Biomedical subjects

E Grossman

Publications and source records attributed to E Grossman.

At least 145 records · Page 8Linked to original sources

PubMed1991

Left ventricular filling and stress response pattern in essential hypertension.

PURPOSE: To evaluate whether impaired left ventricular filling determines the hemodynamic responses to isometric and orthostatic stress in a population with mild essential hypertension. PATIENTS AND METHODS: The study population consisted of 32 patients with essential hypertension who were subdivided into those with preserved left ventricular filling (15 patients) and those with impaired left ventricular filling (17 patients). Echocardiograms were obtained before hemodynamic assessment was performed. Isometric stress and head-up tilt tests were done with a recovery period of at least 10 minutes between each to allow for blood pressure and heart rate to return to baseline. Hemodynamic reassessment was performed during the last minute of each test and at the end of the recovery period. Plasma epinephrine, norepinephrine, and dopamine levels were determined by radioenzymatic method. RESULTS: Isometric stress increased mean arterial pressure by 30% (p less than 0.0001) by an increase in cardiac output (p less than 0.0001) and total peripheral resistance (p less than 0.0001) associated with an increase in plasma catecholamine levels (p less than 0.0001). Patients with preserved left ventricular filling had an increase in arterial pressure predominantly through an elevation in cardiac output (17%, p less than 0.0001) associated with a small increase in plasma norepinephrine levels (p less than 0.05) and in peripheral resistance (11%, p less than 0.05). In contrast, patients with impaired left ventricular filling had an increase in arterial pressure mainly through an increase in peripheral resistance (25%, p less than 0.0001) that was associated with a 45% elevation in plasma norepinephrine levels (p less than 0.0001). Orthostatic stress (passive head-up tilt) caused an exaggerated decrease in stroke volume (p less than 0.01) and cardiac output (p less than 0.01) in patients with impaired left ventricular filling when compared with those with preserved diastolic function. CONCLUSION: Impaired left ventricular filling blunts the response of the heart to isometric and orthostatic stress. As a consequence, hypertensive patients with impaired ventricular filling respond to these stressors with enhanced sympathetic stimulation and exaggerated vasoconstriction.

Adult↗

PubMed1991

Immediate and short-term cardiovascular effects of fosinopril, a new angiotensin-converting enzyme inhibitor, in patients with essential hypertension.

Immediate and short-term cardiovascular effects of a new angiotensin-converting enzyme inhibitor, fosinopril, were assessed in 10 patients with mild to moderate essential hypertension. Administration of a 10 mg oral dose of fosinopril reduced mean arterial pressure (p less than 0.001) as a result of a 24% fall in total peripheral resistance (p less than 0.001). Short-term therapy (12 weeks) maintained the decrease in mean arterial pressure (p less than 0.05) by decreasing total peripheral resistance (p less than 0.01), without reflexive cardiac stimulation or expanding intravascular volume. Renal vascular resistance decreased (p less than 0.05) while renal blood flow, glomerular filtration rate and filtration fraction remained unchanged. The response pattern to mental, isometric and orthostatic stress was similarly unchanged. Left ventricular mass diminished by 11% (p less than 0.01); myocardial contractility was unaffected. Afterload was reduced (p less than 0.05), and velocity of circumferential fiber shortening and stroke volume increased (p less than 0.05). Thus, arterial pressure reduction produced by fosinopril was associated with improved systemic and renal hemodynamics and reduced left ventricular mass.

Adult↗

PubMed1991

Increased plasma levels and blunted effects of brain natriuretic peptide in rats with congestive heart failure.

The hemodynamic and renal effects of brain natriuretic peptide (BNP) were studied in conscious rats with experimental congestive heart failure (CHF) produced by an aortocaval fistula. The peptide had potent hypotensive, diuretic, and natriuretic effects in control rats, all of which were abolished in CHF. Plasma levels of BNP increased time-dependently during the development of CHF, and were more than four-fold higher in sodium retaining rats than in control rats. The data suggest that BNP secretion from the atria is increased in CHF, and that resistance to BNP, in addition to the relative resistance to atrial natriuretic factor, may contribute to sodium retention in CHF.

Animals↗

PubMed1991

Endogenous dopa and dopamine responses to dietary salt loading in salt-sensitive rats.

