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Previous studies have demonstrated variable effects on systemic inflammatory and immune responses following improved periodontal health. This study examined changes in serum levels of the inflammatory mediators IL-1β, IL-6, TNF-α and sICAM-1, and antibodies to Porphyromonas gingivalis, human heat shock protein (hHSP) 60 and P. gingivalis GroEL following improvement in periodontal health in high cardiovascular (CV) risk and low CV-risk patients.Patients retrospectively selected from a longitudinal study, had undergone yearly periodontal examinations and peripheral blood collections. They had demonstrated a quantifiable improvement in periodontal health (60% reduction in number of sites with probing depth ≥ 4 mm from the baseline visit) and could be classified as either high CV-risk (≥ 6 classical risk factors, n = 13) or low CV-risk (≤ 1 classical risk factor, n = 14). Serum levels of the cytokines and antibodies were measured using ELISA.For sICAM-1 and anti-P. gingivalis GroEL and anti-hHSP60 antibodies, most patients recorded decreased levels. Reductions in serum sICAM-1 levels were more notable in low CV-risk patients (p = 0.006); and reductions in levels of anti-P. gingivalis GroEL and anti-hHSP60 antibodies (p = 0.001 and 0.009 respectively) were more notable in high CV-risk patients.This study found that subsequent to improved periodontal health, the anti-HSP (HSP60 and GroEL) antibody response was reduced, particularly for high CV-risk patients. sICAM-1 levels were also lowered, more so for low CV-risk patients.

We have studied the antiemetic effects of propofol when mixed with morphine in a patient-controlled analgesia (PCA) pump after major gynaecological surgery. In a double-blind, randomized, controlled study, 50 women, ASA I or II, received a standardized anaesthetic comprising thiopental, morphine, atracurium, nitrous oxide and oxygen with enflurane, and received postoperative PCA with morphine mixed with either 1% propofol or lvelip. The PCA bolus was morphine 1 mg with propofol 5 mg or lvelip 0.5 ml, with a lockout time of 5 min. Postoperative nausea and vomiting (PONV) were assessed by the nursing staff using a four-point ordinal scale and by the patient using a visual analogue scale for 48 h after surgery. The two groups were similar in the potential factors influencing the incidence of PONV. There were no significant differences between the two groups in any of the study measurements of PONV. There were, no side effects after propofol. Propofol, when mixed with morphine in this dose combination for PCA, did not decrease the incidence of nausea and vomiting in women undergoing major gynaecological surgery.

The total number of neurons in the major laminae of the human entorhinal cortex were estimated with a design-based stereological technique, the optical fractionator. Detailed descriptions of the laminar organization and the cortical limits of the region required for the analysis are provided, along with detailed descriptions of the sampling scheme employed. The individual, mean values, and variances for estimates made in layers II, III, V, and VI are presented and discussed in terms of the precision of the estimation procedure and the results of other studies. Neuron numbers were estimated to be about 1 million layer II cells, 5 million layer III cells, 2 million layer V cells, and 4 million layer VI cells, for a total of slightly more that 13 million neurons in the entorhinal cortex. Combined with data from a similar study carried out in the human hippocampus, the data presented represent the first rigorous stereological evidence of the divergence of entorhinal projections to the hippocampus. The data presented also indicate that projections from layer II of the entorhinal cortex to the dentate gyrus and CA2/3 and projections from layer III of the entorhinal cortex to CA1 differ in the degrees of their divergence.

Cation transport across the red-cell membrane was studied in subjects with essential hypertension and their relatives using rubidium-86 as an analogue of potassium. The activity of the ouabain-sensitive sodium-potassium pump was significantly greater in patients with untreated essential hypertension than in controls (p less than 0.001). No clear separation was seen between normotensive and hypertensive subjects. Activity of the sodium-potassium pump was also increased in a proportion of normotensive relatives of subjects with essential hypertension. Rubidium uptake was significantly lower in normotensive black subjects than in normotensive whites, the difference being in a ouabain-resistant pathway of cation transport. These results provide further evidence that a defect in membrane cation transport contributes to the pathogenesis of essential hypertension.

The interaction between atrial natriuretic peptide (ANP) and the renin-angiotensin-aldosterone (RAA) system was studied in 6 healthy volunteers using the angiotensin-converting-enzyme (ACE) inhibitor, captopril. Each volunteer received, on separate occasions in random order, 48 hours treatment with a) low-dose captopril (6.25 mg twice daily), b) 'high-dose' captopril (25 mg twice daily) and c) placebo prior to an infusion of synthetic human ANP (99-126). Resting plasma ANP levels were significantly (P less than 0.01) higher on treatment with 'high-dose' captopril when compared with low-dose captopril or placebo. 'High-dose' captopril reduced mean arterial blood pressure (BP) and significantly (P less than 0.01) reduced the natriuretic response to the human ANP infusion. These results support the hypothesis that ACE is involved in ANP metabolism. The reduced renal response to ANP during treatment with captopril may reflect the dependence of ANP on adequate renal perfusion pressure and angiotensin II levels to exert its natriuretic effect.

