Effect of different prostaglandins on intrauterine pressure and uterine motility during diestrus in experimental cows

Prostaglandins are widely used in herd management due to their luteolytic properties. They have also a direct effect on the myometrium. We hypothesized, that dissimilar prostaglandin preparations would differ as to their contractile effect. Intrauterine pressure was recorded during the diestrus of lactating dairy cows using a transcervically placed intraluminal pressure microtransducer. After recording physiologic uterine motility for 30 min, prostaglandins (dinoprost, DL-cloprostenol, D-cloprostenol) or a placebo was administered intramuscularly, followed by a 2-h recording period. Significant differences were found for the area under the curve (P < or = 0.05) and mean amplitude (P < or = 0.05), whereas the number of spikes per 15 min and the baseline pressure during the last 3 min of every recording period did not differ significantly among treatments. Peak values for area under the curve and mean amplitude were found between 15 and 30 min after administration of DL-cloprostenol, while dinoprost yielded the steadiest plateau from this period until the end of the recording session. These results contrast with those of earlier studies comparing prostaglandins after intravenous administration.     

Effect of estrogen on cerebrovascular prostaglandins is amplified in mice with dysfunctional NOS

Chronic estrogen treatment increases endothelial vasodilator function in cerebral arteries. Endothelial nitric oxide (NO) synthase (eNOS) is a primary target of the hormone, but other endothelial factors may be modulated as well. In light of possible interactions between NO and prostaglandins, we tested the hypothesis that estrogen treatment increases prostanoid-mediated dilation using NOS-deficient female mouse models, i.e., mice treated with a NOS inhibitor [N(G)-nitro-l-arginine methyl ester (l-NAME)] for 21 days or transgenic mice with the eNOS gene disrupted (eNOS(-/-)). All mice were ovariectomized; some in each group were treated chronically with estrogen. Cerebral blood vessels then were isolated for biochemical and functional analyses. In vessels from control mice, estrogen increased protein levels of eNOS but had no significant effect on cyclooxygenase (COX)-1 protein, prostacyclin production, or constriction of pressurized, middle cerebral arteries to indomethacin, a COX inhibitor. In l-NAME-treated mice, however, cerebrovascular COX-1 levels, prostacyclin production, and constriction to indomethacin, as well as eNOS protein, were all greater in estrogen-treated animals. In vessels from eNOS(-/-) mice, estrogen treatment also increased levels of COX-1 protein and constriction to indomethacin, but no effect on prostacyclin production was detected. Thus cerebral blood vessels of control mice did not exhibit effects of estrogen on the prostacyclin pathway. However, when NO production was dysfunctional, the impact of estrogen on a COX-sensitive vasodilator was revealed. Estrogen has multiple endothelial targets; estrogen effects may be modified by interactions among these factors.     

The action of prostaglandins on GA3 controlled responses I. Induction of barley endosperm acid phosphatase activity by prostaglandins E1 and E2

The effect of PGE₁ and PGE₂ on the induction of acid phosphataseactivity in embryoless barley half-seeds was examined. Thesecompounds were found to promote the total amount of enzyme synthesizedas well as the amount released into the medium to nearly thesame levels obtainable when these seeds are incubated in GA₃or cyclic AMP. The enzyme induction by PGE₁ and PGE₂ was inhibited by cycloheximide,ABA, 6-methyl purine and acetylsalicyclic acid, but not by AMO-1618.A time course for the induction of acid phosphatase activityby PGE₁ and PGE₂ lagged behind by 9 hr a similar time courseobtained when seeds were incubated in GA₃ or cyclic AMP. Someof the implications of these results are discussed. (Received May 6, 1973; )     

Contribution of arterial blood pressure and PaCO2 to the cerebrovascular responses to motor stimulation

Motor stimulation induces a neurovascular response that can be detected by continuous measurement of cerebral blood flow (CBF). Simultaneous changes in arterial blood pressure (ABP) and Pa(CO(2)) have been reported, but their influence on the CBF response has not been quantified. Continuous bilateral recordings of CBF velocity (CBFV), ABP, and end-tidal CO(2) (ET(CO(2))) were obtained in 10 healthy middle-aged subjects at rest and during 60 s of repetitive, metronome-controlled (1 Hz) elbow flexion. A multivariate autoregressive-moving average model was adopted to quantify the relationship between beat-to-beat changes in ABP, breath-by-breath ET(CO(2)), and the motor stimulus, represented by the metronome on-off signal (inputs), and the CBFV response to stimulation (output). All three inputs contributed to explain CBFV variance following stimulation. For the ipsi- and contralateral hemispheres, ABP explained 20.3 ± 17.3% (P = 0.0007) and 19.5 ± 17.2% (P = 0.01) of CBFV variance, respectively. Corresponding values for ET(CO(2)) and metronome signals were 22.0 ± 24.2% (P = 0.008), 24.0 ± 24.1% (P = 0.037), 32.7 ± 22.5% (P = 0.0015), and 43.2 ± 25.1% (P = 0.013), respectively. Synchronized population averages suggest that the initial sudden change in CBFV was largely due to ABP, while the influence of ET(CO(2)) was more erratic. The component due to elbow flexion showed a well-defined pattern, with rise time slower than the main CBFV change but reaching a stable plateau after 15 s of stimulation. Identifying and removing the influences of ABP and Pa(CO(2)) to motor-induced changes in CBF should lead to more robust estimates of neurovascular coupling and better understanding of its physiological covariates.     

Cell membrane mechanism of action of prostaglandins E1 and F2 alpha on thrombocyte function

PGE1 and PGF2 alpha were shown to exert an opposite action on Na, K-ATPase activity and protein fluorescence of the platelet membranes. The effect of the prostaglandins appeared to be unidirectional as regards the erythrocytic membranes. The prostaglandins were demonstrated to increase viscosity of the lipid bilayer and its permeability by uni- and bivalent cations.     

Effect of prostaglandins E1, E2 and F2alpha on neutrophil aggregation.

Recently we have found that chemotactic factors stimulate neutrophils in suspension to aggregate. Because of an obvious analogy to platelet aggregation, we examined the influence of three prostaglandins on this process. Prostaglandins E1, E2 and F2alpha alone did not cause aggregation of the neutrophils but were able to partially inhibit the aggregation response induced by the synthetic chemotactic tripeptide, formyl-methionyl-leucyl-phenylalanine. The minimal inhibitory concentrations for prostaglandins E1, E2 and F2alpha were 10(-7), 10(-6) and 10(-5)M, respectively. These results are similar to those found for the prostaglandin-induced inhibition of platelet aggregation. It may be, therefore, that neutrophil aggregation, like platelet aggregation, is modulated by intracellular prostaglandins and other products of arachidonic acid metabolism.     

Effect of phentolamine on the reflex increase in arterial pressure

Experiments were carried out in anaesthetized and curarized cats to study the effects of the alpha-blocker phentolamine on arterial pressor response to stimulation of group I afferent fibers from gastrocnemius-soleus muscles. It has been found that increasing doses of phentolamine given i.v. cause a decreasing pressor response until complete disappearance occurs at 2.5 mg/Kg. It is concluded that pressor response is present only when the adrenergic control system is effective and, therefore, it is due mainly to an increase in peripheral vascular resistances.