We measured daily urinary excretion rates of dopamine and dopa during dietary salt loading and natriuretic responses to exogenous dopamine in Dahl salt-sensitive (DS), Dahl salt-resistant (DR) and Sprague-Dawley rats. Excretion rates of dopa increased approximately sixfold during salt loading in all rat strains. Maximal urinary dopa responses were attained within 1 day of salt loading. Daily excretion rates of dopamine also increased about five- to sixfold in DS and DR rats and about twofold in Sprague-Dawley rats, with maximal dopamine responses attained by day 5. Dopamine infusion (3 micrograms/kg per min) increased urinary sodium excretion by 406 +/- 132 % (mean +/- s.e.m.) in Sprague-Dawley rats but only 267 +/- 131% and 147 +/- 80% in DS and DR rats (P less than 0.05 for Sprague-Dawley versus Dahl rats). The results demonstrate that salt loading markedly and rapidly increases dopa excretion in rats. Considering values for dopamine excretion in other rat strains, the results suggest that Dahl rats have increased formation of dopamine for a given amount of dopa delivery to the kidney and that this abnormality is unrelated to salt-sensitive hypertension in DS rats. The results also provide in vivo support for the view that the responsiveness of renal dopamine receptors mediating natriuresis is related to production of endogenous dopamine in the kidney.

Animals↗

PubMed1991

Positron emission imaging of cardiac sympathetic innervation and function using 18F-6-fluorodopamine: effects of chemical sympathectomy by 6-hydroxydopamine.

Hypotheses concerning the pathophysiology of hypertension, cardiac failure and other cardiovascular disorders have imputed abnormal cardiac sympathoneural activity. Here we describe a technique to examine cardiac sympathetic innervation and function using positron emission tomographic (PET) scanning after systemic intravenous injection of 18F-6-fluorodopamine, and the effects of chemical sympathectomy by the neurotoxin, 6-hydroxydopamine (6-OHDA). Uptake of 18F-6-fluorodopamine by the heart of anesthetized dogs resulted in striking delineation of the left ventricular myocardium. Myocardial radioactivity declined bi-exponentially, with a half-life of approximately 2 h during the longer phase. In 6-OHDA-treated animals, the ventricular myocardium was barely distinguishable from the chamber; myocardial radioactivity declined rapidly and was virtually absent within 30 min after injection of 18F-6-fluorodopamine. The rates of decline in myocardial radioactivity in dogs treated with 6-OHDA were similar to those in dogs treated with reserpine, but the mechanisms of sympatholysis by these drugs were distinguished by arterial plasma levels of 6-fluorodihydroxyphenylacetic acid (6-FDOPAC). Plasma 6-FDOPAC levels were diminished in 6-OHDA-treated dogs and elevated in reserpinized dogs. The results confirm that, after injection of 18F-6-fluorodopamine, cardiac sympathetic nerve endings are radiolabeled, allowing visualization of sites of sympathetic innervation. Combined assessments of PET time-activity curves and plasma levels of metabolites of 18F-6-fluorodopamine constitute a new, potentially clinically applicable means by which to examine cardiac sympathetic function.

Animals↗

PubMed1991

Correlations between caries prevalence and potential etiologic factors in large samples of 4-5-yr-old children.

A data base containing information on dental caries, oral hygiene, gingival state, Streptococcus mutans and lactobacillus counts, and salivary flow rate and buffer capacity in some 2800 4-5-yr-old South African children was created in 1984. The children were equally distributed in four groups; rural black, urban black, urban Indian, and urban white. In this study, the data were used for simple linear correlations between all the factors including caries as well as stepwise multiple regression analyses between caries prevalence and the independent factors in each of the four groups. The highest r value obtained in the single correlations was 0.56 for dmfs/lactobacillus count in the white group. The overall pattern of the groups did not vary much. In the stepwise multiple regression analyses, lactobacilli entered first in all groups. S. mutans and oral hygiene interchanged as Nos. 2 and 3, and gingival state or buffer capacity came out as No. 4. The highest percentage of caries variability explained by these regressions was 25%, in the urban black group, while the lowest was 12%, in the indian group. It was concluded that our generally accepted etiologic factors are unsatisfactory to explain variation in caries in observational studies, which among other things might be ascribed to the inadequate way these factors generally are measured or estimated.

Black or African American↗

PubMed1991

Yohimbine increases sympathetic nerve activity and norepinephrine spillover in normal volunteers.

