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E F O'Connor

Publications and source records attributed to E F O'Connor.

10 recordsLinked to original sources
PubMed1991

Synergy between tumor necrosis factor and endotoxin decreases early embryo development in vitro.

The purpose of the present study was to investigate the individual and combined effects of low levels of endotoxin and physiological levels of tumor necrosis factor on in vitro fertilization and preimplantation embryo development. B6D2F1 mice were superovulated by utilizing pregnant mare serum gonadotropin and human chorionic gonadotropin. Oocyte-cumulus complexes (3221 oocytes) were collected, pooled, and randomized into control and treatment groups. Sperm were collected from the caudae epididymides of mature male mice and allowed to capacitate. Treatments included culture media supplemented with increasing amounts of endotoxin (0.5, 1.0, and 2.0 ng/ml; sp act, 3000 IU/ng) and/or tumor necrosis factor (1, 10, and 50 pg/ml; sp act, 0.01 IU/pg) throughout the fertilization and preimplantation development process. Percentage cleavage and percentage expanded blastocyst formation were evaluated. No significant effects were observed for percentage cleavage or percentage expanded blastocyst formation in either the endotoxin (E) or the tumor necrosis factor (TNF) groups. The combination of endotoxin and tumor necrosis factor at any of the levels tested did not significantly decrease cleavage; however, percentage blastocyst formation was decreased with any combination of TNF and E (P less than 0.05-P less than 0.001). We conclude that TNF and E exert significant synergistic effects which are detrimental to in vitro preimplantation embryonic development.

Animals↗
PubMed1991

Baroreflex function in chronically stressed borderline hypertensive rats.

A number of previous studies have demonstrated that some aspect of baroreflex function is altered as hypertension develops. However, no studies have determined whether a chronic stressor can alter baroreflex function in the resting state. In the present study, male borderline hypertensive rats (BHR) were divided into three groups: control, stressed daily for 5 weeks, and stressed daily for 11 weeks. At the appropriate time, 7 different dosages of angiotensin II (AII) were given intravenously as a bolus injection. Heart rate (interbeat interval, or IBI) and mean arterial pressure were tracked for 90 subsequent beats. For each group, intercorrelations between pressure and IBI were obtained. In addition, overall means of pressure and IBI for each dosage were computed for each group and plotted. Higher dosages of AII were required to produce a significant correlation between pressure and IBI in the 5-week group compared to control. In the 11-week group, only the highest dosage yielded a significant correlation between pressure and IBI. When data were expressed in terms of the highest pressure and its corresponding IBI for each group, the 5-week-stress group had a shift in set point compared to control. The 11-week group showed a shift in set point and a reduction in gain compared to control animals. The similarity between these findings and those for other models of hypertension is discussed, with special emphasis on the potential role of the central nervous system.

Angiotensin II↗
PubMed1990

Influence of opioid peptides on release from vasopressin and oxytocin neurones of the hypothalamoneurohypophyseal system: effects of naloxone in the conscious rat.

We examined the effects of acute and chronic treatments with naloxone on release of vasopressin and oxytocin from the hypothalamoneurohypophyseal system (HNS) in conscious, chronically instrumented Long-Evans rats. Plasma concentrations of vasopressin-associated neurophysin and oxytocin-associated neurophysin were evaluated before and during an intravenous infusion of 18% saline at 100 microL.kg-1 body weight.min-1 for 60 min. Acute treatment with naloxone (2.75 mumol/kg, intravenous) did not measurably alter basal plasma osmolality or vasopressin-associated neurophysin concentration, but it caused a three-fold rise in basal plasma oxytocin-associated neurophysin concentration (16 +/- 2 to 46 +/- 3 fmol/mL, p less than 0.005). Chronic treatment with naloxone (13.75 mumol/day, subcutaneous pellets) increased plasma osmolality (292 +/- 1 to 300 +/- 2 mosmol/kg H2O, p less than 0.01) by day 5, but it had no measurable effects on basal vasopressin- or oxytocin-associated neurophysin concentration. There were also no significant differences in plasma sodium concentration (144.8 +/- 1.1 vs. 142.2 +/- 1.4 mequiv./L) under both conditions. Acute and chronic treatments with naloxone accompanied by salt loading produced a five- and four-fold decrease in the rates that plasma concentration of vasopressin-associated neurophysin changed with plasma osmolality, compared with untreated salt-loaded control rats. For oxytocin secretion from the HNS, both treatments accompanied by salt loading substantially decreased the threshold for changes in relation to plasma osmolality; the rise in plasma concentration of oxytocin-associated neurophysin was similar at all levels of hyperosmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Lithium chloride stabilizes systolic blood pressure and increases adrenal catecholamines in the spontaneously hypertensive rat.

