacaine before running (26 m min^-1) or continued rest, via previously implanted bilateral brain cannulas aimed at the dorsal aspect of the PVN. Control rats were treated identically to PVN-anaesthetized rats, but were not infused. Blood, for determination of plasma concentrations of metabolites and hormones, was drawn from a tail artery, and ³H-glucose was infused in a tail vein for glucose turnover determinations. At rest, no significant changes in plasma concentrations of metabolites or hormones were induced by anaesthesia of the region of the PVN. During exercise, glucose production and utilization and plasma concentrations of glucose, lactate, glycerol, noradrenaline, adrenaline, corticosterone, and glucagon increased (P < 0.02) and plasma insulin decreased (P < 0.02) in all rats. However, initially in exercise, adrenaline (4.3 ±0.8 vs. 7.9 ± 1.0 nmol 1^-1 in controls, P < 0.05, t= 6 min) and later corticosterone levels (1.37 ± 0.06 vs. 1.69 ± 0.10 nmol 1^-1 in controls, P < 0.05, t = 20 min) were attenuated by PVN anaesthesia. Initially during exercise, glucose utilization was higher and plasma glucose lower in PVN-anaesthetized rats compared to controls (16.6 ± 0.8 vs. 12.7 ± 0.6 μmol min^-1 100 g^-1 and 7.1 ± 0.2 vs. 8.1 ± 0.2 mmol 1^-1, respectively. P < 0.05, t= 6 min) and exercise-induced liver glycogen breakdown was only significant in the controls. In conclusion, the region of the PVN does not influence glucoregulation at rest, but affects glucoregulation during exercise, by stimulating adrenaline and corticosterone secretion during exercise.     

The Impact of heat exposure and repeated exercise on circulating stress hormones

To determine if heat exposure alters the hormonal responses to moderate, repeated exercise, 11 healthy male subjects [age?=?27.1 (3.0) years; maximal oxygen consumption, V˙O_2max?=?47.6 (6.2) ml?·?kg?· min^?1; mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at ≈50% V˙O_2max, separated by a 45-min recovery interval, CEx and HEx conditions), or remained seated for 3?h (CS and HS conditions). Blood samples were analyzed for various exercise stress hormones [epinephrine (E), norepinephrine (NE), dopamine, cortisol and human growth hormone (hGH)]. Passive heating did not alter the concentrations of any of these hormones significantly. During both environmental conditions, exercise induced significant (P < 0.001) elevations in plasma E, NE and hGH levels. At 23°C during bout 1: E?=?393 (199) pmol?·?l^?1 (CEx) vs 174 (85) pmol?·?l^?1 (CS), NE?=?4593 (2640) pmol?·?l^?1 (CEx) vs 1548 (505) pmol?·?l^?1 (CS), and hGH?=?274 (340) pmol?·?l^?1 (CEx)vs 64 (112) pmol?·?l^?1 (CS). At 40°C, bout 1: E?=?596 (346) pmol?·?l^?1 (HEx) vs 323 (181) pmol?·?l^?1 (HS), NE?=?7789 (5129) pmol?·?l^?1 (HEx) vs 1527 (605) pmol?·?l^?1 (HS), and hGH?=?453 (494) pmol?·?l^?1 (HEx) vs 172 (355) pmol?·?l^?1 (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx?=?364 (168) nmol?·?l^?1 vs HS?=?295 (114) nmol?·?l^?1). Compared to exercise at room temperature, plasma levels of E, NE and cortisol were all higher during exercise in the heat (P < 0.001 in all cases). The repetition of exercise did not significantly alter the pattern of change in cortisol or hGH levels in either environmental condition. However, repetition of exercise in the heat increased circulatory and psychological stress, with significantly (P < 0.001) higher plasma concentrations of E and NE. These results indicate a differential response of the various stress hormones to heat exposure and repeated moderate exercise.     

