Capsaicin-insensitive sensory-efferent meningeal vasodilatation evoked by electrical stimulation of trigeminal nerve fibres in the rat. (1/280)

1. Antidromic vasodilatation and plasma extravasation to stimulation of the trigeminal ganglion or its perivascular meningeal fibres was investigated by laser-Doppler flowmetry and 125I-labelled bovin serum albumin in the dura mater and in exteroceptive areas (nasal mucosa, upper eyelid) of anaesthetized rats pretreated with guanethidine and pipecuronium. 2 Trigeminal stimulation at 5 Hz for 20 s elicited unilateral phasic vasodilatation in the dura and lasting response in the nasal mucosa. Resiniferatoxin (1-3 microg kg(-1) i.v.), topical (1%) or systemic capsaicin pretreatment (300 mg kg(-1) s.c. plus 1 mg kg(-1) i.v.) did not inhibit the meningeal responses but abolished or strongly inhibited the nasal responses. Administration of vinpocetine (3 mg kg(-1) i.v.) increased both basal blood flow and the dural vasodilatation to perivascular nerve stimulation. 3. Dural vasodilatation to trigeminal stimulation was not inhibited by the calcitonin gene-related peptide-1 receptor (CGRP-1) antagonist hCGRP8-37 (15 or 50 microg kg(-1) i.v), or the neurokinin-1 receptor antagonist RP 67580 (0.1 mg kg(-1) i.v.) although both antagonists inhibited the nasal response. Neither mucosal nor meningeal responses were inhibited by atropine (5 mg kg(-1) i.v.), hexamethonium (10 mg kg(-1) i.v.) or the vasoactive intestinal polypeptide (VIP) antagonist (p-chloro-D-Phe6-Leul7)VIP (20 microg kg(-1) i.v.). 4. Plasma extravasation in the dura and upper eyelid elicited by electrical stimulation of the trigeminal ganglion was almost completely abolished in rats pretreated with resiniferatoxin (3 microg kg(-1) i.v.). 5. It is concluded that in the rat meningeal vasodilatation evoked by stimulation of trigeminal fibres is mediated by capsaicin-insensitive primary afferents, while plasma extravasation in the dura and upper eyelid and the vasodilatation in the nasal mucosa are mediated by capsaicin-sensitive trigeminal fibres.  (+info)

The effects of ouabain and potassium on peritoneal fluid and solute transport characteristics. (2/280)

BACKGROUND: We reported anomalous transport characteristics of potassium during experimental peritoneal dialysis in rats and suggested that mechanisms of peritoneal potassium transport could be other than simple passive transport. Intracellular transport of potassium in cultured human mesothelial cells was reported to be regulated by three different pathways, such as channels blocked by ouabain, channels blocked by furosemide, and other. OBJECTIVE: To investigate the effect of ouabain on peritoneal potassium and water transport characteristics. METHODS: A single 4-hour peritoneal dwell was performed in 28 Sprague-Dawley rats. To minimize the diffusive transport of potassium, 4.5 mmol/L of KCl was added into conventional dialysis solution with 3.86% glucose [acidic peritoneal dialysis solution (APD)]. To evaluate the effect of the pH of dialysis solution on the transport of potassium and water, 4 mmol/L of NaOH was added into the potassium-containing study solutions [neutral peritoneal dialysis solution (NPD)]. To evaluate the effect of a potassium channel blocker on peritoneal potassium transport ATPase sensitive Na+-K+-transport inhibitor, ouabain (10(-5) mmol/L) was added to dialysis solutions immediately before the dwell study in eight rats with APD (APD-O) and six rats with NPD (NPD-O). Ouabain was not added in eight and six rats with APD and NPD (APD-C and NPD-C, respectively). They were used as control. Infusion volume was 30 mL. The intraperitoneal volume (V(D)) was estimated by using a volume marker dilution method with corrections for the elimination of volume marker, radioiodinated human serum albumin (RISA), from the peritoneal cavity (K(E)). The diffusive mass transport coefficient (K(BD)) and sieving coefficient (S) were estimated using the modified Babb-Randerson-Farrell model. RESULTS: V(D) was significantly higher (p < 0.05 from 90 min to 240 min) and K(E) (0.027+/-0.018 mL/min for APD-O, 0.026+/-0.017 mL/min for NPD-O, and 0.030+/-0.022 mL/min for NPD-C, vs 0.058+/-0.030 mL/min for APD-C, p < 0.05 for each) significantly lower during dialysis with APD-O, NPD-O, and NPD-C than with APD-C. The intraperitoneal glucose expressed as a percentage of the initial amount was significantly higher with APD-O, NPD-C, and NPD-O than with APD-C (p < 0.05 from 90 min to 240 min). K(BD) for sodium was higher during dialysis with ouabain than without ouabain, while K(BD) for urea, glucose, and potassium, and S for urea, glucose, sodium, and potassium did not differ between the four groups. CONCLUSIONS: The physiologic potassium concentration in neutral dialysis solutions and the use of ouabain decreased the intraperitoneal fluid absorption. The diffusive transport coefficient and sieving coefficient for potassium did not differ, while the diffusive transport coefficient for sodium increased during use of ouabain.  (+info)

