Examining the relationship of concurrent obesity and tobacco use disorder on the development of substance use disorders and psychiatric conditions: Findings from the NESARC-III.

Background: Multimorbidity is linked to worse health outcomes than single health conditions. However, recent studies show that obesity may reduce the risk of developing substance use disorders (SUDs), particularly in vulnerable populations. We investigated how comorbid obesity and tobacco use disorder (TUD) relate to the risk of SUDs and psychiatric conditions. Methods: Data was used from 36,309 individuals who completed the National Epidemiological Survey on Alcohol and Related Conditions - Wave III. Individuals who met the DSM-5 criteria for TUD in the last year were defined as the TUD group. Obesity was defined as having a body mass index (BMI) greater than 30 kg/m2. Using this information, individuals were grouped into categories, with people being identified as either having obesity, TUD, both obesity and TUD, or not having either obesity or TUD (comparison). Groups were compared against their comorbid diagnoses of either an additional SUD or psychiatric conditions. Results: Controlling for demographic characteristics, we found that individuals with obesity including those individuals with TUD, had lower rates of comorbid SUD diagnosis than individuals with TUD alone. Additionally, individuals with combined TUD and obesity, and those with TUD alone, had the highest rates of comorbid psychiatric disorder diagnosis. Conclusions: The current study aligns with previous research suggesting that obesity may reduce risk of substance use disorders, even in individuals who have other risk factors promoting harmful substance use (e.g., tobacco use). These findings may inform targeted intervention strategies for this clinically relevant subpopulation.

Ambulatory blood pressure monitoring-derived short-term blood pressure variability in primary hyperparathyroidism.

INTRODUCTION: Primary hyperparathyroidism is associated with a cluster of cardiovascular manifestations, including hypertension, leading to increased cardiovascular risk. PURPOSE: The aim of our study was to investigate the ambulatory blood pressure monitoring-derived short-term blood pressure variability in patients with primary hyperparathyroidism, in comparison with patients with essential hypertension and normotensive controls. METHODS: Twenty-five patients with primary hyperparathyroidism (7 normotensive,18 hypertensive) underwent ambulatory blood pressure monitoring at diagnosis, and fifteen out of them were re-evaluated after parathyroidectomy. Short-term-blood pressure variability was derived from ambulatory blood pressure monitoring and calculated as the following: 1) Standard Deviation of 24-h, day-time and night-time-BP; 2) the average of day-time and night-time-Standard Deviation, weighted for the duration of the day and night periods (24-h "weighted" Standard Deviation of BP); 3) average real variability, i.e., the average of the absolute differences between all consecutive BP measurements. RESULTS: Baseline data of normotensive and essential hypertension patients were matched for age, sex, BMI and 24-h ambulatory blood pressure monitoring values with normotensive and hypertensive-primary hyperparathyroidism patients, respectively. Normotensive-primary hyperparathyroidism patients showed a 24-h weighted Standard Deviation (P < 0.01) and average real variability (P < 0.05) of systolic blood pressure higher than that of 12 normotensive controls. 24-h average real variability of systolic BP, as well as serum calcium and parathyroid hormone levels, were reduced in operated patients (P < 0.001). A positive correlation of serum calcium and parathyroid hormone with 24-h-average real variability of systolic BP was observed in the entire primary hyperparathyroidism patients group (P = 0.04, P = 0.02; respectively). CONCLUSION: Systolic blood pressure variability is increased in normotensive patients with primary hyperparathyroidism and is reduced by parathyroidectomy, and may potentially represent an additional cardiovascular risk factor in this disease.

Ambulatory arterial stiffness indices and non-alcoholic fatty liver disease in essential hypertension.

BACKGROUND AND AIM: Non-alcoholic fatty liver disease (NAFLD) has been found to be strongly related to an increased arterial stiffness in patients with essential hypertension, suggesting a pathophysiologic link between major cardiovascular and metabolic abnormalities associated with liver steatosis and the functional and structural alterations of the arterial wall. The aim of our study was to investigate, in a group of essential hypertensive patients without additional cardiovascular risk factors, the relationship between NAFLD and arterial stiffness. METHODS AND RESULTS: Sixty-eight consecutive patients with essential hypertension underwent 24-h ambulatory blood pressure monitoring (ABPM) and were separated according to the presence (n = 40) or absence (n = 28) of NAFLD at liver ultrasonography. The Ambulatory Arterial Stiffness Index (AASI) and Symmetric AASI (Sym-AASI) were derived from ABPM tracings. Patients with diabetes, obesity, hyperlipidaemia or other risk factors for cardiovascular or liver disease were excluded. Hypertensive patients were compared with a normotensive control group.The two hypertensive groups had comparable age, sex distribution and clinic/ABPM blood pressure levels. In hypertensive patients with NAFLD, body mass index, fasting glucose, insulin, homeostasis model of assessment of insulin resistance index and triglyceride levels were higher, whereas plasma adiponectin was lower than in patients without NAFLD. In hypertensive patients, AASI and Sym-AASI were higher (P < 0.001) than in normotensive subjects, but both indices of vascular stiffness were comparable in patients with and without NAFLD. CONCLUSIONS: In essential hypertensive patients without additional cardiovascular risk factors, NAFLD is associated with insulin resistance but not with increased arterial stiffness.

