Self-reported quality of life in complementary and alternative medicine treatment of chronic rhinosinusitis among African Americans: a preliminary, open-label pilot study.

OBJECTIVE: The southern U.S. region has among the highest incidence of chronic rhinosinusitis (CRS). Historically, African Americans in this region have been a difficult to reach population for clinical research participation. This study's aim was to observe any association between herbal tea consumption and CRS symptoms among African Americans. We recount the volunteers self-reporting of measurements associated with self-treatment of CRS symptoms. DESIGN: The study design was a preliminary, open-label, pilot study. SETTINGS: Volunteers were drawn from Morehouse School of Medicine's outpatient clinics, community multipurpose senior centers, and churches in Fulton and DeKalb Counties, GA. SUBJECTS: One hundred (100) African American volunteers were prescreened, of whom 55 with a clinical diagnosis of CRS met entrance criteria. INTERVENTION: Volunteers self-administered Breathe Easy herbal tea for a duration of 6 weeks. OUTCOME MEASURES: The Chronic Sinusitis Survey (CSS) scale was administered to assess sinus health at baseline and term and overall quality of life was assessed using the Short Form-36 (SF-36) index. RESULTS: Of the 55 volunteers who met entrance criteria, 41 completed the study; groups were q.i.d. (n = 27), t.i.d. (n = 4), b.i.d. (n = 5), and noncompliant (n = 5). For the q.i.d. group (n = 27), there was a significant increase in the CSS symptom score (difference in means 22.0 points; p = 0.020) and CSS total score (11.1 points; p = 0.020). Overall health status (SF-36) reported at baseline was 35% very good; 34% good; and 17% fair. After 6-weeks, the q.i.d. group showed a significant change to 44% good and 45% very good (p = 0.001). CONCLUSIONS: This preliminary pilot study suggests that q.i.d. self-administration of Breathe Easy was associated with improved volunteers' sinus health status (e.g., ability to fall sleep). Our results suggest that this herbal tea may contribute as a complementary therapy for management of CRS among African Americans. To further assess efficacy and applicability to other populations, randomized controlled trials in larger populations are warranted.

PD128,907 induces ocular hypotension in rabbits: involvement of D2/D3 dopamine receptors and brain natriuretic peptide.

The purpose of this study was to determine the potential role of brain natriuretic peptide (BNP) in the PD128,907 (a dopamine D2/D3 receptor agonist)-induced ocular hypotension in rabbits. The effects of topical application of PD128,907 (75, 250, 750 microg) on intraocular pressure (IOP) were investigated. The lowest dose (75 microg) did not alter IOP; while the higher doses (250 and 750 microg) reduced IOP bilaterally. The PD128,907 (250 microg)-induced ocular hypotension, which lasted 3 hours, could be blocked by raclopride (1000 microg), a dopamine D2/D3 receptor antagonist, as well as by sympathetic denervation. Aqueous humor inflow was reduced by intravitreal injection of PD128,907 (10 microg) by 67% at 1 and 2 hours, which then returned to baseline at 3 hours. Furthermore, topical application of PD128,907 (250 microg) elevated aqueous BNP levels by 3-fold at 30 minutes, 6-fold at 1 hour and 5-fold at 2 hours, which could be blocked by pretreatment with raclopride (250 microg). Taken together, PD128,907-induced ocular hypotension by activation of dopamine D2/D3 receptors. This action was associated with reduced aqueous humor inflow and increased aqueous BNP levels.

7-OH-DPAT-induced inhibition of norepinephrine release in PC12 cells.

The purpose of this study was to investigate mechanisms of suppression of norepinephrine release by 7-OH-DPAT, a dopamine D(2)/D(3) receptor agonist, in PC12 cells pretreated with nerve growth factor (NGF). 7-OH-DPAT caused inhibition of basal and K(+)-evoked norepinephrine release, which could be blocked by pretreatment with raclopride, a D(2)/D(3) receptor antagonist. Moreover, dopamine D(2) and D(3 )receptors were identified by immunocytochemistry. Expression of D(2), D(3), and D(4) mRNAs and their proteins were detected using RT-PCR and immunoblotting. Furthermore, 7-OH-DPAT produced no change in cGMP levels; however, 7-OH-DPAT inhibited forskolin-stimulated cAMP accumulation that was antagonized by pretreatment with raclopride. In addition, 7-OH-DPAT inhibited carbachol-induced Ca(2+) transient, conversely, 7-OH-DPAT had no effect on 4-aminopyridine-induced Ca(2+) transient. Taken together, suppression of cAMP accumulation and calcium mobilization by 7-OH-DPAT is involved in the inhibition of norepinephrine release through activation of dopamine D(2)/D(3) receptors.

The role of oxidative stress in salt-induced hypertension.

