FOETAL AND MATERNAL HORMONAL CHANGES PRECEDING NORMAL BOVINE PARTURITION

1977 ◽  
Vol 84 (3) ◽  
pp. 653-662 ◽  
Author(s):  
J. T. Hunter ◽  
R. J. Fairclough ◽  
A. J. Peterson ◽  
R. A. S. Welch

ABSTRACT Successful chronic cannulation of the foetal posterior vena cava and maternal utero-ovarian and jugular veins in five Jersey cows between days 240 and 260 of gestation enabled changes in plasma hormone levels preceding calving to be monitored. All cows delivered live calves within the expected range of gestation for the breed. Corticosteroids were assayed by competitive protein-binding, and prostaglandin F, progesterone, oestrone and oestradiol-17β by radioimmunoassay. Foetal corticosteroids rose slowly from 5.0 ± 0.7 ng/ml at 20 days to 9.3 ± 3.0 ng/ml at 10 days before term, then progressively increased to a mean of 74 ng/ml at calving. Maternal levels remained relatively constant at 5 to 15 ng/ml, though higher concentrations occurred following surgery. Foetal oestrone and oestradiol-17β concentrations were both less than 50 pg/ml and showed little change toward term. The maternal uteroovarian oestrogens increased slowly from 20 to 10 days pre-partum and then rose more rapidly reaching peak levels (2.9 ± 0.6 ng/ml for oestrone and 1.4 ± 0.3 ng/ml for oestradiol-17β) 1 to 4 days before delivery. Maternal progesterone concentrations fell towards term, with a rapid decrease over the last 36–48 h. Prostaglandin F levels showed little change until 36–48 h before calving when they gradually increased until the last 24 h where was a dramatic rise, reaching peak levels (5.7 ± 0.6 ng/ml) during labour.

Reproduction ◽  
1974 ◽  
Vol 36 (2) ◽  
pp. 484-485 ◽  
Author(s):  
C. Nancarrow ◽  
H Hearnshaw ◽  
P. Mattner ◽  
P. Connell ◽  
B. Restall

Author(s):  
Salvatore Spagnolo ◽  
◽  
Luciano Barbato ◽  
Maria Antonietta Grasso ◽  
◽  
...  

Recent perfusion-weighted imaging studies have shown that two clinical pictures characterize multiple sclerosis: intermittent focal inflammatory demyelination and diffuse progressive axonal degeneration. Their etiopathogenesis is not known. We hypothesize that a chronic obstacle to the outflow of blood from the brain can cause these two clinical pictures. We had already shown angiographically that the stenosis of the internal jugular vein causes a systemic-cerebral shunt and a reversal of the venous circulation brain and gives rise to the new circuit that directly connects the superior vena cava system to the straight sinus. This new circuit can cause the BBB to break and new plaques to form. The introduction of near-infrared spectroscopy (NIRS) in cardiac surgery has made it possible to demonstrate that obstruction of the superior vena cava is capable of causing cerebral hypoperfusion, responsible for the progressive degeneration of axons. To confirm the relationship between superior vena cava syndrome and cerebral hypoperfusion, in 35 of the152 patients with multiple sclerosis (MS) and jugular vein stenosis, operated on the plastic of jugular vein enlargement, we measured oxygen saturation in the brain. Material and Methods To measure changes in the oxygen saturation of regional brain tissue (rctSO2) before, during and after clamping the jugular veins, we applied two sensors in the left and right frontal region, and we connected them to a biosignal recorder (Invos-5100 system). Results Closing or opening the IJV produced significant changes in the rctSO2 values. Before clamping, saturations varied between 77% - 78%, while during clamping they decreased reaching values between 48% - 58% (p <0, 05). After declamping, the rctSO2 returned to its starting values. These results confirmed that obstruction of the jugular veins causes a significant reduction in rctSO2 values and cerebral hypoperfusion. Conclusions In MS patients, chronic jugular veins stenosis generates two different clinical pictures: Diffuse cerebral hypoperfusion, documented by the lowering of rctSO2. Systemic-cerebral shunt and inversion of cerebral venous circulation capable of causing a breakdown of the blood-brain barrier (BBB)


