心房钠尿因子对麻醉家兔局部血流的影响

在42只麻醉家兔,观察了静脉注射心房肽Ⅱ(AtriopeptinⅡ,APⅡ)对局部血流量以及动脉内注射 AP Ⅱ 对局部血管阻力的影响。结果如下:(1)静脉注射 APⅡ(30μg/kg)5min后,平均动脉压(MAP)降低11.0±1.5mmHg(n=8,M±SE,下同),与溶剂对照组相比有明显差异(P相似文献   

Effect of thyroidectomy on cardiovascular responses to hypoxia and tyramine infusion in fetal sheep

Fetal sheep were thyroidectomized at 80 days' gestation and reoperated at 118-122 days for insertion of vascular catheters. The effects of hypoxaemia and intravenous tyramine infusion on plasma catecholamine concentrations, blood pressure and heart rate were then determined in experiments at 125-135 days' gestation. Age matched intact fetuses were also studied. Thyroidectomy was associated with increased concentrations of noradrenaline, adrenaline and dopamine in some thoracic and abdominal organs, increased noradrenaline concentrations in the cerebellum, and decreased adrenaline concentrations in the hypothalamus, cervical spinal cord, and superior cervical and inferior mesenteric ganglia. Arterial pressure was significantly lower in the thyroidectomized fetuses (34.0 +/- 0.15 mmHg) than in intact fetuses (44.7 +/- 0.2 mmHg; p less than 0.001). In contrast, plasma noradrenaline concentrations were significantly higher in the thyroidectomized fetuses (2.04 +/- 0.25 ng/ml) compared to the intact fetuses (0.99 +/- 0.08 ng/ml; P less than 0.001). In the intact fetuses there was a significant increase in plasma noradrenaline concentration and blood pressure during hypoxaemia, and bradycardia at the onset of hypoxaemia. In contrast, in the thyroidectomized fetuses hypoxaemia did not cause significant change in plasma catecholamine concentrations, blood pressure or heart rate. Infusion of tyramine produced a 1.9-fold increase of plasma noradrenaline in thyroidectomized fetuses compared to a 9.2-fold increase in the intact fetuses (P less than 0.05). Tyramine infusion caused a similar proportional increase of blood pressure in both thyroidectomized and intact fetuses. Heart rate decreased during the tyramine-induced hypertension in the intact fetus, but increased in the thyroidectomized fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)     

ECG wave form, short term heart rate variability and plasma catecholamine concentrations in intrauterine growth-retarded guinea-pig fetuses

Electrocardiogram waveform, short term heart rate variability and catecholamine concentrations were studied with maternally-induced anesthesia in eleven growth-retarded guinea-pig fetuses and their normal-sized littermates at 63 days of gestation. Intrauterine growth retardation was induced by unilateral uterine artery ligation performed between day 32 and 35. In the growth-retarded group fetal weight was reduced by 45%. Blood gases, acid-base status and oxygen content were similar in the two groups. The growth-retarded guinea-pig fetuses were hypoglycemic and demonstrated a rise in hemoglobin concentration. The T/QRS ratio (T wave amplitude/QRS amplitude) was similar in both groups. The short-term heart rate variability was significantly reduced in the growth-retarded group. Plasma catecholamine concentrations were increased in growth-retarded fetuses but differed only significantly for noradrenaline compared to controls. We suggest that similar T/QRS ratio in both groups of fetuses indicates that aerobic myocardial metabolism is maintained among growth-retarded fetuses. The mechanism behind the reduced variability is unclear.     