It has been difficult to examine clinically the physiological role of central and peripheral alpha 2-adrenoceptors in humans. We simultaneously measured directly recorded peroneal skeletal muscle sympathoneural activity (MSNA) and the rate of appearance (spillover) of norepinephrine (NE) in forearm venous and arterial plasma before and at 15 min during intravenous administration of the alpha 2-blocker yohimbine (Yoh, 125 micrograms/kg bolus, 1 microgram.kg-1.min-1 infusion) in seven normal volunteers. Yoh administration increased mean arterial pressure by 16% (P less than 0.005), heart rate by 8% (P less than 0.05), and forearm vascular resistance by 67% (P less than 0.05). MSNA was increased by 73% (P less than 0.05), NE spillover into arterial blood by 125% (P less than 0.05), and forearm NE spillover (FSO) by 337% (P less than 0.005). Ganglion blockade by trimethaphan during Yoh infusion decreased MSNA to below detection limits and reversed Yoh-induced increases in arterial concentrations of NE and epinephrine. The results demonstrate that Yoh administration increases sympathoadrenal outflow. Because the mean increase of FSO was much larger than that of MSNA, the results suggest that alpha 2-adrenoceptors on sympathetic nerve endings modulate the neuronal release of NE for a given amount of sympathetic nerve traffic in humans; this effect seems prominent in the human limb.

Adrenocorticotropic Hormone↗

PubMed1991

Tracer norepinephrine kinetics: dependence on regional blood flow and the site of infusion.

The rate of appearance of the sympathetic neurotransmitter norepinephrine (NE) in the regional venous drainage (NE spillover) can be estimated based on intravenous or intra-arterial infusions of [3H]NE. The present study examined whether forearm NE spillover (FASO) in humans depends on forearm blood flow (FBF) and on the site of infusion of the tracer. Healthy volunteers underwent infusions of [3H]NE and [3H]isoproterenol (Iso) administered intravenously (n = 21), intra-arterially (n = 32), or by both routes in the same experimental session (n = 7). FBF was manipulated by intra-arterial infusions of the vasodilator sodium nitroprusside (n = 7) or the vasoconstrictor methoxamine (n = 7). Forearm extraction percents of [3H]NE exceeded those of [3H]Iso in all subjects undergoing intravenous infusions (54 vs. 46%, P less than 0.001), whereas extraction percents of [3H]Iso exceeded those of [3H]NE when the tracers were infused intra-arterially. Regardless of the infusion site, FASO was positively correlated with FBF (r = 0.44, P less than 0.005). Nitroprusside increased FBF and FASO, and methoxamine decreased FBF and FASO. When the tracers were added to whole blood, 89% of [3H]NE and 83% of [3H]Iso remained in plasma after 1 min; although no further loss of [3H]NE occurred over time, only 60% of the added [3H]Iso remained in plasma by 20 min. The results indicate that regional NE spillover is flow dependent, complicating inferences about regional sympathoneural activity. Intra-arterial infusion of [3H]NE results in higher estimates of regional NE spillover than does intravenous infusion of the tracer.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Glucagon and clonidine testing in the diagnosis of pheochromocytoma.

We assessed the sensitivity and specificity of glucagon stimulation and clonidine suppression tests in the diagnosis of pheochromocytoma in 113 hypertensive patients, 39 with and 74 without the tumor. In the glucagon stimulation test, blood was sampled 2 minutes after intravenous injection of 0.28 mumol (1 mg) glucagon, and in the clonidine suppression test, blood was sampled 3 hours after administration of oral clonidine, 1.30 mumol (0.3 mg)/70 kg body wt. Baseline levels of catechols in antecubital venous blood were abnormal, with norepinephrine greater than 7.10 nmol/l (1,200 pg/m), epinephrine greater than 1.51 nmol/l (276 pg/ml), norepinephrine/dihydroxyphenylglycol (DHPG) ratio greater than 1.09, or dopa greater than 35.53 nmol/l (7,000 pg/ml), in 30 of 39 patients with pheochromocytoma (sensitivity 77%) and 1 of 74 patients without pheochromocytoma (specificity 99%). Results of the glucagon test were abnormal (norepinephrine greater than 11.83 nmol/l [2,000 pg/ml] or more than threefold increase from baseline) in 25 of 31 patients with pheochromocytoma (sensitivity 81%) and 0 of 72 patients without pheochromocytoma (specificity 100%). Results of the clonidine test were abnormal (after clonidine norepinephrine greater than 2.96 nmol/l [500 pg/ml] or less than 50% decrease from baseline) in 29 of 30 patients with pheochromocytoma (sensitivity 97%) and in 7 of 30 patients without pheochromocytoma (specificity 67%). Very high baseline levels of catechols therefore indicated the presence of pheochromocytoma, but there were several false-negative results when normal levels were obtained. The glucagon test alone was highly specific but not sensitive, and the clonidine test was highly sensitive but less specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗

PubMed1991

High urinary dopa and low urinary dopamine-to-dopa ratio in salt-sensitive hypertension.

