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G H Nelson

Publications and source records attributed to G H Nelson.

At least 37 records · Page 2Linked to original sources
PubMed1993

Endothelium-dependent effects of substance P and calcitonin gene-related peptide on mouse pial arterioles.

BACKGROUND AND PURPOSE: The effects of substance P (SP) and calcitonin gene-related peptide (CGRP) were tested on pial arterioles of mice. This was done because (1) perivascular peptidergic nerves may play an important role in modulation of cerebrovascular responses; (2) there are conflicting data concerning the mechanism of action of CGRP; (3) there are few or no studies directly testing the endothelium dependence of dilation by these peptides in the cerebral circulation; and (4) we wished to extend previous observations of mice by comparing peptidergic responses in the mouse with those published for other species. METHODS: The pial arterioles were monitored in vivo using video microscopy and image-shearing techniques for measuring diameter. Focal endothelial injury was produced with a laser-Evans blue technique. Responses to SP and CGRP were tested before and after endothelial injury. They were also tested before and during treatment with agents that interfere with responses mediated by endothelium-derived relaxing factor (EDRFACh). They were also tested before and during treatment with indomethacin. RESULTS: Both CGRP and SP produced dilation that was blocked by endothelial injury and by agents interfering with responses mediated by EDRFACh. Indomethacin had no effect. CONCLUSIONS: SP and CGRP produce endothelium-dependent dilations. These dilations are probably mediated by EDRFACh. With respect to SP, these results are similar to those reported for other vessels and species. With respect to CGRP, the finding of endothelium dependence has not been previously reported for cerebral vessels. However, very few species have been tested. Reports of other vascular beds in other species sometimes parallel and sometimes contradict our findings with CGRP.

Animals↗
PubMed1993

Estimation of uterine volume with ultrasound in women with endometrial carcinoma.

In calculating uterine volume with ultrasound, it is necessary to calculate the volume of a parallelogram containing the uterus or to assume a specific shape for the uterus. The objective of this study was to determine how much (what percentage) of the parallelogram was actually occupied by the uterus without assuming any specific shape for the uterus. Overall, the volume of the uterus occupies 63% of the volume of the parallelogram. The uterus occupies a greater percentage of smaller parallelogram volumes than larger ones. The data also suggest that the concomitant presence of myomata may be responsible for the positive intercept of the regression line and therefore for the finding that small uteri occupy more than 63% of the parallelogram volume.

Adult↗
PubMed1992

Evaluation of pretreatment transvaginal ultrasonography in the management of patients with endometrial carcinoma.

OBJECTIVE: The objective of this study was to evaluate the usefulness of pretreatment assessment with ultrasonography in patients with endometrial carcinoma. STUDY DESIGN: Fifty patients with endometrial carcinoma diagnosed by endometrial biopsy or curettage were studied before hysterectomy, bilateral salpingo-oophorectomy, and selected lymph node sampling. Ultrasonographic criteria for determination of tumor grade, depth of myometrial invasion, uterine volume, and tumor volume were established. Tumor grade was compared with preoperative and postoperative pathologic diagnoses, depth of invasion was compared with postoperative pathologic evaluation, and uterine volume and tumor volume were compared with postoperative evaluation of tumor grade and depth of invasion. Data were analyzed by chi 2 testing, and, where appropriate, sensitivity, specificity, and accuracy of the ultrasonographic measurements were determined. RESULTS: The following statistically significant correlations (p less than or equal to 0.05) were found. Ultrasonography predicted tumor grade as accurately as preoperative pathologic evaluation did. Depth of invasion less than or equal to 50% or greater than 50% significantly correlated. Uterine volume less than or equal to 200 ml predicted less than or equal to 50% depth of invasion 28 of 32 times. Uterine volume greater than 500 ml was noted in six cases; five of these had grade 2 or 3 tumor and four had depth of invasion greater than 50%. Tumor volume less than or equal to 20 ml predicted a grade 1 tumor in 25 of 39 cases and depth of invasion less than or equal to 50% in 34 of 39 cases. Tumor volume greater than 20 ml correlated with a grade 2 or 3 tumor in 11 of 11 cases and a depth of invasion greater than 50% in seven of 11 cases. In 25 grade 1 tumors diagnosed postoperatively by pathologic study, none was associated with a tumor volume greater than 20 ml. CONCLUSION: Pretreatment ultrasonographic measurements should be of value in the management of patients with endometrial carcinoma.