A fetal-instrumented model to study age-specific responses to leukotriene D4 and prostaglandin D2 in unsedated newborn lambs

Sequential studies of the pulmonary vascular response to leukotriene D4 (LTD4) and prostaglandin D2 (PGD2) in the immediate newborn period were performed in lambs, instrumented in utero and delivered vaginally. Compounds were tested in fully conscious 1.5-day-old lambs and the study was repeated 1 week later. Bolus injections of PGD2 (0.05-2.0 micrograms/kg) or LTD4 (0.01-1.0 micrograms/kg) were made into the main pulmonary artery or aorta while pulmonary blood flow and aortic, pulmonary artery, and left and right atrial pressures were monitored continuously. PGD2 was a systemic constrictor regardless of age. In lambs 1.5 days of age, it decreased pulmonary vascular pressure and resistance by 6% (p less than 0.05) and 15% (p less than 0.05), respectively, while 1 week later it increased pulmonary vascular resistance by 18% (p less than 0.05). In contrast, LTD4 was a pulmonary and systemic vasoconstrictor in both the early and late newborn, the threshold dose being between 0.01 and 0.05 micrograms/kg at either age. The decrease in pulmonary blood flow and the increase in pressure and resistance were greater in older animals. In lambs 1.5 days of age, LTD4 (1 micrograms/kg) increased pulmonary vascular resistance by 66.1% (p less than 0.05) and 1 week later by 210% (p less than 0.001). These sequential observations in the same animal indicate that unlike PGD2, LTD4 is a pulmonary vasoconstrictor regardless of age, and its effectiveness increases significantly with age. These results support previous reports that PGD2 action in the pulmonary circulation changes shortly after birth from dilation to constriction.     

Bestatin results in pathophysiological changes similar to preeclampsia in rats via induction of placental apoptosis.

OBJECTIVE: To establish a rat preeclampsia model with fetoplacental growth restriction caused by bestatin via induction of placental apoptosis. STUDY DESIGN: 200 mg/kg/day of bestatin or saline as a control were infused intraperitoneally into pregnant Wistar rats from 15 days' gestation. In the first experiment, maternal blood pressure and proteinuria were examined during the pre- and postpartum periods. In the second experiment, cesarean sections were performed at 20 days' gestation and the weights of pups and placentas, and levels of proteinuria and placental apoptosis were examined. RESULTS: Physiological decrease of blood pressure in late pregnancy was not detected in the bestatin group but proteinuria level at 20 days' gestation was elevated. The weights of pups and placentas in the bestatin group were significantly lower than those in the controls, bestatin strongly inducing apoptosis in the placenta. CONCLUSION: Bestatin may cause a preeclampsia-like condition through induction of placental apoptosis.     

Foetal circulatory responses to arrest of uterine blood flow in sheep: effects of chemical sympathectomy.

Acute foetal asphyxia, caused by arrest of uterine blood flow, increases both sympathetic activity and peripheral vascular resistance and decreases blood flow to peripheral organs (Jensen et al., J. Dev. Physiol., 9, 543-559). The rapidity and uniformity of this peripheral vasoconstriction suggest that the sympatho-neuronal system may reflexly cause these initial blood flow changes during acute asphyxia. To test this hypothesis, we studied 5 intact and 6 chemically sympathectomized (6-hydroxy-dopamine, 46.1 +/- 6 mg/kg foetal weight) chronically prepared normoxaemic foetal sheep in utero at 0.9 of gestation. Organ blood flows (microsphere method), plasma concentrations of catecholamines, vasopressin, and angiotensin II, acid-base balance and blood gases were measured before, during and after arrest of uterine blood flow for 2 min, i.e., at 0, 1, 2, 3, 4 & 30 min. In intact foetuses there was a progressive increase in arterial blood pressure and a rapid circulatory centralization in favour of the brain stem and heart and at the expense of most of the peripheral organs. The changes in peripheral blood flow during and after asphyxia were well reflected by those in the skin and scalp. In chemically sympathectomized foetuses, arterial blood pressure fell transiently at 1 min of asphyxia and cardiac output was redistributed towards the carcass and intestinal organs at the expense of the heart, spinal medulla, and placenta. We conclude that in foetal sheep at 0.9 of gestation, the short-term adaptation to arrest of uterine blood flow is a rapid and profound peripheral vasoconstriction to effect an increase in arterial blood pressure. This initial response during circulatory centralization, which is necessary to increase or maintain blood flow to the heart, brain stem, and placenta, is blunted by sympathectomy. Thus, the foetal sympatho-neuronal system is important for short-term adaptation to and intact survival of asphyxia.     