The Effect of Aspirin on Recurrent Fetal Loss in Experimental Antiphospholipid Syndrome

PURPOSE: To evaluate the effect of aspirin treatment upon fetal loss in mice with experimental antiphospholipid syndrome (APLS). MATERIALS AND METHODS: Experimental APLS was induced in pregnant mice by passive transfer of mouse monoclonal anticardiolipin antibody. The mice were treated with high (100μg/d) or low (10μg/d) does of aspirin, using vitaminC(100μg/d or 10μg/d)as a control. The mice were assessed for the presence of lupus anticoagulants (prolonged aPTT), thrombocytopenia, degree of fetal resorption rate and mean embryo and placental weights. RESULTS: The mice with APLS had a higher fetal resorption rate(45.7± 12.2% vs 2.5 ± 0.4%, P<0.001), reduced placenta mean weight(104 ± 8 mgvs 169 ±7mg, P<0.001), prolonged aPTT (94± 14sec vs 39±4sec, P<0.001), and reduced mean platelet count(597± 186 ± 10³/mm³vs 847±51 ± 10³/mm³,P<0.001). The groupof mice with APLS, who were treated with low-dose aspirin, had a lower resorption rate (11.1 ±9.3% vs 45.7±12.2%, P<0.001), a higher placenta mean weight (178 ± 8 mg vs 104 ± 8 mg, P<0.001), a higher mean embryo weight (1042 ± 134 mg vs 721±91 mg, P<0.001), and a lower aPTT (58±15 sec vs 94±14 sec, P, <0.001). Micewho were treated with high-dose aspirin also had a lower resorption rate, although not as much as in the low-dose aspirin group (34.2 ± 12.7% vs 45.7 ± 12.2%, P<0.001). CONCLUSION: Aspirin, especially in low dose, has a protective effect against obstetrical complications associated with experimental APLS.     

Carbohydrate and fat metabolism related to blood lactate in boys and male adolescents

The half maximal constant (k _el) of the relative rate of carbohydrate oxidation (relCHO) was individually approximated (relCHO = 100/(1 + k _el/BLC²) as a function of the blood lactate concentration (BLC) in 11 pre-pubertal boys and 11 male adolescents (age: 11.6 ± 0.1 vs. 16.4 ± 0.2 years, height: 151.6 ± 1.7 vs. 182.4 ± 2.3 cm, body mass: 38.2 ± 1.1 vs. 68.7 ± 2.3 kg, all P < 0.001) during incremental cycle ergometry. k _el explained 89.0 ± 2.2 and 91.9 ± 2.2% of the variance of the reliance on CHO in boys and adolescents respectively (both P < 0.001). No difference in k _el [1.34 ± 0.40 vs. 1.48 ± 0.30 (mmol l⁻¹)²] was found between boys and adolescents. The BLC was lower (P < 0.05) in boys when relCHO was higher than 91.2 ± 2.1 and 92.1 ± 1.3% in boys and adolescents respectively. This seems to explain why the reliance on CHO and the BLC are independent of maturation in the moderate and heavy exercise intensity domain and the BLC but not the relCHO which is higher under severe and maximal exercise conditions in more mature subjects.     

Periparturient rise in fecal egg counts associated with prolactin concentration increase in French Alpine dairy goats