Dopamine in urine is derived substantially from renal uptake and decarboxylation of 3,4-dihydroxyphenylalanine (dopa), and increases in excretion of dopa normally parallel increases in excretion of dopamine during salt loading. Since patients with salt-sensitive hypertension may have decreased urinary excretion of dopamine during dietary salt loading, the present study was designed to evaluate the response of dopa to salt loading. Sixteen inpatients with normal-renin essential hypertension ate a constant metabolic diet containing 9 mmol/day sodium for 7 days, followed by the same diet but containing 249 mmol/day sodium for 7 days. Salt sensitivity was defined as an increase in mean arterial pressure of 8 mm Hg between the diets; on this basis, nine patients were salt-sensitive and seven, salt-resistant. The rate of urinary dopa excretion was significantly higher in the salt-sensitive patients throughout the study (mean rates 132 +/- 13 nmol/day in the salt-sensitive group and 78 +/- 9 nmol/day in the salt-resistant group for the 14 days of observation, p less than 0.01). When dietary sodium intake was increased to 249 mmol/day, urinary dopa excretion increased significantly more in salt-sensitive patients than salt-resistant patients. At the end of the high salt diet, dopamine excretion was significantly attenuated in the salt-sensitive patients, despite higher rates of dopa excretion. Thus, the urinary ratio of dopamine to dopa was decreased in salt-sensitive patients, regardless of salt intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Sympathetic reactivity during a yohimbine challenge test in essential hypertension.

Systemic administration of yohimbine augments sympathetic outflow and blocks presynaptic alpha 2-adrenergic receptors, releasing the sympathetic neurotransmitter norepinephrine (NE) into the bloodstream. The present study examined sympathoadrenal and hemodynamic responses to yohimbine in 19 patients with essential hypertension and 19 normotensive control subjects. Baseline mean values for arterial NE, epinephrine, dihydroxyphenylglycol (the main intraneuronal metabolite of NE), spillover of NE into arterial plasma, and corticotropin did not differ between the hypertensive and normotensive groups. Yohimbine (0.125 mg/kg i.v. bolus followed by 0.001 mg/kg/min infusion for a total of 15 minutes) increased mean arterial pressure in all but one subject (by 13 +/- 2% [SEM] in the normotensive and 17 +/- 2% in the hypertensive group) and increased arterial NE levels in all subjects (by 253 +/- 50 pg/ml in the normotensive and 312 +/- 51 pg/ml in the hypertensive group). Among hypertensive patients, pressor, cardiac, output, and arterial NE responses were distributed bimodally. Patients with large hemodynamic and NE responses to yohimbine typically reported a history of anxiety, depression, or other psychopathology and of marked pressor or tachycardic episodes during emotional stress. In the hypertensive and normotensive groups, baseline arterial NE concentrations predicted the magnitude of pressor responses to yohimbine (r = 0.59, r = 0.54,p less than 0.01), whereas baseline mean arterial pressure was unrelated to the pressor response. A yohimbine challenge test can identify patients with pressor hyperresponsiveness and can distinguish patients with pressor hyperresponsiveness due to excessive sympathoadrenal reactivity from patients with enhanced postsynaptic responsiveness to endogenous NE.

Adrenocorticotropic Hormone↗

PubMed1991

Evidence for functional alpha 2-adrenoceptors on vascular sympathetic nerve endings in the human forearm.

