Effect of dietary fish oil on lung lipid profile and hypoxic pulmonary hypertension

The effects of dietary polyunsaturated fats on chronic hypoxic pulmonary hypertension were assessed in rats fed fish oil, corn oil, or a lower fat, "high-carbohydrate" diet (regular) beginning 1 mo before the start of hypoxia (0.4 atm, n = 30 for each). Mean pulmonary arterial pressures were lower in the chronically hypoxic rats fed fish oil (19.7 +/- 1.8 mm Hg) than in the rats fed corn oil (25.3 +/- 1.6 mm Hg) or regular diets (27.5 +/- 1.5 mm Hg, P less than 0.05). The fish oil diet increased lung eicosapentaenoic acid 50-fold and depleted lung arachidonic acid 60% (P less than 0.0001 for each). Lung thromboxane B2 and 6-ketoprostaglandin F1 alpha levels were lower, and platelet aggregation, in response to collagen, was reduced in rats fed fish oil. Chronically hypoxic rats fed fish oil had lower mortality rates than the other hypoxic rats. They also had lower blood viscosity, as well as less right ventricular hypertrophy and less peripheral extension of vascular smooth muscle to intra-acinar pulmonary arteries (P less than 0.05 for each). The mechanism by which dietary fish oil decreases pulmonary hypertension and vascular remodeling during chronic hypoxia remains uncertain. The finding that a fish oil diet can reduce the hemodynamic and morphological sequelae of chronic hypoxia may have therapeutic significance.     

Norepinephrine induces lung vascular prostacyclin synthesis via alpha 1-adrenergic receptors

Sympathetic nerve stimulation can cause pulmonary vasoconstriction related to norepinephrine (NE) release. Because of recent reports that NE caused prostacyclin (PGI2) release from systemic arteries, we wondered whether NE caused pulmonary vascular PGI2 release and whether a feedback mechanism existed whereby PGI2 modulated NE-induced vasoconstriction. NE-induced PGI2 synthesis in rat main pulmonary artery rings was larger than that induced by KCl, passive stretch, or a thromboxane analogue, was alpha-adrenergic receptor dependent, and was enhanced by endothelium removal. The NE-induced PGI2 synthesis was not tightly coupled to the magnitude of the pulmonary artery ring contractile response, and inhibition of NE-induced PGI2 production by cyclooxygenase blockade in either the pulmonary artery ring preparation or in isolated rat lungs perfused with a physiological solution did not augment the magnitude of the contractile response. We concluded that NE is a potent stimulus for PGI2 synthesis in the rat main pulmonary artery ring and in the rat lung, yet PGI2 is not important as a modulator of NE-induced vasoconstriction in the rat lung.     

Three new ground wētā species and a redescription of Hemiandrus maculifrons

Taxonomy lies at the heart of species conservation, yet many large New Zealand orthopterans remain undescribed. Among New Zealand’s anostostomatid wētā, Hemiandrus (ground wētā) is the most speciose genus but also the most poorly characterised and thus most in need of taxonomic and ecological work. Here we redescribe H. maculifrons and describe two new species of ground wētā previously encompassed by the specific name Hemiandrus maculifrons: Hemiandrus luna sp. nov. and H. brucei sp. nov. We also describe a morphologically similar and related species, Hemiandrus nox sp. nov.

http://zoobank.org/urn:lsid:zoobank.org:pub:71EA0879-A2F9-46B2-A105-E97A9AB25061

http://zoobank.org/References/71EA0879-A2F9-46B2-A105-E97A9AB25061     

Benthic insects in Swedish lake-outlet streams: patterns in species richness and assemblage structure