The effects of daily, intraperitoneal injections of LiCl (3 mEq/kg) on systolic blood pressure (SBP) and adrenal catecholamine levels were measured in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKY). Control animals from each strain were injected with equivalent volumes (0.1 ml/100 g b.wt.) of 0.9% saline (0.15 mEq/kg). SBP in LiCl-treated SHR was significantly lower (p less than 0.05) than that of saline-treated SHR (177 +/- 7 vs. 196 +/- 4 mm Hg, respectively) after one week. After two weeks SBP was lower in LiCl SHR than in saline controls, but this difference was not significant. While SBP of both LiCl and saline treated WKY was not significantly different (146 +/- 4 vs. 147 +/- 8 mm Hg, respectively), SBP in both WKY groups remained lower than the SBP for either group of SHR. LiCl induced a significant weight loss in the SHR, but not in the WKY. Adrenal norepinephrine and epinephrine were significantly (p less than 0.05) higher in LiCl-treated rats of both strains; dopamine was also higher in LiCl-treated rats of both strains, but significant only between SHR-LiCl and SHR controls. It appears that LiCl's effect in slowing the development of hypertension is independent of its action on adrenal catecholamines. The SHR's increased sensitivity to LiCl, relative to weight loss and SBP, may reflect differences in genetic or physiological status of the animal compared to WKY. These differences may be associated with alterations in membrane ion transport systems.

Adrenal Medulla↗
PubMed1987

Effects of intraperitoneal injection of lithium chloride on neurohypophyseal activity: implications for behavioral studies.

Intraperitoneal injections of lithium chloride (LiCl) were found to increase the activity of vasopressin-neurons and oxytocin-neurons as indexed by rises in plasma concentrations of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). Plasma VP-RNP increased 12 and 4 times basal levels (greater than or equal to 20 fmol/ml) reaching values of 248 +/- 37 fmol/ml (3.0 mEq LiCl/kg body weight) and 89 +/- 10 fmol/ml (1.5 mEq LiCl/kg body weight) at 60 minutes. OT-RNP rose to 37-and 10-times basal levels (greater than or equal to 20 fmol/ml) with peak values of 749 +/- 100 fmol/ml and 188 +/- 48 fmol/ml ten minutes following injection of 3.0 or 1.5 mEq LiCl/kg body weight. Mean arterial pressure increased in response to lithium treatment by 31 +/- 6 mm Hg at 60 minutes in rats receiving 3.0 mEq LiCl/kg and by 22.5 +/- 5 mm Hg at 10 minutes in rats receiving 1.5 mEq LiCl/kg over pretreatment values (125 +/- 3 mm Hg). Heart rate decreased from a pretreatment value of 422 +/- 12 beats/min to 367 +/- 48 beats/min at 10 minutes and to 341 +/- 27 beats/min at 20 minutes for rats treated with the high and low dose of lithium, respectively. These findings suggest that the behavioral effects of LiCl could result from multiple mechanisms and involve its acute release of vasopressin and oxytocin. It is also possible that changes in cardiovascular function may act as cues when LiCl is used as an aversive stimulus.

Animals↗
PubMed1986

Acute infusion of lithium chloride raises blood pressure in the conscious rat.