The role of alpha 2-adrenoceptors on vascular sympathetic nerve endings in modulating release of the sympathetic neurotransmitter norepinephrine (NE) in humans was examined by measuring the regional rate of appearance of NE in forearm venous plasma (forearm NE spillover [FSO]) in 32 healthy volunteers during intra-arterial infusion of drugs acting at adrenoceptors or directly on vascular smooth muscle. Simultaneous intra-arterial infusions of tracer amounts of [3H]NE were used to calculate the extraction rate of NE in the forearm. Methoxamine or propranolol with epinephrine (PRO + EPI) was used to stimulate alpha-adrenoceptors, yohimbine was used to inhibit alpha-adrenoceptors, and sodium nitroprusside (NIP) was used to produce increases in forearm blood flow directly. Sympathetic efferent activity was manipulated by systemic intravenous infusions of NIP or trimethaphan. Yohimbine and NIP increased and PRO + EPI and methoxamine decreased NE FSO, without effects on systemic blood pressure, heart rate, or arterial levels of catechols. Changes in FSO were flow dependent; therefore, the slope of the relation between the changes in FSO and forearm blood flow was used to evaluate the effects of each drug on regional sympathoneural activity. During administration of yohimbine, the mean slope of the relation between the change in estimated FSO and the change in forearm blood flow was about four times that of the mean slope during administration of NIP (F = 6.35, p less than 0.05). The slopes of the relations between changes in FSO and forearm blood flow were unaffected by systemic trimethaphan or NIP infusion, indicating that the activity of alpha 2-adrenoceptors was not altered during inhibition or reflexive stimulation of sympathetic outflow. The results suggest that alpha 2-adrenoceptors modulate release of NE from vascular sympathetic nerve endings in humans and that the function of these receptors is unchanged during acute changes in junctional NE concentrations.

Adult↗

PubMed1990

Opposite effects of endothelin-1 and Big-endothelin-(1-39) on renal function in rats.

Bolus injections of Big-endothelin-(1-39) (Big-ET; 0.1-3.0 nmol/kg) induced a dose-dependent diuretic and natriuretic response in conscious Sprague-Dawley rats. Endothelin-1-(1-21) (ET-1; 1 nmol/kg) induced an opposite effect with almost complete renal shut down. Renal blood flow did not change with Big-ET but was reduced by half with ET-1. Although the maximal pressor responses of the two peptides were comparable the renal resistance did not change with Big-ET but increased 4-fold with ET-1. These data suggest that Big-ET may have a different mechanism of action than ET-1.

Anesthesia↗

PubMed1990

Increased spillover of dopa into arterial blood during dietary salt loading.

1. We measured urinary excretion rates of dopamine (3,4-dihydroxyphenethylamine) and dopa (3,4-dihydroxyphenylalanine) and the spillover rate of dopa into arterial blood during dietary salt loading in conscious Dahl salt-sensitive and salt-resistant rats with intact or denervated kidneys. 2. Dopa spillover was calculated from the steady-state clearance of intravenously infused L-[3H]dopa and arterial levels of endogenous dopa. 3. Daily excretion rates of dopa and dopamine increased by about sixfold during salt loading in both rat strains. Bilateral renal denervation delayed these increases and the natriuretic responses. 4. During dietary salt loading, dopa spillover increased to approximately the same extent as simultaneously measured dopamine excretion. 5. The results suggest that increases in urinary excretion of dopamine during dietary salt loading can be accounted for by increases in the release of dopa into the bloodstream and that the renal nerves contribute to the dopa and dopamine excretory responses.

Animals↗

PubMed1990

The initial vasodilation and the later vasoconstriction of endothelin-1 are selective to specific vascular beds.

The regional hemodynamic effects of endothelin-1 (ET-1) were studied in Wistar-Kyoto rats. Endothelin-1 caused a transient increase in blood flow in the carotid and femoral arteries but a decrease in flow in the renal and mesenteric arteries. The resistance in the carotid and femoral beds decreased while it increased in the renal and mesenteric beds. Subsequently there was a variable increase in resistance in all vascular beds with a maximal increase in the renal bed. Thus, ET-1 initially causes a selective vasorelaxation in musculocutaneous beds but not in visceral beds; the cause of this selectivity is unknown.

Animals↗

PubMed1990

Sodium intake modulates renal vascular reactivity to endothelin-1 in Dahl rats.

