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Biomedical subjects

C H Sawyer

Publications and source records attributed to C H Sawyer.

At least 19 recordsLinked to original sources
PubMed1993

Comparison of German and United States malpractice systems.

Germany has successfully contained overall health-care costs while providing virtually universal access to high quality services. The country's medical and legal systems create a climate characterized by less pressure for malpractice litigation and greater efficiency of resolution. This analysis reviews characteristics that may be useful in reducing the $20 billion annual costs associated with medical malpractice in the United States. Some features of the German model may be unattractive. Further investigation appears warranted.

Cost Control↗
PubMed1987

Hypothalamic control of ovulation and behavioral estrus in the cat.

The estrous cat ordinarily ovulates only after a complex mating behavior pattern which involves an elaborate after reaction. The present experiments were designed to determine whether identical or separate hypothalamic areas control mating behavior and the release of an ovulatory surge of pituitary gonadotropin. With stereotaxic methods under chloralose anesthesia the hypothalami of naturally estrous or estrogen-gonadotropin-primed queens were stimulated bilaterally in one of the following regions: medial basal hypothalamus including the premamillary area (MBH) and the anterior hypothalamus including both medial and lateral divisions (AH, MAH, LAH). At the end of the stimulation period (5 V, 30 c/s, 5 ms duration, 30 s off for 30 min) bilateral anodal electrolytic lesions were made at the stimulation sites (3 mA for 30 s) with the central tips of the bipolar electrodes. Characteristically, ovulation was induced by stimulating the MBH but not the AH. Furthermore, the MBH lesions usually caused ovarian atrophy which led to anestrus, but the cats mated normally if supplied with exogenous estrogen. The anterior lesions left the ovaries in good trophic condition, and they could be ovulated by stimulating the MBH. However, the cats with anterior hypothalamic lesions in either the medial or lateral position repeatedly refused to accept the male even when primed with exogenous estrogen. The results from these combined stimulation and lesion experiments in the female cat indicate that a hypothalamic sex behavioral area lies rostral to and discrete from a tubero-mamillary area controlling the release of pituitary gonadotropin.

Animals↗
PubMed1986

Ovarian steroid modulation of norepinephrine action on luteinizing hormone release. Analogous effects in male and female rats.

The modulatory actions of ovarian steroids on the norepinephrine (NE) induced alterations in luteinizing hormone (LH) secretion were examined in male and female rats. Long-term (4 weeks) castrated male and female rats bearing chronic third-ventricle cannulae were implanted with intra-atrial catheters. Animals were bled sequentially at 5- or 15-min intervals for 4-6 h, and plasma LH secretory patterns were determined by radioimmunoassay. After a 2- to 3-hour control bleeding period, castrated unprimed rats received an intracerebroventricular (ICV) infusion of 0.3 mumol of arterenol bitartrate or vehicle. Blood sampling was continued for an additional 2-3 h after infusion. In female rats NE caused a rapid and potent inhibition of episodic LH secretion which was characterized by decreases in mean plasma LH, mean pulse amplitude, and pulse frequency. Similarly, ICV infusion of NE into male rats resulted in decreased mean plasma LH and pulse frequency. In a second series of experiments, castrated male and female rats were primed with estrogen and progesterone 2 days prior to the bleeding/infusion session. Animals were bled sequentially and infused with 0.3 mumol arterenol bitartrate or vehicle during a morning or afternoon session. ICV infusion of vehicle had no effect on plasma LH in either sex regardless of the time of day. NE infusion into estrogen and progesterone primed female rats resulted in significant elevations of plasma LH during both morning and afternoon periods. In estrogen and progesterone primed male rats, NE infusion resulted in a marked facilitation of LH release, similar to that observed in female rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity Cycles↗
PubMed1986

Activation of the CNS noradrenergic system may inhibit as well as facilitate pituitary luteinizing hormone release.

Earlier work established that neural secretion of luteinizing hormone-releasing hormone (LH-RH) and the resultant release of pituitary gonadotropins could be facilitated by activating alpha-receptors of a central noradrenergic (NA) system. The present study emphasizes that central NA mechanisms may also inhibit LH release largely through activation of beta-adrenergic receptors.

Animals↗
PubMed1986

Episodic patterns of luteinizing hormone and follicle-stimulating hormone release: differential secretory dynamics and adrenergic control in ovariectomized rats.