Innate immunity, through late complement components activation, contributes to the development of early vascular inflammation and morphologic alterations in experimental diabetes.

OBJECTIVE: To verify if innate immunity, and namely the assembly of terminal complement complex (TCC) could be involved in the development of early diabetic vascular damage. METHODS AND RESULTS: At first in 2 groups of diabetic or non-diabetic Wistar rats the occurrence of basal or stimulated stable adherence to the endothelial layer and extravasation of circulating fluorescently-labelled leukocytes was assessed by using an in vivo videomicroscopy technique. In a second part of the study, the development of vascular damage in short term diabetes was studied in the genetically C6 deficient rats of the PVG strain, and compared with those observed in the wild-type C6 sufficient animals. Here, the analysis of mesentery vascular expression of mRNA for vascular cell adhesion molecule (VCAM)-1, transforming growth factor-ß (TGF-ß), connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF), the evaluation of intravascular protein levels of VCAM-1, TGF-ß, CTGF, proliferative cell nuclear antigen (PCNA), as well as the assessment of structural changes and Complement components deposition at the mesentery arterial vascular wall were also performed. CONCLUSIONS: Leukocyte trafficking, mesentery arteries hypertrophy, extracellular matrix deposition, local vascular gene and protein expression of VCAM-1, TGF-ß, CTGF and PCNA, as well as PGDF gene expression were all increased by short term diabetes, but all significantly reduced in the C6 deficient diabetic animals, thus suggesting an active role for TCC in the development of vascular inflammation in the early phases of experimental diabetes.

Fluvastatin treatment inhibits leucocyte adhesion and extravasation in models of complement-mediated acute inflammation.

Complement activation plays a relevant role in the development of tissue damage under inflammatory conditions, and clinical and experimental observations emphasize its contribution to inflammatory vasculitides. Statins have recently been shown to reduce cardiovascular morbidity independently of plasma cholesterol lowering and in vitro studies support a direct anti-inflammatory action of these drugs. The aim of this study was to verify the in vivo effect of fluvastatin on complement-mediated acute peritoneal inflammation. The effect of oral treatment with fluvastatin was investigated in normo-cholesterolaemic rats that received intraperitoneal injection of either yeast-activated rat serum (Y-act RS) or lipopolysaccharide to induce peritoneal inflammation monitored by the number of PMN recruited in peritoneal fluid washes. In addition, vascular adherence and extravasation of leucocytes were evaluated by direct videomicroscopy examination on mesentery postcapillary venules topically exposed to Y-act RS. The number of PMN in the peritoneal washes of rats treated with fluvastatin was 38% lower than that of untreated animals (P < 0.05) 12 h after LPS injection, and was even lower (56%) in rats treated with Y-act RS already 8 h after injection (P < 0.02). Firm adhesion to endothelium and extravasation of leucocytes evaluated under direct videomicroscopy observation were significantly inhibited in fluvastatin treated rats (77% and 72%, respectively; P < 0.01), 120 min after treatment with Y-act RS. Our results demonstrate that fluvastatin inhibits in vivo complement-dependent acute peritoneal inflammation and suggest a role for statins in preventing the inflammatory flares usually associated with complement activation in chronic diseases, such as SLE or rheumatoid arthritis.

Pulse pressure responses in patients treated with Valsartan and hydrochlorothiazide combination therapy.

In a randomized, double-blind, parallel-group study of middle-aged and elderly patients, we examined the effects of treatment with the angiotensin receptor blocker valsartan (Val) in combination with hydrochlorothiazide (HCTZ) on pulse pressure (PP). After a 2-week washout period, patients entered a 4-week single-blind Val 160 mg once daily run-in period before randomization to one of three treatment groups: Val 160 mg (n = 666), Val 160 mg/HCTZ 12.5 mg (n = 670) or Val 160 mg/HCTZ 25 mg (n = 666), once daily for eight weeks. Sitting PP at baseline was similar in all groups. From baseline to randomization, Val monotherapy reduced PP by 4.7 +/- 10.2 mmHg (mean +/- SD). At the end of the study, overall reductions in PP were 6.7 mmHg for Val 160/HCTZ 12.5 and 7.5 mmHg for Val 160/HCTZ 25. Val monotherapy reduced PP in mild-to-moderate hypertensive patients. Val combined with HCTZ provides an additional dose-related reduction in PP.