A new complement function: solubilization of antigen-antibody aggregates. (3/280)

Antigen-antibody aggregates are solubilized when incubated with fresh serum at 37 degrees, yielding immune-complexes of relatively small molecular weight which contain antigen, antibody, and complement (C3)determinants. Solubilization is complement-dependent,requires free Mg++ but not Ca++, and proceeds in sera from C4- or C5-deficient animals. It is accelerated in the presence of Ca++ in normal or C4-deficient guinea pig serum, suggesting involvement of the Cl-bypass activation of the properdin system. Immune precipitates can also be solubilized by monovalent fragments (Fab) of antibodies directed against determinants of the antibody molecules included in the antigen-antibody lattice. Similarly, it is suggested that complement-mediated solubilization might be induced by the combination of a complement fragment with the antibody in the immune-aggregate.  (+info)

Errors in estimating lung liquid volume in fetal lambs when using radiolabeled serum albumin and blue dextran. (4/280)

Fetal lung liquid volume is usually determined by using radio-iodinated serum albumin (RISA) or blue dextran (BD) as volume tracers. We tested the reliability of both tracers at 124 (G124) and 142 days of gestation (G142; term = G147) when the labels were employed simultaneously. We measured the proportion of label bound reversibly to the lung, or apparently lost from the lung compartment, by washing out the lung with saline and 5% albumin. At G124, volume estimates with the two labels were similar. At G142, the volume estimate with BD (36.3 +/- 8.7 ml/kg of body wt) was higher (P < 0. 05) than with RISA (22.3 +/- 3.5 ml/kg). This difference resulted from reversible binding of BD, because 5% albumin washout released 38.5 +/- 4.0% of the BD added at the start of the experiment but a lesser amount of RISA (9.8 +/- 0.7%; P < 0.05). At G142, when RISA was used alone, its reversible binding was 1.3 +/- 0.2%. Background absorbance increased during experiments, giving rise to an apparent increase in BD concentration. We conclude that RISA is an effective tracer for lung liquid volume determination in the fetal lamb, whereas our findings of substantial epithelial binding of BD and large changes in background absorbance demonstrate that, under the conditions of our experiments, BD is a poor tracer close to term.  (+info)

Role for endogenous endothelin in the regulation of plasma volume and albumin escape during endotoxin shock in conscious rats. (5/280)

To explore the role of endogenous endothelin (ET) in the regulation of vascular functions, we studied the effects endothelin receptor blockade on blood pressure, plasma volume and albumin escape during endotoxin shock in conscious, chronically catheterized rats. Red blood cell volume and plasma volume were determined by using chromium-51-tagged erythrocytes and iodine-125-labelled albumin, respectively. Intravenous injection of lipopolysaccharide (LPS, 10 mg kg(-1)) resulted in hypotension, haemoconcentration, and increased total-body albumin escape, which is reflected by a 30% reduction in plasma volume. Plasma ET-1 concentrations increased 2.1 fold and 5.4 fold at 30 and 120 min post-LPS, respectively. LPS-induced losses in plasma volume and albumin escape were significantly attenuated by pretreatment of animals with the dual ET(A)/ET(B) receptor antagonist bosentan (17.4 micromol kg(-1), i.v. 15 min prior to LPS) or the ET(A) receptor antagonist FR 139317 (3.8 micromol kg(-1), i.v.) during both the immediate and delayed phases of endotoxin shock. The inhibitory actions of bosentan and FR 139317 were similar. Both antagonists augmented the hypotensive action of LPS. Administration of bosentan or FR 139317 70 min after injection of LPS also attenuated further losses in plasma volume and increases in total body and organ albumin escape rates with the exception of the lung and kidney. These results indicate a role for endogenous endothelin in mediating losses in plasma volume and albumin escape elicited by LPS predominantly through activation of ET(A) receptors, and suggest that by attenuating these events, ET(A) or dual ET(A)/ET(B) receptor blockers may be useful agents in the therapy of septic shock.  (+info)