Effect of metabolic acidosis on fetal renal haemodynamics

The effects of metabolic acidosis on renal haemodynamics and intrarenal blood flow distribution was studied in two groups of chronically-catheterized fetal sheep between 122 and 130 days of gestation. One group (experimental group) was studied before and during infusion of 1.1 M lactic acid, whereas the second group received on infusion of dextrose 5% (w/v) in water and served as a time-control group. Infusion of lactic acid for 2 h decreased fetal arterial pH from 7.37 +/- 0.01 to 6.95 +/- 0.02, did not change arterial blood pressure, but produced a significant decrease in renal blood flow (41 +/- 3 to 33 +/- 7 ml/min, P less than 0.05) and a significant increase in renal vascular resistance (1.42 +/- 0.13 to 1.86 +/- 0.18 mmHg/ml/min, P less than 0.05). Moreover, a significant decline in cortical blood flow was also observed in the outer portion of the renal cortex during lactic acidosis. Taken together, these results suggest that metabolic acidosis produces significant changes in fetal renal haemodynamics not associated with changes in arterial blood pressure.     

The effects of prostacyclin and thromboxane analogue (U46619) on the fetal circulation and umbilical flow velocity waveforms

In placental insufficiency and pre-eclampsia the relative production rates of prostacyclin and thromboxane by the placenta and umbilical vessels are altered and the Doppler umbilical flow velocity waveform shows a high resistance pattern. To investigate the control of umbilical placental blood flow by those eicosanoids either prostacyclin (10 micrograms/min), or the thromboxane analogue U46619 (10 ng/min) was infused into the distal aorta of 12 chronically catheterized fetal lambs at day 125. Thromboxane produced a rise in mean arterial pressure and a rise in the systolic diastolic ratio of the umbilical artery flow waveform (2.6 to 3.1; P less than 0.05). Umbilical blood flow did not change and there was no evidence of altered flow to other organs. Prostacyclin caused a fall in fetal mean arterial pressure and a decrease in the umbilical artery systolic diastolic ratio (2.9 to 2.4; P less than 0.05). Prostacyclin produced a three-fold increase in lung perfusion (and the onset of fetal breathing movements) and this was associated with a 90% reduction in muscle blood flow (hindlimb muscle flow reduced from 12.5 to 1.1 ml.min-1 100g-1; P less than 0.01). We conclude that the local release of thromboxane in the fetal placental vascular bed could account for the rise in systolic diastolic ratio seen in umbilical placental insufficiency.     

Effects of indomethacin on fetal renal function, renal and umbilicoplacental blood flow and lung liquid production.

The effects of indomethacin (10 mg/kg i.v. to the ewe and 12 mg/kg i.v. to the fetus) were examined in 8 chronically catheterized fetal sheep (117-138 days gestation). These doses suppressed fetal 6-keto-prostaglandin F1 alpha and thromboxane B2 levels. Fetal arterial PO2 increased (P < 0.01); PCO2 (P < 0.001) and pH fell (P < 0.001) and arterial pressure did not change. Placental blood flow increased in 4 of the 5 fetuses in which blood flows were measured. Lung liquid flow rate fell (P < 0.001). Fetal renal blood flow did not change but its distribution did, i.e. flow to the inner part of the renal cortex decreased (P < 0.05). Urine flow rates did not change but there was a natriuresis (P < 0.02), kaliuresis (P < 0.02) and chloriuresis (P < 0.02). Urinary osmolality rose (P < 0.001) and free water clearance fell (P = 0.004). It is concluded that when indomethacin is administered to both ewe and fetus, the resulting fall in prostaglandin I2 and thromboxane A2 levels causes marked changes in fetal blood gas status, renal function and lung liquid production. These effects are more profound than those seen when indomethacin is given only to the fetus. They do not however, explain the reason why clinical use of indomethacin is associated with a reversible oligohydramnios.     