BACKGROUND: Impairment of endothelial function during hypertension is associated with increased production of superoxide radicals and reduced antioxidants. We investigated the involvement of oxidative stress in Dahl salt-sensitive (SS) and salt-resistant (SR) rats. METHODS: For a 2-week period, male rats were fed either high salt (HS; 8% sodium chloride) or low salt (LS; 0.3% sodium chloride) diets. Before and weekly on the diets, mean arterial pressure (MAP) and heart rate were measured by tail-cuff plethysmography. At the end of the experiment, plasma and tissue samples were collected for analysis of nitric oxide, prostacyclin, glutathione, and isoprostane. RESULTS: The MAP was increased in SS rats on HS diet, but not in those on a LS diet or in SR rats on either diet. Plasma levels of nitric oxide were reduced in SS rats on HS diet. Plasma prostacyclin levels in SS rats on either diet were lower than SR on LS diet. Increased dietary salt reduced plasma prostacyclin levels in SR, but not in SS rats. Plasma total 8-isoprostane was elevated in both SS and SR rats on HS diet compared with either strain on LS diet. Plasma levels of total glutathione were reduced in SS compared with SR rats, regardless of the level of dietary salt intake. The whole blood ratio of reduced-to-oxidized glutathione (GSH/GSSG) as well as the kidney total glutathione were lower in SS rats on HS diet. Aortic superoxide production in both strains on HS diet was increased compared with the animals on LS diet. CONCLUSIONS: These data suggest that HS diet may indirectly induce endothelial dysfunction through intermediate mechanisms that are associated with oxidative stress.

4-aminopyridine transiently increases intraocular pressure in rabbits.

The purpose of this study is to determine the mechanisms of action involved in the ocular hypertension induced by 4-aminopyridine (4-AP), a voltage-dependent potassium (K+) channel blocker, in rabbits. Topical application of 4-AP elevated intraocular pressure (IOP). This action caused increases in the aqueous flow rate as well as aqueous levels of protein and norepinephrine. In isolated iris-ciliary body preparations, 4-AP (0.01, 0.1, 1 mmol/l) caused dose-related increases in field-stimulated norepinephrine release by 43, 222 and 243%, respectively. Taken together, the IOP-elevating effect evoked by 4-AP was associated with enhancement of aqueous norepinephrine levels and norepinephrine release from sympathetic nerves of the iris-ciliary body. These results demonstrate that the 4-AP-sensitive K+ channels in sympathetic nerves and the ciliary epithelium are the potential sites of action of the 4-AP-induced ocular hypertension.

Effect of losartan on oxidative stress-induced hypertension in Sprague-Dawley rats.

BACKGROUND: Hypertension induced by oxidative stress has been demonstrated in normal rats. In the current study, we investigated the effect of the oral AT(1) receptor blocker losartan (10 mmol/kg/day) on oxidative stress, induced by glutathione (GSH) depletion (using buthionine-sulfoximine, BSO, 30 mmol/L/day in the drinking water), in Sprague-Dawley rats. METHODS: Mean arterial pressure (MAP) was measured by tail-cuff plethysmography and the plasma levels of total 8-isoprostane, nitric oxide, prostacyclin, thromboxane A(2), angiotensin II, aldosterone, and aortic cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were determined by enzyme immunoassay. Plasma, heart, and kidney GSH were analyzed by high-performance liquid chromatography. Aortic and renal superoxide production was determined by fluorescence spectrometry. RESULTS: In the BSO-treated group, MAP, angiotensin II, isoprostane, thromboxane A(2), and superoxide were elevated; whereas prostacyclin, GSH, cAMP, and cGMP were reduced, compared to control. Losartan alone reduced MAP, and increased renal GSH, plasma nitric oxide, angiotensin II, aldosterone, and aortic cGMP. When administered concurrently with BSO, losartan reversed the BSO-induced elevation of MAP, superoxide, and thromboxane A(2) as well as the reduction in prostacyclin and aortic cAMP levels, but did not significantly alter the reduction in GSH or the elevation in angiotensin II and aldosterone. CONCLUSIONS: Losartan attenuates BSO-induced hypertension, which appears to be mediated, in part, by angiotensin II and the prostanoid endothelium-derived factors.

Acute inhibition of glutathione biosynthesis alters endothelial function and blood pressure in rats.