1. We studied how species richness of three hierarchical insect species groups, namely all benthic, lotic and filtering taxa, were related to a number of environmental variables in a data set from fifteen Swedish lake outlets. 2. In partial least-squares analyses, we found that size-related factors (stream width, discharge) and velocity-related factors (current velocity, substratum particle size) were positively associated, and productivity-related factors (chlorophyll a, seston energy, conductivity) negatively associated, with the species richness of the three groups. 3. The weak and negative relationship of richness with productivity largely negated theoretical predictions, whereas the species-environment results corroborated earlier findings from running water systems. 4. The most important factors associated with the species composition of the lake outlets studied included pH, lake area, discharge, channel width and detritus. 5. Of the filter feeders, most species of blackflies (Diptera: Simuliidae) showed a negative relationship with pH. 6. A nested subset analysis demonstrated that species-poor sites did not have a subset of species found at more species-rich sites in any of the three hierarchical groups.     

Pulmonary vascular reactivity: effect of PAF and PAF antagonists.

We investigated the effects of two different platelet-activating factor (PAF) antagonists, SRI 63-441 and WEB 2086, on PAF-, angiotensin II-, and hypoxia-induced vasoconstrictions in isolated rat lungs perfused with a physiological salt solution. Bolus injection of PAF (0.5 micrograms) increased pulmonary arterial and microvascular pressures and caused lung edema. Both SRI 63-441, a PAF-analogue antagonist, and WEB 2086, a thienotriazolodiazepine structurally unrelated to PAF, completely blocked PAF-induced vasoconstriction and lung edema at 10(-5) M. At a lower concentration (10(-6) M), WEB 2086 was more effective than SRI 63-441. WEB 2086 also blocked the pulmonary vasodilation induced by low-dose PAF (15 ng) in blood-perfused lungs preconstricted with hypoxia. SRI 63-441 and CV 3988 (another PAF analogue antagonist), but not WEB 2086, caused acute pulmonary vasoconstriction at 10(-5) M and severe lung edema at a higher concentration (10(-4) M). PAF-induced but not SRI- or CV-induced pulmonary vasoconstriction and edema were inhibited by WEB 2086. In addition, SRI 63-441 potentiated angiotensin II- and hypoxia-induced vasoconstrictions. This effect of SRI 63-441 is not due to PAF receptor blockade because 1) addition of PAF (1.6 nM) to the perfusate likewise potentiated angiotensin II-induced vasoconstriction and 2) WEB 2086 did not cause a similar response. We conclude that both SRI 63-441 and WEB 2086 are effective inhibitors of PAF actions in the rat pulmonary circulation. However, antagonists with structures analogous to PAF (SRI 63-441 and CV 3988) can have significant pulmonary vasoactive side effects.     

Leukotriene C4 production during hypoxic pulmonary vasoconstriction in isolated rat lungs

Leukotriene inhibitors preferentially inhibit hypoxic pulmonary vasoconstriction in isolated rat lungs. If lipoxygenase products are involved in the hypoxic pressor response they might be produced during acute alveolar hypoxia and a leukotriene inhibitor should block both the vasoconstriction and leukotriene production that occurs in response to hypoxia. We investigated in isolated blood perfused rat lungs whether leukotriene C₄ (LTC₄) could be recovered from whole lung lavage fluid during ongoing hypoxic vasoconstriction. Lung lavage from individual rats had slow reacting substance (SRS)-like myotropic activity by guinea pig ileum bioassay. Pooled lavage (10 lungs)_as analyzed by reverse phase high performance liquid chromatography had an ultraviolet absorbing component at the retention time for LTC₄. At this retention time the element had both LTC₄ immunoreactivitiy by radioimmunoassay, and SRS myotropic activity by bioassay. LTC₄ was not found during normoxic ventilation, during normoxic ventilation after a hypoxic pressor response, or during vasoconstriction elicited by KCL. Diethylcarbamazine citrate, a leukotriene synthesis blocker, concomitantly inhibited the hypoxic vasoconstriction and LTC₄ production. Thus 5-lipoxygenase products may play a role in the sequence of events leading to hypoxic pulmonary vasoconstriction.