Oxidative stress contributes to chronic leg vasoconstriction in estrogen-deficient postmenopausal women.

Basal whole leg blood flow and vascular conductance are reduced in estrogen-deficient postmenopausal compared with premenopausal women. The underlying mechanisms are unknown, but oxidative stress could be involved. We studied 9 premenopausal [23 +/- 1 yr (mean +/- SE)] and 20 estrogen-deficient postmenopausal (55 +/- 1 yr) healthy women. During baseline control, oxidized low-density lipoprotein (LDL), a marker of oxidative stress, was 50% greater in the postmenopausal women (P < 0.001). Basal whole leg blood flow (duplex ultrasound of femoral artery) was 34% lower in the postmenopausal women because of a 38% lower leg vascular conductance (P < 0.0001); mean arterial pressure was not different. Intravenous administration of a supraphysiological dose of the antioxidant ascorbic acid increased leg blood flow by 15% in the postmenopausal women as a result of an increase in leg vascular conductance (both P < 0.001), but it did not affect leg blood flow in premenopausal controls or mean arterial pressure in either group. In the pooled subjects, the changes in leg blood flow and leg vascular conductance with ascorbic acid were related to baseline plasma oxidized LDL (r = 0.46 and 0.53, P < 0.01) and waist-to-hip ratio and total body fat (r = 0.41-0.44, all P < 0.05). Our results are consistent with the hypothesis that oxidative stress contributes to chronic leg vasoconstriction and reduced basal whole leg blood flow in estrogen-deficient postmenopausal women. This oxidative stress-related suppression of leg vascular conductance and blood flow may be linked in part to increased total and abdominal adiposity.     

Maximal vascular leg conductance in trained and untrained men

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.     

Insignificant response of the fetal placental circulation to arterial hypotension in sheep

Infusion of the angiotensin-converting enzyme inhibitor enalaprilat into fetal sheep caused a profound arterial hypotension within days. Five fetal lambs were infused with enalaprilat for 8 days starting at day 128 of gestation. Total accumulated dose was 0.30 ± 0.11 mg/kg. Arterial pressure decreased from 43.6 to 25.6 mmHg; venous pressure did not change. Biventricular output was not statistically significantly changed; placental blood flow decreased almost in proportion to the decrease in pressure but the increase in somatic flow was not statistically significant. There were no significant changes in pressure 30 min after the initial 50-μg loading dose of enalaprilat. However, the arterial pressure responses to test doses of ANG I were largely abolished. After 1 day, however, there was a significant decrease in somatic vascular resistance, which became stronger with time, but almost no decrease in the placental resistance. We conclude that the fetal somatic circulation exhibits a slow but strong decrease in resistance but that the response to hypotension is weak or absent in the fetal placenta, possibly because it is already fully relaxed.     

Placental blood flow in rats fed alcohol before and during gestation

Female Sprague-Dawley rats were either given 20% alcohol in drinking water and solid diet $\text{ad libitum}$ (alcohol group) or were pair-fed to the alcohol group (pair-fed group) or were given water and solid diet $\text{ad libitum (ad libitum}$ group) for four weeks. They were then mated and the alcohol group was changed to 30% alcohol in water. On day 20 of gestation each rat was injected with ⁵⁷Co-labeled microspheres into the left ventricle and radioactivity was determined in the placentas and kidneys. Cardiac output and blood flow to the placentas and kidneys was calculated. Fetuses and placentas were weighed, and the osmolality of the maternal plasma and water content of the muscle was determined. Cardiac output and blood flow to the kidneys did not differ among the three groups. Blood flow to the placenta, whether expressed as m1/min/g placenta or m1/min/placenta, or as % of cardiac output was significantly reduced in the alcohol group compared with the pair-fed and $\text{ad libitum}$ groups, which did not differ from one another. Fetuses were significantly lighter and placentas were significantly heavier in the alcohol group than in the other two groups. Plasma osmolality was increased and muscle water was decreased about 7% in the alcohol group, indicating a moderate degree of dehydration. It is concluded that chronic alcohol consumption leads to a redistribution of blood, with less blood supplying the placentas. This may contribute to the growth retardation seen in fetal alcohol syndrome.     