1980 ◽  
Vol 238 (4) ◽  
pp. H599-H603 ◽  
Author(s):  
M. E. Burt ◽  
J. Arbeit ◽  
M. F. Brennan

A system is described for chronic cannulation of the thoracic aorta and superior vena cava in the rat. This system employs a protective stainless steel coiled spring and water tight swivel and allows chronic infusion of solutions and simultaneous intermittent blood sampling for prolonged periods of time in the undisturbed unanesthetized rat. The rats (200-250 g) lost approximately 25 g in the immediate postoperative period, but then gained weight at a relatively normal rate (cannulated rats, 2.23 g/day; control rats, 2.29 g/day).


2008 ◽  
Vol 33 (6) ◽  
pp. 426-428 ◽  
Author(s):  
Madhavi Tripathi ◽  
Rajnish Sharma ◽  
Abhinav Jaimini ◽  
Namita Singh ◽  
Sanjiv K. Saw ◽  
...  

1978 ◽  
Vol 87 (3) ◽  
pp. 617-624 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.


1983 ◽  
Vol 96 (1) ◽  
pp. 155-161 ◽  
Author(s):  
C. H. Tyndale-Biscoe ◽  
L. A. Hinds ◽  
C. A. Horn ◽  
G. Jenkin

Concentrations of progesterone, prolactin, LH and 13,14 dihydro-15-keto-prostaglandin F2α (PGFM) were measured in plasma of eight tammar wallabies at 8-hourly intervals during the end of pregnancy and post-partum oestrus initiated by removing the pouch young, and during the end of the oestrous cycle, similarly initiated. In the non-pregnant cycle oestrus occurred 29·7 ± 0·7 (mean ±s.e.m.) days after initiation of the cycle, was preceded by a slow decline in progesterone concentration from 1·6 nmol/l to less than 0·64nmol/l and was followed by a preovulatory peak of LH 5·3± 3·9 h later. In the pregnant cycle birth occurred 26·1±0·2 days after removing the pouch young and was followed 8·0 ± 2·1 h later by oestrus and 16·0± 2·5 h by an LH peak. The latter events thus occurred 3·2 days earlier in the pregnant than in the non-pregnant cycle. Parturition coincided with a very rapid decline in progesterone and a transient high peak of prolactin. In two females sampled less than 25 min after parturition there was a transient peak of PGFM but in all others the concentrations of PGFM remained basal throughout. It is suggested that the fetus and/or placenta is involved in both the premature decline in progesterone and the initiation of parturition and that onset of oestrus and ovulation, being a consequence of a decline in progesterone, are therefore also determined by the fetus.


1984 ◽  
Vol 64 (3) ◽  
pp. 655-665 ◽  
Author(s):  
R. M. LIPTRAP ◽  
P. A. GENTRY

A significant increase (P < 0.01) in plasma fibrinogen values and a concurrent decrease in hematocrit values were observed at parturition in seven sows. Plasma fibrinogen values remained elevated and those of the hematocrit remained depressed through the 7-day postpartum period. Although the mean value was not statistically significant, a transient decrease in circulating platelet numbers was observed for each pregnant sow shortly before parturition. Values for 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) rose markedly at parturition. Injection of prostaglandin F2 alpha (PGF2 alpha) into four ovariectomized sows and two castrated boars resulted in a statistically significant increase in plasma fibrinogen levels (P < 0.01) and a transient decrease in platelet counts (P < 0.01). In four ovariectomized sows, administration of progesterone (1 mg/kg body weight) also produced a small elevation in fibrinogen values. The fibrinogen response in sows was not directly related to the amount of progesterone since no further increase occurred when the dose of hormone was doubled. Fibrinogen values in four castrated boars were unaffected by injection of either dose of progesterone. No changes were observed in the circulating activity of other coagulation proteins at the time of parturition and these were not altered by administration of estrogen, progesterone or PGF2 alpha. Key words: Pigs, parturition, coagulation factors, hormones


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5000-5000
Author(s):  
Meera Sridharan ◽  
Aref Al-Kali ◽  
Aneel A. Ashrani ◽  
Kebede Begna ◽  
Michelle Elliott ◽  
...  