The effects of acute infusion of lithium chloride (LiCl) were studied on mean arterial pressure (MAP) and magnocellular activity as shown by the concentrations of vasopressin-associated neurophysin ([VP-RNP]) and concentrations of oxytocin-associated neurophysin ([OT-RNP]) in plasma in conscious Long-Evans rats. Chronically-cannulated rats were infused intravenously at 10 microliter/100 g body wt/min with 13% LiCl for 20 min (total dose = 6.16 mequiv./kg body wt) or 0.65% LiCl for 60 min (total dose = 0.92 mequiv./kg body wt). Effects of 13% LiCl on mean arterial pressure were also examined in vasopressin-deficient homozygous Brattleboro rats. For Long-Evans rats, infusion of 13% LiCl produced rapid and significant (P less than 0.001) increases in mean arterial pressure, the concentration of lithium in plasma ([Li+]), plasma osmolality (Posmol), [VP-RNP], [OT-RNP] and significant decreases in heart rate and sodium concentration in plasma ([Na+]). For similar changes in plasma osmolality, lithium had a greater effect than sodium on mean arterial pressure, [VP-RNP], [OT-RNP]. For the 20 min infusion of 13% LiCl, there was a significant relationship (P less than 0.033) between delta MAP and log delta[VP-RNP] with a slope of 11.9 mmHg fmol-1 ml-1 (r = 0.5678). Unlike that of Long-Evans rats, infusion of 13% LiCl only did not produce significant changes of mean arterial pressure in Brattleboro rats. For Long-Evans rats, infusion of 0.65% LiCl resulted in more gradual and smaller elevations of blood pressure, [Li+] and smaller decreases in heart rate with no significant changes in plasma osmolality, [Na+], [VP-RNP] and [OT-RNP].(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Identification and localization of catecholamines in the nervous system of Limulus polyphemus.

The concentrations of various catecholamines in the nervous system of the horseshoe crab Limulus polyphemus have been determined by high-performance liquid chromatography with electrochemical detection. Dopamine, norepinephrine, epinephrine, and their precursor L-Dopa were present in appreciable quantities in discrete regions of the central nervous system and cardiac ganglion. The catecholamines were localized more precisely by use of the glyoxylic-acid-histofluorescence technique of de la Torre and Surgeon (1976). Catecholamine fluorescence appeared in protocerebral and tritocerebral neuropile, including regions of the central body and optic medulla. Posterior to these brain areas, tracts extended through the circumesophageal ganglionic ring and laterally out each of the pedal ganglia. Small clusters of large fluorescent somata were present in the protocerebrum. No fluorescence was observed in the corpora pedunculata.

Animals↗
PubMed1979

Liquid chromatographic demonstration of catecholamine release in fish heart.

High-pressure liquid chromatography (HPLC) was used to assay for catecholamines released into the heart of the goldfish (Carassius auratus L.) upon stimulation of vagal nerve fibers. Stimulation induced the release of norepinephrine, epinephrine and dopamine into the lumen of the perfused, isolated heart. The results suggest that heart activity in teleosts is directly modulated by functional adrenergic, cardioacceleratory nerve fibers.

Animals↗
PubMedDate not supplied

Single-step isolation and sequencing of vasopressin and oxytocin precursors.

The pre- and post-Golgi processing of preprovasopressin and prepro-oxytocin was evaluated by microsequencing for incorporated radiolabel. 35S-Cysteine and 3H-fucose were microinjected into rat supraoptic nuclei (SON), and proteins and peptides related to the biosynthesis of vasopressin (VP) and oxytocin (OT) were isolated at various times from the supraoptic nuclei and neural lobe by employing a one-step procedure of high performance liquid chromatography (HPLC). These proteins and peptides were recognized through their binding to specific antibodies against VP, OT, and rat neurophysins (RNPs), and by their binding to ConA-Sepharose. Two immunoreactive glycoproteins related to VP biosynthesis were recovered from the SON and both contained fucose and had a 35S-cysteine placement consistent with the location of the hormone sequence at the N-terminus. SDS-electrophoresis revealed the major protein form to be 21,000 daltons and the minor protein form to be 19,000 daltons. One nonglycosylated protein of 16,000 daltons related to oxytocin biosynthesis was recovered from the SON, and this protein also had a 35S-cysteine placement consistent with an N-terminal OT sequence. These data provide the first sequential evidence that prior to, or shortly after, packaging in the Golgi the preprohormones of VP and OT have lost their entire leader-peptide structures.

Animals↗