1. The systemic and renal haemodynamic responses to endothelin-1 (ET1) were evaluated and compared to Angiotensin II (AII) in anaesthetized Dahl salt-sensitive (DS) and salt-resistant (DR) rats on either low (0.1% NaCl in diet) or high (8% NaCl in diet) salt intake. 2. Baseline mean arterial pressure on low salt diet was similar in both strains, while on high salt diet it was 73 +/- 4 mmHg in DR rats and 119 +/- 8 mmHg in DS rats (P less than 0.05). Baseline renal blood flow (RBF) and renal vascular resistance (RVR) were similar in all groups. 3. AII in bolus injection induced a short, dose-dependent increase in blood pressure and renal vascular resistance and a fall in renal blood flow. The maximal pressure increase was significantly greater in DS rats on high salt diet than that in each of the other groups (P less than 0.05). The fall in renal blood flow and the increase in renal vascular resistance were attenuated in both strains on low salt diet. 4. ET1 induced an initial decrease followed by a prolonged increase in blood pressure; both phases were similar in all groups. However, renal vascular reactivity to ET1 was markedly modulated by salt intake. On low salt diet, following a bolus injection of ET1 (1 nmol/kg), RBF decreased by 34% in DR and by 20% in DS rats, while on high salt diet RBF decreased by 76% in DR and by 80% in DS rats (P less than 0.05 high vs low salt).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1990

Role of atrial appendages in modulating stimulated plasma atrial natriuretic peptide levels in conscious rats.

To evaluate the role of the atrial appendages in modulating plasma levels of atrial natriuretic peptide (ANP), we applied a series of both acute and chronic stimuli in conscious, chronic, bilaterally atrial-appendectomized (APP) and sham-operated control rats. Basal plasma ANP levels and urinary sodium excretion were normal in all rats after APP. The release of ANP was markedly blunted to acute volume expansion (+67% vs. +357% in controls, P less than 0.01) but was only moderately reduced after norepinephrine infusion (+106% vs. +212%, P less than 0.05) and was normal after acute salt load [+148% vs. +180% in controls, not significant (NS)]. Furthermore, plasma levels of ANP were increased normally in APP rats treated with deoxycorticosterone acetate (270 + 18 vs. 296 + 14 pg/ml in controls, NS) and in APP rats with congestive heart failure induced by a large arteriovenous (a-v) fistula between the aorta and the vena cava (306 +/- 18 vs. 302 +/- 12 pg/ml, NS). Sodium excretion patterns were similar in chronically stimulated APP and control rats. The results demonstrate that, although APP reduces the response of ANP release to acute volume expansion, it does not do so to other stimuli of either acute or chronic nature, suggesting that there is no permanent defect in the ability of APP rats to secrete ANP. These studies confirm that the atria are the major source for ANP release into the circulation after acute intravascular volume expansion. However, other tissue sources may contribute significantly to the levels of circulating ANP in response to this and other acute and chronic stimuli.

Animals↗

PubMed1990

Supragingival irrigation with 0.06% chlorhexidine in naturally occurring gingivitis. I. 6 month clinical observations.

The purpose of this study was to assess the efficacy of supragingival irrigation with 0.06% chlorhexidine gluconate (CHX) on naturally occurring gingivitis. The relative benefit of CHX irrigation in comparison with CHX rinsing, water irrigation, and normal oral hygiene was evaluated. In a blind, placebo-controlled 6-month study 222 patients were assigned to one of four groups: Group 1: Once daily irrigation with 300 ml water followed by irrigation with 200 ml 0.06% chlorhexidine gluconate (experimental); Group 2: Twice daily rinsing with 15 ml 0.12% chlorhexidine (positive control); Group 3: Once daily irrigation with 500 ml water (irrigation control) and Group 4: Sodium fluoride dentifrice for normal oral hygiene only (negative control). All groups used the same sodium fluoride dentifrice for tooth brushing. At baseline, 3 months, and 6 months patients were examined for Gingival Index (GI), Bleeding on Probing (BOP), Plaque Index (PLI), Pocket probing depth (PD), Calculus Index (CI), and stain. After the baseline visit all patients received a supra- and subgingival oral prophylaxis. At 6 months GI and BOP were significantly (P less than or equal to 0.05) reduced by adjunctive CHX irrigation (42.5% and 35.4%, respectively), CHX rinse (24.1% and 15.0%), and water irrigation (23.1% and 24.0%) compared to tooth brushing alone. Plaque was significantly (P less than or equal to 0.05) reduced only by CHX irrigation (53.2%) and CHX rinse (43.3%) while calculus and staining were significantly (P less than or equal to 0.05) increased in the two chlorhexidine groups (276.4% (irrigation) and 273.2% (rinse)). Although significant (P less than or equal to 0.05), pocket probing depth reduction was minimal after CHX irrigation (4.6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