Plasmodium berghei: malaria infection causes increased cardiac output in rats, Rattus rattus

Thirty-two 4-week-old male Wistar rats were infected with Plasmodium berghei malaria. On Days 12 through 14, blood volume, arterial blood pressure, right ventricular pressure, heart rate, cardiac output, stroke volume, hematocrit, and vascular resistances were determined. All of the cardiovascular parameters measured, with the exception of calculated pulmonary vascular resistance, changed progressively as the peripheral blood parasitemia increased. With a rising parasitemia, cardiac output increased, despite a reduced heart rate. The highest parasitemia of 63% was accompanied by a doubling of the normal cardiac output. The relationship between parasitemia and cardiac output can be described by the equation, cardiac output = (6.14) x % parasitemia + 452 ml/min/kg. The mean arterial blood pressure was lower than controls when parasitemia exceeded 20%, whereas systolic right ventricular pressure was elevated only at the highest parasitemias. When noninfected control rats were compared with those animals having parasitemias greater than 40%, in the infected animals, mean arterial pressure was 28% lower (P less than 0.01) and systolic right ventricular pressure rose by 21% (P less than 0.02). A 50% decline was observed in the total peripheral vascular resistance (P less than 0.01), although the pulmonary resistance was apparently unchanged. With P. berghei infection, there is also a marked anemia, an increase in plasma volume, and a 16% increase in blood volume (% body weight). It is concluded from these results that although the hemodynamic changes previously reported in the literature indicate that infection with malaria may result in focal blockages in microvessels and poor tissue perfusion, the total systemic effect, in the rat, is an increase in cardiac output secondary to a reduced peripheral resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fetal pulmonary vasodilation and vasoreactivity during metabolic acidaemia

We studied the pulmonary vascular response to progressive metabolic acidaemia and to an abrupt increase in oxygen tension during metabolic acidaemia in 8 chronically-prepared fetal sheep. Left pulmonary artery blood flow was measured by electromagnetic flow transducer. Two and a half hour infusion of NH4Cl into the fetal inferior vena cava caused pH to fall to 6.94 +/- 0.01 from 7.37 +/- 0.01 (P less than 0.001). During this period of progressive metabolic acidaemia, left pulmonary artery blood flow increased from a baseline value of 60 +/- 8 to 105 +/- 14 ml.min-1 (P less than 0.002). Pulmonary artery pressure did not change significantly and calculated pulmonary vascular resistance fell indicating fetal pulmonary vasodilation. PO2 rose significantly (19.8 +/- 0.7 to 24.1 +/- 1.8 torr; P less than 0.03) and oxygen saturation fell (54.6 +/- 2.8% to 38.9 +/- 3.5%; P less than 0.001) confirming a rightward shift of the oxyhaemoglobin dissociation curve. During acidaemia, administration of 100% oxygen to the ewe further increased fetal PO2 to 37.9 +/- 2.3 torr within 10 min (P less than 0.001) and this increase in PO2 was accompanied by an increase in left pulmonary artery blood flow (P less than 0.001), a fall in pulmonary artery pressure (P less than 0.03) and a decrease in pulmonary vascular resistance (P less than 0.001) indicating further vasodilation. The response of the fetal pulmonary circulation to a 2-h period of increased oxygen tension was qualitatively similar in acidaemic and non-acidaemic fetuses. We conclude that the progressive metabolic acidaemia imposed by these experimental conditions increases pulmonary blood flow likely through an increase in fetal PO2 and that metabolic acidaemia does not block the normal vasodilatory response to an increase in oxygen tension.     