Abrupt occurrence of high fever and rash in a patient treated with sulphasalazine for psoriatic arthritis.

We report a singular clinical condition observed following a short duration treatment with sulphasalazine (SSZ) in a 64-year-old woman affected by psoriatic arthritis. Two weeks after starting treatment, a high degree, subcontinuous fever occurred, together with systemic discomfort, fatigue, headache, and ultimately a moderate wakefulness impairment. Upon admission to the hospital, a malar rash became evident. Modest notes of hepatotoxicity were also evident. All of the symptoms suddenly resolved after SSZ withdrawal. The markers of hepatitis become negative just 2 months later. It is interesting to note that after dismissal, in order to counteract the severe arthritic conditions and the presence of a type 2 diabetes, a combined therapy with methotrexate and cyclosporin had to be used, with no renal or hepatic side effects and remarkable therapeutic effects. No markers of autoimmunity were found in this patient. The chronology and the clinical events here described may confirm the hypothesis of a idiosyncratic reaction to SSZ, closely resembling a rare, sometimes irreversible, condition known as "the 3 week sulphasalazine syndrome".

Comparison of benazepril-amlodipine and captopril-thiazide combinations in the management of mild-to-moderate hypertension.

OBJECTIVE: To compare the efficacy and tolerability of benazepril 10 mg + amlodipine 5 mg combination (BZ+AM) versus captopril 50 mg + hydrochlorothiazide 25 mg (CP+HT) combination. MATERIAL: 405 outpatients with mild-to-moderate arterial hypertension not adequately controlled by a monotherapy with ACE inhibitors or calcium channel blockers or diuretics entered this multicenter, double-blind, randomized, parallel-group study. METHOD: After a 2-week placebo run-in, 397 patients with sitting diastolic (D) blood pressure (BP) > 95 mmHg and/or sitting systolic (S) BP > 160 mmHg were randomized to receive either BZ+AM (201 patients) or CP+HT (196 patients) once daily for 12 weeks. Main outcome measure was sitting DBP and SBP values at the end of active treatment. The response rate was defined as the proportion of patients with either a final sitting DBP < 90 mmHg or decreased by at least 10 mmHg or a sitting SBP < 150 mmHg or decreased by at least 20 mmHg from baseline. RESULTS: The DBP and SBP values obtained with BZ+AM were, respectively, 2.7 and 3.7 mmHg lower than those obtained with CP+HT (both p < 0.001 vs. CP+HT). The response rate in the BZ+AM group (94.8%) was better than that observed in the CP+HT group (86.0%, p = 0.004). The incidence of adverse events was similar with the 2 treatment regimens (17.9% for both). CONCLUSIONS: These data suggest a higher antihypertensive efficacy of the fixed combination BZ 10 mg+AM 5 mg as compared with CP 50 mg+HT 25 mg.

Modulation of incipient glomerular lesions in experimental diabetic nephropathy by hypotensive and subhypotensive dosages of an ACE inhibitor.

A glomerular permeability defect occurs early in the course of type 1 diabetes and precedes the onset of microalbuminuria and renal morphological changes. Recently, ACE inhibitors have been shown to prevent loss of glomerular membrane permselective function, but the mechanism of this nephroprotective effect is still being debated. The objective of the present study was to evaluate the effects of hypotensive and subhypotensive dosages of the ACE inhibitor quinapril ex vivo and of its active metabolite quinaprilat in vitro on the glomerular albumin permeability (P(alb)) defect in the early phases of experimental diabetes. For the ex vivo study, six groups of male Wistar rats were evaluated for 4 weeks. One group served as a nondiabetic control (C); the other five groups were rendered diabetic and included untreated diabetic rats (D) and diabetic rats receiving quinapril at the dosages of 5 (DQ1), 2.5 (DQ2), 1.25 (DQ3), and 0.625 (DQ4) mg. kg(-1). day(-1). Dosage-dependent effects of quinapril on systolic blood pressure and the glomerular filtration rate were observed. In contrast, control of P(alb) in isolated glomeruli exposed to oncotic gradients, proteinuria, and glomerular and tubular hypertrophy was obtained with subhypotensive dosages (DQ3 and DQ4 groups) of the ACE inhibitor. In the in vitro study, quinaprilat reduced P(alb) significantly in concentration ranges from 10(-6) to 10(-14) mol/l compared with results in control glomeruli. The effect on P(alb) may have occurred by mechanisms different from kidney ACE inhibitor. These study results indicated that ACE inhibitor treatment prevents the early onset of the P(alb) defect in experimental diabetes. This effect seemed to occur independently of systemic or glomerular hemodynamic changes and, at least partially, from kidney ACE inhibition.