Adult↗
PubMed1992

The endothelium-dependent effects of thimerosal on mouse pial arterioles in vivo: evidence for control of microvascular events by EDRF as well as prostaglandins.

Thimerosal causes synthesis and/or release of both endothelium-derived relaxing factor (EDRF) and prostaglandins from conductance vessels in vitro. We tested its effects and mechanism of action on mouse pial arterioles in vivo using intravital microscopic techniques. Topical thimerosal dilated pial arterioles. This effect was eliminated by endothelial injury produced by a laser/Evans blue technique. Dilation was also eliminated by topical L-NMMA, a reported inhibitor of EDRF synthesis. Topical thimerosal also reduced the incidence of platelet adhesion/aggregation ("capture") at a site of minimal endothelial damage. This effect was eliminated by L-NMMA pretreatment. The ability of thimerosal to dilate arterioles was eliminated not only by treatments thought to eliminate synthesis/release of EDRF, but also by cyclooxygenase inhibitors. However, inhibition of platelet adhesion/aggregation was not affected by cyclooxygenase inhibition. Thimerosal significantly increased production of prostaglandin E2 recovered from a closed cranial window. We conclude that the dilating effects of thimerosal on diameter require two endothelium-derived agents: EDRF and one or more prostaglandins acting in concert. However, the inhibiting effect of thimerosal on local platelet adhesion/aggregation appears to be caused only by an increase in EDRF at the injured site.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

L-arginine suffusion restores response to acetylcholine in brain arterioles with damaged endothelium.

Minor endothelial injury was produced in pial arterioles by a laser-Evans blue technique. This technique previously has been shown to prevent relaxation of the arterioles by topical acetylcholine (ACh) or bradykinin, agonists whose actions are known to be endothelium dependent in most vascular beds. L-Arginine is thought to be the precursor of the endothelium-derived relaxing factor (EDRF) that mediates the response to ACh. To further test this hypothesis and to begin exploration of the intracellular effects of the laser injury, we used the laser to eliminate the response to ACh and then attempted to restore the responsivity by suffusing the arterioles with 10(-3) L-arginine for 10 min before testing with ACh. This treatment restored the response. In contrast, over the same time period, responses failed to recover in arterioles that were never exposed to L-arginine or in arterioles that were only exposed to L-arginine at the time of retest with ACh. D-Arginine failed to restore the response to ACh. L-Arginine failed to restore the response to bradykinin. The data support the hypothesis that L-arginine acts as a substrate for synthesis of "classical" EDRF in brain microvessels in vivo. The data suggest that laser-Evans blue injury either depletes the endothelium of L-arginine or interferes with conversion of L-arginine to EDRF. Increasing the substrate by exposing the vessels to L-arginine for 10 min permitted ACh to release sufficient EDRF to elicit dilatation. The data also support conclusions from earlier studies that in this vascular bed the dilations produced by ACh and bradykinin are mediated by different EDRF.

Acetylcholine↗
PubMed1992

L-NMMA in brain microcirculation of mice is inhibited by blockade of cyclooxygenase and by superoxide dismutase.

As previously reported, NG-monomethyl-L-arginine (L-NMMA) constricted pial arterioles, inhibited dilation of pial arterioles by acetylcholine (ACh) or L-arginine (L-Arg), and enhanced platelet adhesion/aggregation at sites of endothelial damage. However, all of these effects were inhibited by local application of 20 micrograms/ml indomethacin (Indo). When 100 micrograms/ml acetylsalicylic acid were used instead of Indo, the acid also blocked the effects of L-NMMA. Superoxide dismutase (SOD; 50 U/ml) blocked the constriction produced by L-NMMA and also blocked the constriction produced by N omega-nitro-L-arginine (NNA). SOD also prevented L-NMMA from blocking dilation by ACh. SOD itself had no effect on diameter or on the response to ACh, norepinephrine, or BaCl2. The effects of L-NMMA and of Indo were also selective. Thus L-NMMA did not inhibit dilation by prostacyclin or bradykinin, and Indo did not inhibit dilation by prostacyclin. Indo did not interfere with the ability of arginase to enhance platelet adhesion/aggregation or with the ability of ACh or L-Arg to inhibit adhesion/aggregation. We conclude that in mouse cerebral microcirculation the ability of L-NMMA and NNA to constrict arterioles, the ability of L-NMMA to inhibit dilation by ACh or L-Arg and the ability of L-NMMA to enhance platelet adhesion/aggregation are all related to interference with phenomena dependent on "classical" endothelium-derived relaxing factor (EDRFACh). However, in this preparation the action of L-NMMA or NNA may not be due to competitive inhibition of the enzyme producing EDRFACh from L-Arg. Rather, L-NMMA and NNA appear to activate cyclooxygenase with resultant production of superoxide, which inactivates EDRFACh.