Previous data on periparturient relaxation of immunity during gastrointestinal nematode infection in goats are scarce and conflicting; one study carried out in fiber (Angora) goats showed a positive association of fecal egg counts with prolactin concentrations around parturition, whereas the two other available studies dealing with dairy goats, gave divergent results. The objectives of the study were thus to assess the occurrence of a periparturient rise in fecal egg counts in dairy goats and to examine a possible relationship between the level of milk production and the intensity of the periparturient rise. A total of 28 French Alpine grazing dairy goats naturally infected with Teladorsagia, Trichostrongylus, and Oesophagostomum were allocated into two groups according to their reproductive status; group 1 (n = 7) consisted of nonpregnant lactating animals in the 3^rd month of lactation, whereas group 2 (n = 21) was composed of dry goats at 6 weeks before term. Fecal egg counts, pepsinogen and phosphate blood concentrations, blood eosinophil counts, and prolactin concentrations were individually monitored at weekly intervals for 12 weeks (from midwinter to early spring). The mean fecal egg counts were significantly higher in pregnant goats during the 2 weeks before (668 versus 242 eggs per gram of feces (epg), P < 0.05) and the 2 weeks after (962 versus 279 epg, P < 0.01) parturition as compared with nonpregnant lactating animals. No significant difference was seen in the composition of larval cultures between the two groups of animals, with Oesophagostomum infective larvae being found predominantly, particularly at the time of parturition. Pepsinogen and phosphate concentrations as well as blood eosinophil counts were similar between the two groups throughout the survey and indicated a moderate larval challenge. The mean prolactin concentration measured in pregnant goats was significantly higher (P < 0.01) at the time of parturition (298 versus 130 ng ml⁻¹) and at 4 weeks after parturition (387 versus 193 ng ml⁻¹) than that determined in nonpregnant animals. Furthermore, a significant correlation (r _s = 0.30, df = 79; P < 0.01) between fecal egg counts and prolactin concentrations was recorded for the pregnant goats during the 4-weeks period around parturition. Received: 2 April 1998 / Accepted: 8 June 1998     

Effects of water deprivation and hyperhydration in pregnant and lactating goats

The response to 30 h water deprivation was studied in 7 goats during the last month of pregnancy and during lactation with anestrus as the control period. Plasma osmolality and plasma Na concentration increased by about 4% in pregnant and lactating goats and by about 2% in anestral goats. Plasma AVP concentration rose by about 7 pg/ml in pregnant and lactating goats, but only by about 3 pg/ml during anestrus. PRA was elevated in pregnant animals, but dehydration caused only a minor further rise. Total plasma protein concentration was low in pregnant goats and did not increase during water deprivation, but it did so in lactating animals. Neither the hematocrit nor the plasma K concentration changed in response to dehydration. GFR fell by about 24% in pregnant goats and by 22% in lactating animals, but remained unchanged during anestrus. ERPF fell by 20% in lactating animals, but no consistent effect of the dehydration was seen during pregnancy and anestrus. Urine flow decreased by about 75% during pregnancy, 55% during lactation and 65% during anestrus with the highest urine osmolality observed during anestrus. Milk production was only slightly reduced, but the milk osmolality increased in parallel with that of the blood plasma. When allowed to drink at the end of the water deprivation period, pregnant goats immediately drank 2.5 +/- 0.5 litres, lactating goats 3.3 +/- 0.9 litres and anestral goats 1.1 +/- 0.3 litres. When hyperhydrated, pregnant goats excreted the excessive water more readily and showed less response to exogenous AVP than lactating and anestral animals. In conclusion, pregnant and lactating goats are obviously more susceptible to a shortage of water supply than anestral animals but can easily excrete an excess of water.     

Long-lasting coronary vasoconstrictor effects and myocardial uptake of endothelin-1 in humans

The effect of intravenous administration of the endothelium-derived vasoconstrictor peptide endothelin-1 (ET-1 0.2, 1 and 8 pmol kg^?1 min^?1) on coronary blood flow in relation to plasma ET-1 as well as blood lactate and glucose levels were investigated in six healthy volunteers. Coronary sinus blood flow was measured by thermodilution. Administration of ET-1 elevated arterial plasma ET 35-fold, dose-dependently increased mean arterial blood pressure from 95±5 mmHg to 110±6 mmHg (P<0.01) and reduced heart rate from 64±4 beats min^?1 to 58±4 beats min^?1 (P<0.05) at 8 pmol kg^?1 min^?1. Coronary sinus blood flow was reduced maximally by 23±4% (P<0.01) and coronary vascular resistance increased by 48±11% (P<0.01). Coronary sinus oxygen saturation decreased from 35±1% to 22±2% at 2 min after the infusion (P<0.01). A coronary constrictor response was observed at a 4-fold elevation in plasma ET. The reduction in coronary sinus blood flow lasted 20 min and coronary sinus oxygen saturation was still reduced 60 min after the infusion. Myocardial oxygen uptake or arterial oxygen saturation were not affected by ET-1. Myocardial lactate net uptake decreased by 40% whereas glucose uptake was unaffected. At the highest infusion rate there was a net removal of plasma ET by 24±3% over the myocardium (P<0.05). The results show that ET-1 induces long-lasting reduction in coronary sinus blood flow via a direct coronary vasoconstrictor effect in healthy humans observable at a 4-fold elevation in plasma ET-1. Furthermore, there is a net removal of circulating ET-1 by the myocardium.     