A multicenter, randomized double-blind study of valsartan/hydrochlorothiazide combination versus amlodipine in patients with mild to moderate hypertension.

OBJECTIVE: To compare the antihypertensive efficacy and tolerability of a once-daily fixed valsartan/hydrochlorothiazide (HCTZ) combination and amlodipine in subjects with mild-to-moderate hypertension. SUBJECTS AND SETTING: In this multicentre, double-blind, randomized, comparative trial, 690 patients with sitting systolic blood pressure (BP) > or = 160 mmHg and sitting diastolic BP > or = 95 mmHg at the end of a 2-week placebo wash-out period were randomized to valsartan-based treatment (n = 342) or amlodipine (n = 348). METHODS: The patients received valsartan 80 mg o.d. or amlodipine 5 mg o.d for 4 weeks; in the case of an unsatisfactory blood pressure response, the treatments could be respectively changed to the fixed combination of valsartan 80 mg + HCTZ 12.5 mg o.d. or amlodipine 10 mg o.d. for a further 8 weeks. RESULTS: Both treatment approaches decreased systolic blood pressure and diastolic blood pressure to the same extent. The rate of responders to treatment at the end of fourth week (before up-titration) was 57.4% among the valsartan-treated patients and 61.9% among the amlodipine-treated patients (ns). At the end of the study, the rate of responders was not significantly different between the two groups (74.9 versus 72.1%). Valsartan-based treatment had a slightly lower incidence of adverse events (1.5 versus 5.5%; P = 0.006). CONCLUSIONS: The results of this trial demonstrate that the valsartan/hydrochlorothiazide combination and amlodipine are equally effective in lowering BP, and that the combination is better tolerated.

Mechanics of the carotid artery wall and baroreflex sensitivity after acute ethanol administration in young healthy volunteers.

The effects of ethanol administered orally (300 mg/kg in 250 ml of water) or intravenously (7.5 mg.min(-1).kg(-1) in 250 ml of saline over 40 min) on common carotid haemodynamics, wall mechanics and baroreflex sensitivity were compared with the effects of the intravenous infusion of 250 ml of saline. Ethanol or saline was administered to 10 healthy volunteers after 30 min of supine rest, and measurements were obtained 40 min (median; range 34-46 min) after administration. After ethanol administration, the plasma alcohol level rose from 0 to 0.3+/-0.07 g/l. Mean arterial blood pressure had risen slightly at 20 min, but was normalized by 40 min, the time at which the haemodynamic study was performed. Heart rate decreased after infusion of either saline or alcohol, but was unchanged after oral ethanol administration. Both oral and intravenous ethanol administration were associated with significant decreases in baroreflex sensitivity, carotid shear stress and blood velocity, compared with resting values, while the mean carotid artery diameter was increased, and blood viscosity and mean blood flow were unchanged. No changes were observed in these parameters after saline administration. Ethanol, administered either intravenously or orally, increased the stiffness of the carotid artery and decreased the pulsatility (systo-diastolic changes) of its diameter. A direct, statistically significant correlation was found between the decrease in shear stress and the decrease in baroreflex heart rate control sensitivity after both modes of alcohol administration, while no such correlation was found between the increase in the Peterson elastic modulus and the decrease in carotid diameter pulsatility on the one hand or the decrease in baroreflex sensitivity on the other. In conclusion, reduced shear stress associated with vasodilatation of the carotid artery wall may contribute to the decrease in baroreflex sensitivity observed after acute ethanol administration.

Haemoconcentration, shear-stress increase and carotid artery diameter regulation after furosemide administration in older hypertensives.