Long term (4 weeks) ovariectomized rats were bled sequentially at 5-min intervals for 5 h via indwelling intraatrial cannulas. Plasma LH and FSH secretory patterns were determined from the same plasma samples by RIA. Hormonal profiles were subjected to power spectral analysis to determine periodicities of plasma LH and FSH. Distinct and regular release patterns were observed for LH, with significant periodicities between 20-40 min. In contrast to LH, FSH oscillations were neither as distinct nor as regular. However, significant periodicities in FSH (50-60 min) were often detected. At times, plasma LH and FSH appeared to be synchronized, but there were numerous instances of differential secretion. The effects of intracerebroventricular infusion of norepinephine (NE) and clonidine (an alpha 2-agonist) were tested in another group of animals. After a 2- to 3-h control bleeding period each animal bearing a chronic third ventricle cannula received an intracerebroventricular infusion of 0.3 mumol NE, clonidine, or vehicle. Blood sampling was continued for 2-3 h after infusion. Intracerebroventricular infusion of NE caused rapid and potent inhibition of LH secretion with FSH affected to a lesser extent. NE infusion decreased mean plasma LH levels and LH pulse amplitude while causing a marked increase in pulse period. Although mean FSH levels declined after NE infusion, secretory episodes of FSH were detectable even in the absence of pulsatile LH secretion. Infusion of an equimolar dose of clonidine produced a biphasic response in LH, a transient elevation followed by a decrease in overall plasma levels. In contrast to LH, plasma FSH levels showed only a delayed decrease after clonidine infusion. No significant changes in pulse amplitude or pulse period for either gonadotropin were observed. These data show that plasma FSH, like LH, oscillates in a periodic manner, but when compared with episodic LH secretion there are both quantitative and qualitative differences. Although the neural mechanisms involved in periodic LH release are also involved to a lesser extent in FSH secretion, it appears that independent regulatory mechanisms exist for LH and FSH as well.

Animals↗
PubMed1985

Postcastration rise in plasma gonadotropins is blocked by a luteinizing hormone-releasing hormone antagonist.

The dependence of the acute increases in plasma gonadotropins following castration on luteinizing hormone-releasing hormone (LHRH) was assessed with the use of a potent LHRH antagonist [ALHRH; (Nac-L-Ala1,p-Cl-D-Phe2,D-Trp3,6) LHRH]. Blood samples were collected from male and female rats at the time of castration and 2, 4, 8, 12, 24 and 48 h following and plasma gonadotropin levels were determined. Immediately following castration (diestrus I for females) animals received one of the following treatments: females-vehicle, 100 micrograms ALHRH, 50 micrograms estrogen benzoate (EB), or 100 micrograms ALHRH + 50 micrograms EB; males-vehicle, 100 micrograms ALHRH, 500 micrograms testosterone propionate (TP), or 100 micrograms ALHRH + 500 micrograms TP. ALHRH blocked the selective increase in plasma follicle-stimulating hormone (FSH) observed in female rats as well as the parallel increases in both gonadotropins seen in male rats following castration. Administration of EB or ALHRH + EB to females significantly suppressed both gonadotropins compared with control levels. However, EB alone did not completely block the rise in plasma FSH in females. In males, all three treatments significantly suppressed the increases in both gonadotropins when compared with control levels. These data demonstrate that hypothalamic LHRH plays an essential role in the acute elevations of plasma gonadotropins following castration in rats. In addition, these data suggest that the selective rise of FSH in females is dependent on LHRH stimulation of pituitary gonadotropes.

Animals↗
PubMed1984

Differential gonadotropin secretion: blockade of periovulatory LH but not FSH secretion by a potent LHRH antagonist.

The dependence of periovulatory gonadotropin secretion on LHRH was assessed with the use of a potent LHRH antagonist [ ALHRH ; (Nac-L- Ala1 ,p-Cl-D-Phe2,D-Trp3,6)LHRH]. Blood samples were collected hourly from 14.00 h proestrus (P) through 09.00 h estrus (E) from intact cycling female rats. ALHRH was administered at 09.00 or 13.00 h P before the proestrous increases in gonadotropins had commenced or at 23.00 h P after the LH and primary FSH surges had occurred but preceding the secondary FSH surge. Antagonist given at 09.00 or 13.00 h P completely blocked the LH release with levels remaining undetectable in most animals (less than 30 ng/ml) throughout the sampling period. However, administration of antagonist at these times failed to block completely the primary FSH surge although peak values were reduced when compared with controls, which displayed normal gonadotropin surges. In addition, ALHRH administered at 23.00 h failed to alter the magnitude or other characteristics of the secondary FSH surge when compared with controls. The present study demonstrates that the estrous surge of FSH in the rat is independent of acute hypothalamic release of LHRH. Furthermore, although the proestrous release of FSH is to a large extent LHRH dependent, our data suggest that some other mechanism may also contribute to this primary FSH surge.