The cardiovascular and biochemical responses during acute oxidative stress induced by D,L-buthionine-(S,R)-sulfoximine (BSO) were investigated in Sprague-Dawley rats. Mean arterial pressure, heart rate and vascular reactivity were measured after subcutaneous injection of BSO (4 mmol/kg). Control rats received saline. Levels of GSH and GSSG in blood and tissues as well as renal superoxide were determined. Nitric oxide, prostacyclin and thromboxane A(2) in plasma and aorta, and isoprostane in plasma were also measured. Blood pressure was elevated at 24 h (121+/-2 vs. 104+/-2 mm Hg), with increased reactivity to phenylephrine (by a 59+/-4 vs. 45+/-2 mm Hg change), and impaired response to sodium nitroprusside (by a -35+/-2 vs. -63+/-2 mm Hg change), P<0.05. The GSH:GSSG ratio was reduced at 8 and 24 h in blood (4.1+/-0.6 and 5.1+/-0.3, respectively, vs. 8.5+/-0.2), and at 8 h in the aorta (1.0+/-0.2 vs. 2.9+/-0.5), heart (1.6+/-0.3 vs. 2.3+/-0.1) and kidney (2.1+/-0.2 vs. 3.7+/-0.4), P<0.05. Superoxide fluorescence was increased at 24 h via NADH (4131+/-194 vs. 2853+/-199), NADPH (2874+/-272 vs.1479+/-257) and succinate (2475+/-133 vs. 1594+/-2150), P<0.05. Plasma prostacyclin was reduced at 8 and 24 h (36+/-4 and 52+/-13, respectively, vs. 310+/-44 pg/ml), P<0.001, whereas nitric oxide was reduced at 24 h (6.4+/-1 vs. 22+/-2 microM), P<0.01. Also at 24 h, thromboxane A(2) was increased both in plasma (374+/-154 vs. 61+/-10 pg/ml) and the aorta (174.4+/-38 vs. 27+/-3.4 pg/mg), P<0.05. Thus, acute BSO-induced oxidative stress alters blood pressure and endothelial function by mechanisms involving increased plasma levels and aortic release of thromboxane A(2) and reduced nitric oxide and prostacyclin.

Effect of palm oil on oxidative stress-induced hypertension in Sprague-Dawley rats.

BACKGROUND: Oxidative stress, associated with increased plasma isoprostane (ISO) and reductions in plasma glutathione (GSH), has been shown to cause severe hypertension in normal rats. Palm oil (PO), with an unsaturated-to-saturated fatty acid ratio close to one and rich in antioxidant vitamins, has been investigated for its beneficial effects on arterial thrombosis and atherosclerosis. In this study, the effect of PO on oxidative stress induced by inhibition of GSH synthesis (using buthionine sulfoximine [BSO]) was examined. METHODS: Sprague-Dawley rats were separated into two groups and received either natural vitamin-rich PO (Carotino, 5 g/kg daily) or water by gavage. After 4 weeks, they were further divided between receiving either BSO (30 mmol/L/day in the drinking water) or drug-free water for an additional week. Mean arterial pressure (MAP), heart rate (HR), and body weight (BW) were measured before and weekly during the experiment. The levels of plasma ISO, nitric oxide (NO), prostacyclin (PGI2), and thromboxane A2 (TXA2) were determined by enzyme immunoassay, and plasma, heart, and kidney GSH by high-performance liquid chromatography. RESULTS: The PO reduced the age-dependent increase in MAP, and the pressor response to BSO, without changing the HR or BW compared to the BSO and control groups. It also elevated PGI2, NO, and aortic cGMP, but decreased TXA2 and aortic cAMP. In addition, the BSO-induced increase in ISO and TXA2, and the reduction in kidney GSH were attenuated by PO. However, the PO effect on NO, PGI2, cGMP, and TXA2 was partly counteracted by BSO. CONCLUSIONS: Palm oil reduces BSO-induced oxidative stress and attenuates hypertension by mechanisms involving changes in endothelium-derived factors.

High performance liquid chromatographic assay for the quantitation of total glutathione in plasma.

A simple and widely used homocysteine HPLC procedure was applied for the HPLC identification and quantitation of glutathione in plasma. The method, which utilizes SBDF as a derivatizing agent utilizes only 50 microl of sample volume. Linear quantitative response curve was generated for glutathione over a concentration range of 0.3125-62.50 micromol/l. Linear regression analysis of the standard curve exhibited correlation coefficient of 0.999. Limit of detection (LOD) and limit of quantitation (LOQ) values were 5.0 and 15 pmol, respectively. Glutathione recovery using this method was nearly complete (above 96%). Intra-assay and inter-assay precision studies reflected a high level of reliability and reproducibility of the method. The applicability of the method for the quantitation of glutathione was demonstrated successfully using human and rat plasma samples.

1A-779 attenuates angiotensin-(1-7) depressor response in salt-induced hypertensive rats.

Chronic infusion of angiotensin-(1-7) [Ang-(1-7)] lowers blood pressure in salt-induced and spontaneously hypertensive (SHR) rats. In the present study, we have examined the acute effect of Ang-(1-7) in salt-induced hypertension using Dahl salt-sensitive rats placed on low (0.3%) or high (8.0% NaCl) salt diets for 2 weeks. Rats fed a high salt diet showed a greater rise in BP than those fed a low salt diet. Ang-(1-7) (24 microg/kg) reduced mean arterial pressure (MAP), enhanced the release of prostacyclin and nitric oxide, and suppressed thromboxane A(2) levels. A-779 (48 microg/kg, i.v), a selective Ang-(1-7) antagonist, partially blocked these effects of Ang-(1-7). The Ang-(1-7)-induced depressor response observed in these animals was related to an increase in vasodilatory prostanoids, a decrease in the constrictor prostanoid thromboxane A(2), and an increase in nitric oxide levels in both plasma and isolated aortic rings.