Renal tubular transport and metabolism of carboxyamidated and glycine-extended gastrins in pigs

Renal handling of postprandial and intravenously administered gastrin was investigated in anaesthetised pigs. The fractional extraction of postprandial carboxyamidated and glycine-extended gastrin in the kidneys was 0.21 ± 0.01 and 0.16 ± 0.02, but the respective urinary clearance comprised only 0.57 ± 0.03 and 0.44 ± 0.05% of the GFR (P < 0.02). The respective total body clearance of carboxyamidated and glycine-extended gastrin-17 (gastrin-17 and gastrin-17Gly) during continuous infusion was 22.9 ± 1.5 and 19.6 ± 1.4 mL kg^?1 min^?1 (NS), and the renal fractional extraction of the peptides was 0.31 ± 0.03 and 0.29 ± 0.05, respectively. The kidneys accounted for 8% of total body clearance of gastrin-17. Renal filtration rate of gastrin-17 exceeded renal extraction rate (9.739 ± 0.487 vs. 6.407 ± 0.321 pmol min^?1). Urinary clearance of gastrin-17 and gastrin-17Gly amounted only 0.91 ± 0.16 and 0.13 ± 0.03%, respectively, of the GFR (P < 0.01), but urinary excretion rate correlated with the filtered amount of the peptides (r = 0.93, P < 0.01). Neither was a renal plasma threshold recorded nor was a T_m value for tubular uptake or degradation of gastrin achieved in spite of supraphysiological plasma levels of the peptides. The results indicate that filtered gastrin is almost completely removed in the renal tubules, primary by metabolism although part of the absorbed peptides may be returned to the circulation in intact form. The process for uptake or metabolism has a high capacity but varies with the molecular form of gastrin.     

Effects of intensified endurance training on the concentration of Na,K-ATPase and Ca-ATPase in human skeletal muscle

Thirty-nine moderately endurance trained males increased their normal training programme of 2.2 h week^-1 with an average training intensity of 65 % of maximum heart rate (HR_max) to 2.7 h week^-1 and a mean intensity of 78% of HR_max. Performance tests and measurements of the total concentrations of Na,K-ATPase (³H-ouabain binding) and Ca-ATPase, fibre type distribution and fibre area were performed in biopsies from the vastus lateralis muscle before and after increased training. The 6 weeks of training elevated Vo_2max from 54.9 + 3.1 to 58.3±3.0 ml 0₂ min^-1 kg^-1 (P < 0.0001). Exercise time to exhaustion at 86% of Fo_2max (pre-training) increased from 35 ±8 to 61 + 17 min (P < 0.0001). The concentration of Ca-ATPase was unaffected by the intensified training (6.74 ± 1.03 vs. 6.68+ 1.07 nmol g wet wt^-1), but the concentration of Na,K-ATPase increased from 307±43 to 354 + 59 pmol g wet wt ' (P < 0.0001). The relative distribution of FT-fibres was correlated with the concentration of Ca-ATPase (r = 0.72, P < 0.0001). The data support the view that intensive training induces an upregulation of the concentration of skeletal muscle Na,K-ATPase, but no change in the total capacity for reaccumulation of Ca²⁺ into the SR. There was no correlation between the concentrations of Na,K-ATPase, Ca-ATPase and indices of endurance performance.