Animals↗
PubMed1992

Postcesarean endometritis: a brief review and comparison of three antibiotic regimens.

Three different antibiotic regimens (trospectomycin plus azteonam, clindamycin plus azteonam, and triple antibiotics-ampicillin plus clindamycin plus gentamicin) were all effective in treating patients with postcesarean endometritis. Patients are frequently cured clinically despite the fact that the offending organisms may be isolated in post-treatment cultures. Treatment of postcesarean endometritis without obtaining endometrial cultures is acceptable gynecologic practice. Obtaining post-treatment cultures is clearly not cost effective nor clinically beneficial. Drug treatment efficacy should be evaluated by clinical response. This communication is the first to report the new antibiotic, trospectomycin, in the treatment of postcesarean endometritis. Further clinical trials are currently underway.

Anti-Bacterial Agents↗
PubMed1991

Agents that modify EDRF formation alter antiplatelet properties of brain arteriolar endothelium in vivo.

In the presence of circulating Evans blue a helium-neon laser injures the endothelium of brain surface arterioles in situ. The injury is known to selectively eliminate endothelium-dependent responses. The present study documents in mice the fact that such endothelial sites become selectively attractive to passing platelets that have been activated as a result of more severe injury upstream. We then test the hypothesis that the "capture" of platelets at the downstream site is due to loss of "classical" endothelial-dependent relaxing factor of acetylcholine (EDRFACh) at that site. EDRFACh is known to inhibit platelet adhesion/aggregation and is synthesized from L-arginine. We show that agents that would either enhance or reduce the synthesis of local EDRFACh reduce or increase the incidence of capture as predicted by the hypothesis. Thus NG-monomethyl-L-arginine (L-NMMA) and arginase that would reduce synthesis of EDRFACh enhanced platelet capture. L-Arginine, which would enhance synthesis of EDRFACh, inhibited platelet capture. In addition, L-NMMA and arginase enhanced platelet aggregation over the more severely damaged site upstream from the site of capture. Ex vivo studies of platelets harvested from treated mice showed that the platelets themselves were unaffected by the treatments that, except for arginase given intravenously, all involved topical application of the tested drugs.

Acetylcholine↗
PubMed1990

Tone regulates opposing endothelium-dependent and -independent forces: resistance brain vessels in vivo.

Pial arterioles on the surface of the mouse brain were observed with television microscopy and measured with an image-splitting technique. Previous studies showed that, in this vascular bed, serotonin (5-HT) and high-dose histamine produced endothelium-dependent constriction that masked and overwhelmed an endothelium-independent relaxation produced by the same agonists. Low-dose histamine produced relaxation. In the present studies we compared the responses to these agonists before and after alterations in tone. Preconstriction with uridine 5'-triphosphate caused reversal of the responses to 5-HT or high-dose histamine. These agonists now relaxed the arterioles to diameters greater than their original base line. Prerelaxation by nitroprusside caused reversal of the response to low-dose histamine. The agonist now constricted the arterioles to diameters smaller than their original base line. The data show, in vivo, in resistance vessels, that initial tone is an important determinant of the final effect or relative strengths of competing, opposing, endothelium-dependent and -independent forces triggered by a single agonist.

Animals↗
PubMed1990

Endothelium-dependent L-Arg- and L-NMMA-sensitive mechanisms regulate tone of brain microvessels.