Animals↗
PubMed1983

Thyroid stimulating hormone and prolactin secretion: reduced sensitivity to TRH-stimulated prolactin release after midpregnancy in rats.

Prolactin (PRL) and thyroid stimulating hormone (TSH) plasma concentrations were measured during the latter part of the dark period in early and mid-late pregnancy in the rat. On Days 4-5 and 7-8 of pregnancy, plasma PRL concentrations surged between 22:00 and 06:00 hr and TSH values increased between 22:00 and 02:00 hr. While the TSH pattern was maintained during the second-half of pregnancy, surges in PRL release ceased and PRL levels remained at less than 10 ng/ml. The effects of thyrotropin releasing hormone (TRH) administration on PRL and TSH secretion were then measured to determine whether the second-half of pregnancy is associated with a decrease in sensitivity to an agent that can stimulate PRL release. Injection (iv) of cannulated pregnant rats with a low dosage (20 ng) of TRH stimulated a twofold increase in plasma TSH during both early (Days 5-9) and later (Days 14-18) pregnancy but did not change plasma PRL levels. Treatment with a high dosage (2 micrograms) of TRH induced a sixfold rise in plasma TSH during both phases of gestation. The higher dose of TRH also stimulated elevations in plasma PRL during early and mid-late pregnancy; however, both the absolute increase in the amount of PRL in plasma and the percentage increase over baseline levels were greater from Days 5-9 than from Days 14-16 of gestation. These data indicate that the neuroendocrine sensitivity to factors that stimulate PRL secretion changes as pregnancy progresses, and suggest that nocturnal secretion of PRL and TSH during pregnancy may be regulated, in part, by a common trophic factor.

Animals↗
PubMed1982

Electrophysiologic correlates of steroid modulation of luteinizing hormone release.

In both ovariectomized (OVX) and steroid-primed OVX freely moving rats, attempts were made to correlate the effects of intraventricular norepinephrine (NE) on multiunit activity (MUA) of different brain regions with NE-induced alterations in blood LH levels. MUA-recording electrodes were implanted in the diagonal band of Broca (DBB), medial preoptic area (MPOA), arcuate nucleus (ARC) and/or ventromedial hypothalamic nucleus (VMH). Steroid priming included 50 micrograms estradiol benzoate (EB) and 25 mg progesterone (P) 3 days prior to experiment. The unanesthetized animals were bled via indwelling atrial cannulas before and after intraventricular infusion of NE (10 micrograms in 2 microliters over 2 min). In OVX-primed rats NE lengthened the interval between episodic LH peaks and decreased mean blood LH levels. In contrast, in OVX-EBP-primed rats, NE stimulated an LH surge. Concurrent recording of MUA revealed that, in OVX-unprimed rats, NE dramatically depressed MUA in both DBB-MPO and ARC-VMH neurons. However, in OVX-EBP-primed rats, while still markedly inhibiting ARC-VMH units, NE failed to depress MUA recorded in DBB-MPO sites (some units were actually excited by NE), perhaps reflecting the higher ratio of LHRH neurons/inhibitory neurons in DBB-MPO.

Action Potentials↗
PubMed1982

Differential effects of central adrenoceptor agonists on luteinizing hormone release.

This study examined the alterations in episodic luteinizing hormone (LH) release in response to third ventricle infusions of various alpha- and beta-adrenoceptor agonists in ovariectomized (OVX) rats as well as the effects of steroid priming with 50 micrograms estradiol benzoate (EB) and 25 mg progesterone (P) on the LH responses to these agonists. Unanesthetized rats with indwelling atrial cannulae were bled at 10-min intervals for 0.5-1.5 h prior to infusion and up to 1.5 h following infusion of equimolar amounts (0.06 or 0.3 mumol in 2 microliters saline adjusted to pH 5.5 and infused slowly over a 2-min period) of norepinephrine (NE), phenylephrine (Phen, alpha 1-agonist), isoproterenol (Iso, beta-agonist) or clonidine (Clon, alpha 2-agonist). In unprimed OVX rats, 0.06 mumol NE induced a significant lengthening (by approximately 121%) of the episodic interval between the peak LH levels and caused a decrease in mean blood LH levels of approximately 24%, which began almost immediately and lasted for approximately 1 h after infusion. When administered in the same manner and dosage, both alpha- and beta-adrenergic agonists were similarly effective in suppressing pulsatile LH release in OVX unprimed rats, with the following rank order being apparent: Clon greater than NE congruent to Phen greater than Iso. However, in OVX-EBP-primed rats, while 0.06 mumol NE significantly stimulated LH release, none of the other adrenoceptor agonists administered at this dosage was effective in altering the low nonpulsatile levels of blood LH characteristic of the steroid-primed animal. Nevertheless, at a concentration 5 times higher (0.3 mumol) Clon and Phen did induce LH surges while Iso, even at this higher dose, was not stimulatory to LH release. These results suggest that the inhibitory action of NE on LH secretion in OVX rats may be exerted via activation of both alpha- and beta-adrenoceptors, whereas primarily alpha-adrenoceptors are responsible for mediating the NE-induced stimulation of LH release in OVX steroid-primed animals.