The blood supply to the heart and brain in the growth retarded guinea pig fetus

Blood flow to the heart and brain of 31 control and 15 growth retarded (IUGR) guinea pig fetuses was measured between 60-64 days of pregnancy by the microsphere technique. The animals were anaesthetized with diazepam and pentobarbitone. Brain weight was reduced by 11% in IUGR fetuses from 2.61 +/- 0.03 to 2.33 +/- 0.05 g and heart weight by 39% from 0.42 +/- 0.01 to 0.25 +/- 0.01 g, compared to a decrease in body weight of 42% from 83.6 +/- 2.3 to 48.2 +/- 2.2 g. The myocardial blood flow of control animals was negatively correlated to arterial O2 content (r = 0.78, P less than 0.001) and arterial pH (r = 0.68, P less than 0.001). Brain blood flow was inversely correlated to arterial O2 content in control fetuses (r = 0.79, P less than 0.001). Eight regions of the brain were examined: cerebral hemispheres, caudate nucleus, hippocampus, thalamus + hypothalamus, cerebellum, pons, and medulla. Regional blood flows were significantly correlated to fetal oxygenation in the controls. Growth retarded fetuses were characterized by poor oxygenation (arterial O2 content less than or equal to 2.5 mM) and were frequently acidaemic (pH less than 7.20). No relation could be demonstrated between the myocardial or cerebral blood flows of IUGR fetuses and arterial O2 content or pH. It is concluded that growth retarded fetuses are unable to maintain O2 delivery to the brain and myocardium by increases in blood flow. Although O2 extraction could be increased to meet the O2 requirements of the heart, IUGR fetuses had a lower rate pressure product, suggesting a decline in myocardial O2 consumption.(ABSTRACT TRUNCATED AT 250 WORDS)     

Umbilical cord compression produces pulmonary hypertension in newborn lambs: a model to study the pathophysiology of persistent pulmonary hypertension in the newborn

We investigated the effects of chronic intrauterine hypoxaemia produced by prolonged partial umbilical cord compression on the circulation shortly after birth in lambs. Vascular catheters were inserted in 10 fetal sheep at 120 to 130 days gestation to measure descending aortic blood gases, arterial pH, and arterial O2 saturation. An inflatable silicone rubber balloon cuff was also placed around the umbilical cord. After recovery and the return of descending aortic blood gases to the normal range, the balloon was gradually inflated, decreasing the PaO2 from 21.2 +/- 3.6 to 17.5 +/- 1.3 mm Hg and the arterial O2 saturation from 57.1 +/- 9.2% to 37.2% +/- 5.2. After 14.3 +/- 3.7 days of partial umbilical cord compression, the lambs were delivered by Caesarean section, instrumented to measure systemic and pulmonary arterial, right atrial and pulmonary arterial wedge pressures, pulmonary and systemic blood flows, and mechanically ventilated. Five normal lambs were also studied. From 60 to 120 min after delivery, when compared to normal lambs, the umbilical compression lambs had an increased pulmonary arterial pressure (P less than 0.05) pulmonary vascular resistance (P less than 0.05), and right atrial pressure (P less than 0.05) with similar arterial blood gases. In both groups, hypoxic ventilation produced an increase in pulmonary arterial pressure (P less than 0.05) which on return to room air ventilation decreased to baseline in the normal lambs but not in the umbilical cord compression lambs (P less than 0.05). Prolonged partial umbilical cord compression produces chronic fetal hypoxaemia and pulmonary arterial hypertension after birth. This may represent a model to study the pathophysiology of persistent pulmonary hypertension syndrome.     

