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Biomedical subjects

B Hammond

Publications and source records attributed to B Hammond.

At least 37 records · Page 2Linked to original sources
PubMed1985

The oxygen free radical system: potential mediator of myocardial injury.

The sequential univalent reduction of oxygen gives rise to very reactive intermediate products including superoxide anion radical, hydrogen peroxide and free hydroxyl radicals. Normally, the tissue concentration of these intermediate products of oxygen is severely limited; however, if oxygen free radicals are produced in excess of the capacity of the tissues to eliminate them, they may cause serious damage. The biochemistry and possible sources of free radical generation in animal models of ischemic/reperfusion injury are reviewed. The ability of scavengers of oxygen free radicals to improve mechanical, mitochondrial and sarcoplasmic reticulum function in animal models of ischemic/reperfusion injury suggests that oxygen free radicals are partly responsible for myocardial injury in these models. Future research should be directed at establishing the relevance of oxygen radical-mediated myocardial injury in the experimental setting to analogous clinical situations.

Acute Disease↗
PubMed1985

The pulmonary hypertension of sclerosing agents is prevented by cyclooxygenase inhibitors.

Sodium morrhuate and sodium tetradecylsulfate are injected during endoscopic sclerotherapy to control variceal bleeding. When administered to sheep they cause transient pulmonary hypertension and increase protein poor lung lymph flow. To determine the etiology of these alterations, we studied three groups of sheep after establishing acute lung lymph fistulas. In Group 1, indomethacin or ibuprofen was infused. In Group 2, 2.5 cc of sodium morrhuate was injected alone (2A) or after indomethacin or ibuprofen pretreatment (2B). In Group 3, 2.5 cc of sodium tetradecylsulfate was given intravenously either alone (3A) or after indomethacin or ibuprofen (3B). When sclerosing agents were given alone (Group 2A and 3A) pulmonary artery pressures increased three-fold at 30 seconds postinjection to 37 +/- 4.4 and 39 +/- 5.7 mmHg respectively with a slow return to baseline over two hours. Lymph flow increased significantly from 1.3 +/- 1.5 to 2.7 +/- 1.5 cc/30 minutes after sodium morrhuate and from 1.2 +/- .62 to 2.7 +/- 1.7 cc/30 mins at 30 minutes after sodium tetradecylsulfate and the lymph/plasma albumin ratio fell. Increased lymph flow persisted through 120 minutes. In those animals receiving a sclerosing agent after indomethacin or ibuprofen (2B and 3B) there was no change in pulmonary artery pressure, lymph flow, lymph plasma albumin ratio, or lung wet weight to dry weight ratios. We conclude that the pulmonary hypertension and increased protein poor lymph flow are mediated by prostaglandins.

Animals↗
PubMed1985

Oxygen radicals in the adult respiratory distress syndrome, in myocardial ischemia and reperfusion injury, and in cerebral vascular damage.

Recent work suggests that oxygen radicals may be important mediators of damage in a wide variety of pathologic conditions. In this review we consider the evidence supporting the participation of oxygen radicals in the adult respiratory distress syndrome, in ischemia reperfusion injury in the myocardium, and in cerebral vascular injury in acute hypertension and traumatic brain injury. In the adult respiratory distress syndrome there is active sequestration of polymorphonuclear neutrophils in the pulmonary vascular system. There is evidence that activation of these neutrophils results in the production of oxygen radicals which injure the capillary membrane and increase permeability, leading to progressive hypoxia and decreased lung compliance which are hallmarks of the syndrome. In acute arterial hypertension or experimental brain injury oxygen radicals are important mediators of vascular damage. The metabolism of arachidonic acid is the source of oxygen free radical production in these conditions. In myocardial ischemia and reperfusion injury, the ischemic myocyte is "primed" for free radical production. With reperfusion and reintroduction of molecular oxygen there is a burst of oxygen radical production resulting in extensive tissue destruction. Myocardial ischemia--reperfusion injury shares in common with the other two syndromes activation of the arachidonic acid cascade and acute inflammation. Thus it would appear that the generation of toxic oxygen species may represent a final common pathway of tissue destruction in several pathophysiologic states.