Animals↗
PubMed1982

Postpartum luteinizing hormone release and maternal behavior in the rat after late-gestational depletion of hypothalamic norepinephrine.

The effects of depletion of hypothalamic norepinephrine (NE) during late pregnancy on the postpartum ovulatory LH surge, the onset and maintenance of maternal behavior and lactation were examined in adult female rats. Bilateral transections of the ascending noradrenergic pathways (ANP) between days 14 and 17 of gestation resulted in a 70% depletion in hypothalamic NE content when assayed on day 6 postpartum. In spite of this depletion in hypothalamic NE content, a postpartum ovulatory surge of LH was observed in transected rats at 18:00 h on either the day of parturition or 1 day later. The magnitude of the LH surge in experimental animals at this time appeared equal to that of controls. A second group of transected and sham-transected rats was tested for maternal responsiveness postpartum and through day 6 postpartum. Primiparous transected females displayed normal maternal behavior during this period with only minor disruptions in nest-building behavior. The lactational performance of transected rats, however, was inferior to that of sham-transected animals. The hypothalamic content of NE in females that showed impairment of lactation was consistently below the NE content found in the controls. The importance of the noradrenergic system in the control of maternal behavior is discussed, and it is proposed that noradrenergic involvement in maternal behavior is modulatory rather than directly regulatory.

Animals↗
PubMed1981

Effects of intraventricular norepinephrine on preoptic-anterior hypothalamic electrical activity in the freely-moving rat: modulation by ovarian steroid hormones.

In freely-moving female rats the effects of intraventricular infusion of norepinephrine (NE) on multiunit activity (MUA) were examined in the Diagonal Band of Broca (DBB), medial preoptic area (MPOA) and anterior hypothalamic area (AHA), regions containing neurons producing luteinizing hormone-releasing hormone (LHRH). NE was infused at a dosage known to depress plasma LH levels in ovariectomized (OVX) rats and elevate plasma LH concentrations in OVX-estrogen-progesterone-primed (EBP) animals. It was found that in adult OVX rats MUA in the brain areas listed above was almost invariably inhibited by NE (20 of 23 cases or 87%; the other three cases showed no change in electrical activity). However, after priming with estrogen and progesterone only about one-third of the OVX-EBP rats gave an inhibitory response, with another one-third showing no change in MUA and the final one-third of the cases actually giving an excitatory MUA response to NE--the DBB neurons being the most positive in the regard. Thus it appears that responsiveness of LHRH and/or adjacent neurons to the modulatory action of NE may itself be modulated by the influence of gonadal steroids.

Animals↗
PubMed1981

The effects of stimulation and lesion of raphe nuclei on luteinizing hormone release in estrogen-progesterone-treated ovariectomized rats.

A study was made of the effects of electrochemically stimulating (ECS) and destroying the midbrain dorsal and median raphe nuclei on the estrogen-progesterone- (EP) induced surge of pituitary LH release in ovariectomized rats. ECS and lesions were produced simultaneously with anodal direct current through a chronically implanted stimulation-lesion electrode. Blood for LH assay was collected through a chronic intra-atrial cannula positioned on the day of first treatment with progesterone. ECS of the raphe nuclei exerted a strong inhibition of the LH surge when compared with sham stimulation. On the second EP treatment the onset of the LH surge was advanced both in sham-stimulated animals and in rats with raphe lesions resulting from the anodal direct current of the initial ECS. It was suggested that this apparent facilitation of the LH surge on the second EP treatment was the results of reduced stress or an altered hormonal milieu and not a consequence of destroying the raphe nuclei. The results confirm in a chronic preparation that stimulation of raphe nuclei depresses the EP-induced LH surge and that subsequently in the absence of the raphe nuclei the LH response to EP treatment is apparently normal.

Animals↗