The antihypertensive actions of the beta-adrenergic blocking agent, prindolol, and of the diuretic, hydrochlorothiazide, were analysed in a double-blind randomized 2 X 2 factorial trial in 16 patients. There were four eight-week phases in which patients received prindolol alone, hydrochlorothiazide alone, prindolol plus hydrochlorothiazide in combination, and no treatment. Both drugs were given in fixed doses: prindolol, 10 mg three times per day; hydrochlorothiazide, 50 mg per day. Blood pressure was measured weekly, alternately at the outpatient clinic and at home. Supine mean arterial pressure (MAP) in resting patients fell from 127 mm Hg in the placebo phase to 117 mm Hg with hydrochlorothiazide alone, 116 mm Hg with prindolol alone, and 111 mm Hg with the combination of prindolol and hydrochlorothiazide. (The standard error of difference between treatments was +/-3-58). A mean factorial effect of -7 mm Hg for hydrochlorothiazide (P less than 0-01) and -8 mm Hg for prindolol (P less than 0-01) was obtained, and the two drugs acted in an additive manner. The effects on standing blood pressure in resting patients were similar. No serious side effects were noted.

Twenty-two young normotensive male subjects, 12 with an established family history of essential hypertension, were put on a low-followed by a high-sodium diet. Plasma from each dietary period was tested for inhibitory activity on Na-K-ATPase using three different techniques: measurement of 22Na efflux rate, measurement of 3H ouabain binding characteristics and a bioluminescent adenosine triphosphate assay. The high-sodium diet was associated with a diminished ouabain-sensitive sodium efflux rate constant in the whole group; however, no circulating inhibitor could be detected in the plasma. Those with and those without a family history of essential hypertension were indistinguishable. The results suggest that young normotensive individuals with a genetic predisposition to essential hypertension do not produce a circulating inhibitor of sodium-potassium adenosine triphosphatase (Na-K-ATPase) in response to a high-sodium challenge.

In a cross sectional study of 137 women of childbearing age (16-40) the effects of normal pregnancy, hypertensive pregnancy, and oral contraceptives on red cell electrolyte content and sodium efflux rates were examined and the results compared with values in a control group of normotensive, non-pregnant women. Efflux rate constants were significantly increased in normotensive pregnancy and in women taking oral contraceptives. This was associated with a significant increase in sodium permeability in the contraceptive group. A much larger increase in sodium permeability and efflux rate constant was seen in the hypertensive group. The results permit a hypothesis that the hormonal changes induced by pregnancy and oral contraceptives increase membrane permeability to sodium and stimulate sodium efflux. The rise in blood pressure associated with use of oral contraceptives may have a similar aetiology to that occurring in pregnancy induced hypertension.

To examine the interrelationship of blood pressure, ethnic origin, genetic predisposition to hypertension, and cellular sodium handling, 49 hypertensive and 70 normotensive subjects were studied. Those with a positive family history of essential hypertension were found to have higher intracellular sodium levels and lower ratios of intracellular potassium to sodium than those without, regardless of their blood pressure. Only hypertensive subjects with a positive family history had depressed sodium efflux rate constants. Hypertensive subjects with no family history of essential hypertension had normal intracellular sodium levels and sodium pump activity. Black subjects had significantly higher levels of intracellular sodium than whites, regardless of blood pressure. Black hypertensive subjects had higher plasma sodium and lower plasma potassium concentrations than normotensive subjects did. These results suggest that cellular sodium handling is more closely associated with a genetic predisposition to essential hypertension than to hypertension itself and cast doubt on the significance of abnormalities of cellular sodium handling in the development of essential hypertension.

The activity of the erythrocyte ouabain sensitive Na/K ATPase pump was studied in 20 Type 1 diabetics, 15 Type 2 diabetics and 20 healthy controls. All diabetics were normotensive, caucasian and non-obese diabetics. The diabetics were assessed for retinopathy and had HbA1 estimated. The erythrocyte sodium concentration, membrane permeability to sodium and ouabain-sensitive sodium efflux rate constant (ERCos) were determined. The Type 1 diabetics had a significantly reduced ERC, mean +/- SD 0.198 +/- 0.028 hr-1 vs control 0.264 +/- 0.054 hr-1 (p less than 0.001). A similar reduction in ERCos was seen in the Type 2 diabetics when compared to controls (0.229 +/- 0.059 hr-1 p less than 0.005). There was also a significant difference between the 2 groups of diabetics (p less than 0.05). There was no significant difference in intracellular sodium concentrations. Membrane permeability was reduced in the Type 1 diabetics (3.69 +/- 0.79 mmol/kg dry wt/hr) compared to the control group (4.56 +/- 0.79 mmol/kg dry wt/hr, p less than 0.01). Diabetic control (HbA1) was positively correlated with ERCos, but no significant differences were seen in the ERCos between complicated and uncomplicated Type 1 diabetics. In vitro studies of normal erythrocytes did not show an effect on pump activity of increasing glucose or insulin concentration during a preincubation study. These results demonstrate that there is a reduction in activity of the ouabain-sensitive Na/K ATPase pump and a reduction in membrane permeability on the diabetic erythrocyte which is most marked in Type 1 diabetics.