Animals↗
PubMed1982

Release of toxic microvesicles by Actinobacillus actinomycetemcomitans.

Oral isolates of Actinobacillus actinomycetemcomitans (strain Y4) release spherical microvesicles in large numbers during normal growth. The biological activities of these products were studied, and it was estimated that approximately 1/10 of their dry weight was made up of heat- and proteolysis-resistant endotoxin. The chicken embryo lethality and bone-resorbing activity of the microvesicles were heat stable but proteolysis sensitive. Other laboratories have reported the presence of a heat- and proteolysis-sensitive leukotoxin in similar preparations. Accordingly, the microvesicles released by strain Y4 may contain, in addition to endotoxin, several potent substances which are highly toxic and active in bone resorption, and these may be significant factors in the pathogenesis of periodontal diseases.

Actinobacillus↗
PubMed1981

Chemotactic response to some arachidonic acid lipoxygenase products in the rabbit eye.

The effects of arachidonic acid, its cyclo-oxygenase and lipoxygenase products and the synthetic chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (FMLP) on leukocyte accumulation in the aqueous humour and intraocular pressure in the rabbit were studied in vivo. Substances were injected into the anterior chamber of the eyes of anaesthetised rabbits using a closed circuit perfusion system. Injection of arachidonic acid, prostaglandins E1 and E2, and the monohydroperoxy and hydroxy acids of the lipoxygenase pathway did not result in any significant accumulation of leukocytes in the anterior chamber. In contrast, FMLP and 5,12-diHETE (Leukotrine B4) resulted in significant dose dependent accumulation of leukocytes into the aqueous humour. Leukocytes appeared in the aqueous humour between 2 and 3 h after the injection of either FMLP or LTB4 and the response was maximal at 4 h. None of the lipoxygenase products tested had any effect on intraocular pressure in contrast to the profound effects observed with arachidonic acid and the E type prostaglandins. FMLP had a small but significant effect on intraocular pressure at the highest dose tested for leukocyte accumulation. These results indicate that the effects of the cyclo-oxygenase products of arachidonate metabolism are mainly vascular in the rabbit eye in contrast to the predominantly cellular effects of lipoxygenase products. Thus in the eye, the interaction of cyclo-oxygenase and lipoxygenase products of arachidonate metabolism may be important in the development of both acute and chronic ocular inflammation.

Animals↗
PubMed1979

Estrogenic activity of the insecticide chlordecone (Kepone) and interaction with uterine estrogen receptors.

The chlorinated insecticide chlordecone (Kepone) interacts with the estrogen receptor system in the rat uterus in vitro and in vivo. It competes with estradiol for binding to the cytoplasmic receptor in vitro and also induces nuclear accumulation of estrogen receptor sites in uteri in vitro. When injected into immature rats, chlordecone translocates estrogen receptor sites to the uterine nucleus, increases uterine weight, and stimulates the synthesis of the progesterone receptor, an estrogen receptor-mediated process. Its slow onset of action but prolonged duration of interaction with estrogen receptor and stimulation of uterine weight gain and progesterone receptor synthesis indicates that, although it has an affinity for receptor only 0.01-0.04% that of estradiol, its considerable estrogenic activity may likely be derived from its long half-life and bioaccumulative character.

Animals↗
PubMed1976

Simple method of determining the axial length of the eye.

By photographing the corneal reflex in two positions of gaze and measuring the radius of curvature of the cornea it is possible to calculate the radius of rotation of the eye. The measurements obtained in this way showed a high correlation with refraction in a series of 80 eyes. The axial length obtained by this method was about 3 mm greater than that obtained by ultrasonographic or x-ray methods, and the reasons for the discrepancy are discussed.

Anthropometry↗
PubMedDate not supplied

Operation cataract.

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Aged↗