Abstract Background Tunneled central venous catheters have traditionally been used for administration of chemotherapy (chemo) for acute leukemia treatment. Peripherally inserted central catheters (PICC) are increasingly being used, but there is an increased risk of PICC-associated thrombosis (PAT). There is limited information on management of PAT in this subgroup of patients (pt). Methods In this retrospective cohort study we investigated the primary management of PICC related upper extremity venous thrombosis (TB) in pt with hematologic malignancy undergoing chemo at Mayo Clinic Rochester.  Eligible pt were 18 years and older, had documentation of PICC placement at our institution, initiation of chemo within a week of PICC placement, and the TB was objectively documented by compression venous ultrasound (CVU).   Superficial venous TB (SVT) was defined as TB of subcutaneous veins (basilic and cephalic) and deep venous TB (DVT) defined as TB of brachial, axillary, subclavian, or innominate superior vena cava and internal jugular veins. We retrospectively stratified initial management (IM) into 1) PICC removal alone (PR), 2) PR and therapeutic anticoagulation (AC), 3) AC alone, and 4) conservative management (CM) consisting of symptomatic care and observation.  We also investigated factors influencing IM of PAT.  Long term outcomes including incidence of pulmonary embolism (PE), post phlebitic syndrome and recurrence of TB were noted. Results Between 2006 and 2012, 190 pt with AML (n=160), MDS or MDS/MF (n=10), or ALL (n=20) met our study criteria.  Overall, 40/190 (21.6%) developed PAT: AML n=38, ALL n=1, MDS/MF n=1. SVT occurred in 16/40 (40%) pt and DVT occurred in 24/40 (60%) pt. IM is shown in Table 1. One pt with SVT received AC for 6 weeks as well as PR.  In this pt, IM included AC because of proximity of TB to deep veins. 7 pt had a follow up (f/u) CVU within 3 months demonstrating: TB progression (prog, n=1, IM with PR alone but with prog AC was started); TB stability (stab, n=2, both IM with PR alone) and TB resolution/improvement (R/I, n= 4, 2 IM with PR and 2 IM with CM)  In the 5 pt with CM, 2 pt had f/u CVU demonstrating improvement, one pt had charted clinical improvement , and 2 pt had no charted clinical f/u. Of DVT pt on AC (n=14), 5 pt completed at least 2 months of AC.  Reasons for early cessation (n=9) of AC included thrombocytopenia (tcp, n=4), hematoma (n=1), hematuria (n=1), subarachnoid hemorrhage (n=1), and unknown (n=1).   One pt died 2 days after presence of DVT was noted. Two pt initially treated with PR alone developed a second TB with placement of a new PICC on contralateral arm and AC was subsequently initiated (duration: 3 months (n=1), and 8 days (n=1)). 14 pt with DVT had f/u CVU within 3 months which demonstrated prog (n=2), stab (n= 8), or R/I ( n=4) of TB (Table 2). The 2 pt with TB prog subsequently received longer term AC guided by platelet count.   In 5 pt with PICC not initially removed, 3 pt had PR after completion of chemo. (1-4 days), one pt had PR at discharge (27 days from TB), and one pt had PICC in place on discharge. One pt with DVT experienced a PE within one year f/u.  This pt had initially completed 3 days of AC which was stopped because of tcp. Conclusion In this cohort of patients with PAT, the most common IM consisted of PR, which appeared to result in a low recurrence rate among pt with SVT.  In pt with DVT, the role of AC remains to be defined given the abbreviated course of AC in most pt.  Though, the lack of CVU followup in all pt limits conclusions, there appeared to be a low rate of symptomatic prog.  Initiation of AC was largely guided by platelet count and degree of occlusive symptoms. Thrombocytopenia was also the most commonly cited reason for discontinuing AC.  Close clinical follow up aided by the use of CVU was integral to ensure that PAT did not lead to further adverse events. Disclosures: No relevant conflicts of interest to declare.


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