Pial arterioles on the surface of the mouse brain were observed via television microscopy and measured with an image-splitting technique. The vessels were dilated by L-arginine (L-Arg) in concentrations as low as 10(-5) M and were constricted in dose-dependent manner by NG-monomethyl-L-arginine (L-NMMA). Both the dilation and the constriction were abolished by endothelial damage. This damage was produced over a short segment of endothelium by a well-established technique that involves exposing the endothelium to a helium-neon laser in the presence of intravascular Evans blue dye. In arterioles that were responsive to 10(-5) M L-Arg, five other L-amino acids, also at 10(-5) M, failed to have any effect. The data provide direct evidence for the endothelium-dependent nature of the responses to L-Arg and L-NMMA in vivo in a defined segment of the cerebral vasculature. L-NMMA inhibited dilation by either L-Arg or acetylcholine. The data are consistent with data from in vitro studies and from studies demonstrating that L-NMMA acutely raises blood pressure. From all these earlier studies it has been hypothesized that there is a continuously acting, endothelium-dependent, L-Arg-dependent, and L-NMMA-inhibitable mechanism tending to relax blood vessels. The mediator of this mechanism is thought to be the endothelium-dependent relaxing factor for acetylcholine. Our data suggest that this mechanism is acting in the resistance vessels of the brain in vivo.

Acetylcholine↗
PubMed1990

Leukotriene constriction of mouse pial arterioles in vivo is endothelium-dependent and receptor-mediated.

The diameters of pial arterioles of mice were monitored in vivo with an image-splitting technique and television microscopy. Concentrations of leukotriene C4 as low as 10(-7) M constricted the arterioles. The leukotriene C4-D4 receptor blocker ICI 198615 (10(-8) M) inhibited the response. Endothelial injury by helium-neon laser/Evans blue technique eliminated the constriction and unmasked a slight but consistent relaxation that was not inhibited by 10(-8) M ICI 198615. Since leukotrienes are produced by the brain and enter the cerebrospinal fluid in ischemia, head trauma, and subarachnoid hemorrhage, the possibility that leukotrienes C4 and D4 contribute to decreases in cerebral blood flow during these conditions should be considered. However, the present data makes such a possibility far less likely because the endothelium is frequently injured in these conditions, and therefore the ability of leukotrienes to constrict vessels would be severely curtailed.

Animals↗
PubMed1990

Histamine elicits competing endothelium-dependent constriction and endothelium-independent dilation in vivo in mouse cerebral arterioles.

We used television microscopy and an image-splitting technique to monitor the changes in diameter produced by histamine applied locally to mouse pial arterioles in vivo. A high dose (50 micrograms/ml, 3 X 10(-4) M) of histamine constricted the arterioles, whereas lower doses (20 and 10 micrograms/ml) relaxed them. Constriction was blocked and dilation occurred when selective injury of the endothelium was produced by light from a helium-neon laser in the presence of intravascular Evans blue. From this we conclude that the constriction was endothelium-dependent and was caused by the release of an endothelium-derived constricting factor. Constriction was also blocked by each of two antagonists of the H1 histamine receptor and by pretreatment of the arterioles with indomethacin. H1 blockade unmasked a dilating action of 1 micrograms/ml histamine, a dose too low to affect the diameter of arterioles not treated with the H1 blocker. An H2 blocker interfered with the relaxation by low-dose (10 micrograms/ml, 6 X 10(-5) M) histamine. These data indicate that for mouse pial arterioles, histamine can interact with H1 receptors on the endothelium to release an endothelium-derived constricting factor that causes constriction of the underlying muscle while simultaneously interacting with H2 receptors in the muscle that mediate relaxation of the vessel.

Animals↗
PubMed1990

Comparison of the complement-fixation and agar gel immunodiffusion tests for diagnosis of subclinical bovine paratuberculosis.

The performance of the serum complement fixation (CF) test was compared with that of a serum agar gel immunodiffusion (AGID) test on 74 subclinically infected and 154 uninfected cattle in 6 commercial midwestern dairy herds with Mycobacterium paratuberculosis infection and on 30 cattle in a herd that was free of infection. Infection status of cattle within herds was established by performance of a series of 3 or more fecal cultures and of ileocecal lymph node cultures of culled cattle. In cattle with subclinical infection detected by culturing, the sensitivity estimates of the CF and AGID tests were 10.8% (3.6% SE) and 18.9% (4.5% SE), respectively. In the cattle classified as disease free, the specificity estimates of the CF and AGID tests were 97.4% (1.3% SE) and 99.4% (0.6% SE), respectively. Neither set of estimates was significantly different. Negative test results obtained with the use of either test in apparently normal cattle from suspect herds should be interpreted with caution because both tests suffer from low sensitivities in subclinically infected animals. However, the AGID test may be more useful in regulatory situations in which the CF test is currently used because the AGID test is easier to perform and to interpret.