Protective effect of lung inflation in reperfusion-induced lung microvascular injury. (6/280)

We used the isolated-perfused rat lung model to study the influence of pulmonary ventilation and surfactant instillation on the development of postreperfusion lung microvascular injury. We hypothesized that the state of lung inflation during ischemia contributes to the development of the injury during reperfusion. Pulmonary microvascular injury was assessed by continuously monitoring the wet lung weight and measuring the vessel wall (125)I-labeled albumin ((125)I-albumin) permeability-surface area product (PS). Sprague-Dawley rats (n = 24) were divided into one control group and five experimental groups (n = 4 rats per group). Control lungs were continuously ventilated with 20% O(2) and perfused for 120 min. All lung preparations were ventilated with 20% O(2) before the ischemia period and during the reperfusion period. The various groups differed only in the ventilatory gas mixtures used during the flow cessation: group I, ventilated with 20% O(2); group II, ventilated with 100% N(2); group III, lungs remained collapsed and unventilated; group IV, same as group III but pretreated with surfactant (4 ml/kg) instilled into the airway; and group V, same as group III but saline (4 ml/kg) was instilled into the airway. Control lungs remained isogravimetric with baseline (125)I-albumin PS value of 4.9 +/- 0.3 x 10(-3) ml x min(-1) x g wet lung wt(-1). Lung wet weight in group III increased by 1.45 +/- 0.35 g and albumin PS increased to 17.7 +/- 2.3 x 10(-3), indicating development of vascular injury during the reperfusion period. Lung wet weight and albumin PS did not increase in groups I and II, indicating that ventilation by either 20% O(2) or 100% N(2) prevented vascular injury. Pretreatment of collapsed lungs with surfactant before cessation of flow also prevented the vascular injury, whereas pretreatment with saline vehicle had no effect. These results indicate that the state of lung inflation during ischemia (irrespective of gas mixture used) and supplementation of surfactant prevent reperfusion-induced lung microvascular injury.  (+info)

Ciliary ganglion stimulation. I. Effects on aqueous humor inflow and outflow. (7/280)

Stimulation of the ciliary ganglion in an enucleated, arterially perfused cat eye preparation produced a sustained increase in aqueous humor formation and an increase in the rate of aqueous humor outflow. The increased aqueous humor formation induced by ciliary ganglion stimulation has been found to be pressure-dependent and therefore suggests that ultrafiltration may be the underlying mechanism of action. No change in capillary permeability of the ciliary body could be demonstrated.  (+info)

The effect of various immunosuppressive agents on mouse peritoneal macrophages and on the in vitro phagocytosis of Escherichia coli O4:K3:H5 and degradation of 125I-labelled HSA-antibody complexes by these cells. (8/280)

Large doses of hydrocortisone, cyclophosphamide, and methotrexate injected subcutaneously, and whole-body irradiation (500 rads) caused a reduction in the number of peritoneal cells (PE cells) obtained after intraperitoneal injection of the treated mice with proteose-peptone. The same dose of cyclophosphamide and irradiation induced morphological changes in PE macrophages. There were more giant cells in the peritoneal exudates from treated mice as compared to control mice. 'Pharmacological' and larger doses of hydrocortisone, methotrexate and azathioprine or anti-lymphocyte globulin had no effect on the in vitro phagocytic capacity of proteose-peptone-stimulated mouse PE macrophages. This also applied to doses of up to 50 mg/kg of cyclophosphamide. In contrast, whole-body irradiation (500 rad) and 100 mg/kg of cyclophosphamide decreased the phagocytic capacity of mouse macrophages in vitro and reduced the ability of PE cells to degrade 125I-labelled HSA-antibody complexes in vitro. The greatest effect was noted 4-5 days after whole-body irradiation or four to five subcutaneous injections of cyclophosphamide.  (+info)