Left ventricular systolic time intervals and plasma noradrenaline concentrations during acute hypovolaemia in newborn infants

Left ventricular systolic time intervals and plasma noradrenaline concentrations were determined in twelve newborn infants during acute moderate hypovolaemia. Rapid withdrawal of 8.5 ml of blood per kg body weight shortened the left ventricular ejection time from 204 to 176 msec (P less than 0.001) and increased the plasma noradrenaline concentration from 3.4 to 4.0 nmol/l (P less than 0.05). Systemic blood pressure was unchanged. It is concluded that even a moderate reduction in blood volume is associated with marked changes in left ventricular dynamics. The shortening of left ventricular ejection time during hypovolaemia probably reflects left ventricular adaptation to decreased volumes and response to increased noradrenaline release.     

Pressure-flow relations of diaphragm and vital organs with nitroprusside-induced vasodilatation

We determined maximal conductance in the diaphragm and other vital organs in 14 anesthetized dogs, weighing 22.8 +/- 4.2 kg, which were given maximal vasodilating doses of nitroprusside (mean dose 13.9 +/- 4.3 micrograms X kg-1 X min-1) and the blood pressure was lowered in stages by hemorrhage. Blood flow in the diaphragm, brain, heart, kidney, gut, and quadriceps was measured with radiolabeled microspheres. To ensure maximal vasodilatation of diaphragmatic vessels, we stimulated the phrenic nerves to produce diaphragmatic contractions at 0.3 Hz. The mean cardiac output was 2.13 +/- 0.42 l/min (thermodilution) before nitroprusside and 4.68 +/- 1.45 after (P less than 0.001). Nitroprusside failed to break the autoregulation of the brain. Pressure-flow relations (P-F) in other regions were linear (r = 0.70 +/- 0.03, P less than 0.001) and blood pressure at zero flow (X-intercept) was always greater than venous pressure (diaphragm = 11, kidney = 19, heart = 8, gut = 8, quadriceps = 32 mmHg). The flow to the diaphragm (Qdi) could be predicted by Qdi (ml X min-1 X g-1) = [(3.13 +/- 0.56) X Pa X 10(-2)] -0.52 (r = 0.71), where Pa is mean arterial pressure. The maximal vascular conductance (i.e., slope of the P-F relation) of the diaphragm was 27% of the conductance in the kidney, 87% of the value in the gut, and 42% of that in the heart. In conclusion the maximal diaphragmatic blood flow at a given blood pressure is much larger when the muscle is stimulated than is observed in spontaneously breathing animals.     

Circulating PgF2alpha and nutritional parameters at parturition in dairy cows with and without retained placenta: Relation to prepartum diet

Reproductive and biochemical parameters were studied at parturition in multiparous single-carrying Holstein cows. These were compared in animals with (n=14) and without (n=40) a retained placenta and then according to 2 prepartum diets (corn silage/concentrate, n=44; grass silage/concentrate, n=10) in cows with and without retained placentas. Cows with retained placentas had a 4-day shorter gestation period and gave birth to 5 kg-lighter calves than cows without retained placentas. Furthermore, their plasma PGFM -PgF2alpha main metabolite- (3325 vs 5675 pg/ml; P<0.01) and glucose (79.2 vs 95.2 mg/100ml; P<0.05) levels were lower and their protein concentration was higher (85.7 vs 76.5 g/l; P<0.05) than those of cows without retained placentas. Retained placenta incidence in cows fed grass-silage was higher than in cows fed corn-silage (60% vs 18.2%; P<0.05). Cows with retained placentas and fed corn silage had shorter gestation lengths, gave birth to lighter calves, and had less circulating glucose at calving (77.6 vs 96.5 mg/100ml; P<0.05) than cows without retained placentas and fed the same forage. Cows with retained placentas and fed grass silage had less PGFM (2172 vs 4530 pg/ml; P<0.05) than cows without retained placentas and fed the same forage. Calving number, sex ratio and preceeding milk yield were not different between the two groups of cows whatever their prepartum diet. In the dairy cow, retained placenta could be due to a PgF2alpha or an energy deficiency at calving. Roles of the dietary polyunsaturated fatty acids toward the Pg synthesis and of the energy supply before calving in relation to retained placenta are discussed here.