Animals↗
PubMed1989

Effect of fetal sex and race on amniotic fluid lecithin concentration.

Amniotic fluid lecithin phosphorus concentration (AF-Lec) was measured in 209 healthy women at 31.7-42.7 weeks gestation. The patients were divided into four groups according to race and fetal sex. No differences in AF-Lec between black and white nor between male and female fetuses were found. The relationship of AF-Lec to gestational age and the incidence of "mature" AF-Lec was not different among the four groups. We conclude that there is no effect of fetal sex, race, or the interaction between them on fetal lung development as measured by AF-Lec.

Adult↗
PubMed1989

Chicago sky blue and a helium neon laser abolish endothelium dependent relaxation in vivo in the microcirculation.

Chicago sky blue, also known as Niagara sky blue, is a vital dye that can successfully be used as an intravascular energy absorbing target for the light from a helium-neon (HeNe) laser. The result of this light/dye interaction is endothelium damage which can be controlled by adjusting the duration of the laser exposure and the amount of dye injected intravenously. The endothelial damage probably is the result of the heat generated by the dyes absorption of energy at the interface between plasma and endothelium. The most minimal damage resulted in selective loss of the dilation normally produced by acetylcholine and bradykinin, two endothelium dependent dilators. The dilation produced by sodium nitroprusside, a dilator acting directly on vascular smooth muscle, was preserved. More severe injury (i.e. more prolonged exposure to light and/or more dye, resulted in local platelet aggregation at the site of laser impact.

Acetylcholine↗
PubMed1988

One day of estradiol treatment enhances platelet aggregation at the site of microvascular injury without altering aggregation ex vivo.

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol placebo. On the day following implantation platelet aggregation was produced in arterioles on the brain surface (pial arterioles) by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .01) in the estradiol treated mice. In contrast to this enhancement of aggregation, when platelets were tested ex vivo in platelet rich plasma (PRP), aggregation to sodium arachidonate or to ADP was not altered in estradiol treated mice. Thus the enhanced aggregation observed in injured pial arterioles of estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. Rather enhanced aggregation may reflect an effect of estradiol on endothelium or adjacent tissue. This effect was produced within 24 hours of achieving pregnancy levels of estradiol. The rapidity of the effect is of interest in light of earlier studies showing a similar in vivo action following 7-14 days of high estradiol levels. The rapid effect suggests that an action on megakaryocytes is an unlikely explanation for the results.

Animals↗
PubMed1988

Fetal lung maturity in diabetic pregnancies: relation among amniotic fluid insulin, prolactin, and lecithin.

Insulin, prolactin, and lecithin phosphorus levels were measured in 97, 62, and 44 amniotic fluid samples from third trimester normal, gestational diabetic, and insulin-dependent diabetic patients, respectively. There was no difference in lecithin phosphorus concentration (index of fetal lung maturity) among the three groups. The amniotic fluid insulin level was significantly higher in insulin-dependent diabetic patients, whereas there was no difference in amniotic fluid prolactin levels among the groups. Correlations of amniotic fluid prolactin levels with both lecithin phosphorus and insulin levels were not statistically significant in any of the groups. This is probably because amniotic fluid prolactin is decidual, rather than fetal, in origin. Even though amniotic fluid insulin levels, which reflect fetal levels, were significantly higher in insulin-dependent diabetic patients, there was no difference in the amniotic fluid lecithin phosphorus concentration in diabetic pregnancies compared with that in normal pregnancies. Moreover, there was a positive, and not a negative, correlation between amniotic fluid insulin and amniotic fluid lecithin phosphorus levels in diabetic pregnancies. These results do not support the theory that fetal hyperinsulinemia results in delayed pulmonic maturation in diabetic pregnancies.

Adult↗