The aim of the present study was to determine whether changes of carotid wall shear stress induced by changes in blood viscosity after diuretic administration cause carotid arterial dilatation in elderly hypertensives, as reported in the cat. Arterial wall shear rate (ultrasound technique, profilmeter FRP III), the systo-diastolic diameter (echotracking technique) and the mean blood flow velocity and volume of the common carotid artery, the blood viscosity (rotational viscometer) and the finger arterial blood pressure (Finapress Ohmeda) were measured in 12 young volunteers (aged 25+/-2 years) and in 12 elderly hypertensives (aged 80+/-4 years) treated with short-acting calcium antagonists up to 24h before the study, both at baseline and after intravenous furosemide infusion (0.5mg/min), when the haematocrit had increased by at least two percentage points. After furosemide administration the mean arterial blood pressure decreased and blood viscosity and carotid systolic shear stress increased in both groups. However, common carotid artery diameter increased only in the young controls but not in the elderly hypertensives. These data show that an increase in carotid shear stress caused by haemoconcentration induces carotid vasodilatation only in young healthy subjects, and not in elderly hypertensives. This effect may be related to impaired endothelium function and/or arterial wall mechanics.

The Society of Nuclear Medicine in the new millennium.

The Society of Nuclear Medicine (SNM), which was first organized in January 1954 by 12 men at the Davenport Hotel in Spokane, WA, has evolved into an international educational organization. It has more than 15,000 members, including physicians, scientists, technologists, and industrialists. The SNM has embarked on a new strategic plan that will make it the premier educational and scientific organization representing the specialty of nuclear medicine. The role of the Society in the new millennium and its relationship with other international nuclear medicine societies continue to evolve. The opportunity for joint educational programs, interchange of ideas, research, an international journal, educational activities, and the sharing of professional experiences awaits the SNM and its members in the new millennium. The Society has also reached out to other organizations and physicians who are involved in the clinical practice of nuclear medicine to forge new alliances that will strengthen the specialty of nuclear medicine. These alliances will allow nuclear medicine physicians to speak with a unified voice when faced with regulatory and reimbursement issues and will help in advancing the research, education, and clinical mission of the SNM.

Systemic and regional haemodynamic effects of aortofemoral angiography.

UNLABELLED: The aim was to investigate the regional and systemic haemodynamic consequences of bolus injection of fluids with different physical properties in the course of routine aortography. Iopamidol was compared with an equiosmolar solution of mannitol and with a 0.9 N saline solution. Continuous blood flow and Pulsatility Index (PI), as an index of regional vascular resistance, were measured by Doppler technique. Finger arterial pressure and heart rate were monitored at the time and for 3 min following each intraaortic bolus injections. The patients who underwent routine aortography were grouped according to the site of the flow measurements: common femoral artery, common carotid artery and brachial artery. Flow changes induced by the bolus infusion were evident for all the fluids but only at the femoral artery level. After an immediate (3 +/- 2 s) and brief (2 +/- 2 s) but marked reduction of flow and in-phase increase of PI following the bolus, further haemodynamic changes were observed only in the femoral artery, with a peak at 35 +/- 10 s and returning to baseline values after 70 +/- 15 s, in terms of both increased mean blood velocity and decreased PI. Saline and mannitol induced overall blood velocity alterations of 54% and 80%, respectively, and PI reductions of 44% and 57% compared with those induced by iopamidol. In the other vascular areas there was only a 17 +/- 2% increase of the physiological early diastolic backflow at the brachial artery level. Blood pressure decreased and heart rate increased in phase with the flow changes of the femoral artery. IN CONCLUSION: (1) a dramatic rheodynamic perturbation at the site of injection induces a vasodilating stimulus; (2) the haemodynamic response following injection results in marked vasodilation of only the tributary vascular bed; (3) flow steal may occur from other beds towards the lower limb vascular beds owing to vascular impedance imbalance; (4) a reduction of systemic arterial pressure is induced in phase with the regional vascular events and a reflex increase of the heart rate; and (5) the physical properties of the injected fluids influence the intensity of the perturbation, although the decisive triggering factor is the counterflowing bolus per se.

Albumin permeability in isolated glomeruli in incipient experimental diabetes mellitus.

AIMS/HYPOTHESIS: The pre-clinical phase of diabetic nephropathy is characterised by increased glomerular filtration rate and episodes of microalbuminuria. The cause of the microalbuminuria has been variably ascribed to alterations of the size or charge selective barriers of the glomerulus or both or as a consequence of the haemodynamic changes. Our aim was to investigate very early albumin permeability alterations in isolated glomeruli which were not subject to perfusion pressure. METHODS: Isolated glomeruli were studied from 120 male Wistar rats, divided into three groups: streptozotocin-treated, streptozotocin-treated with insulin pellet implants, and controls. From each group ten animals were killed at 7, 14, 28, and 56 days after induction. Study variables included blood pressure, proteinuria, iopamidol clearance, albumin permeability and glomerular area. Subsequently, albumin permeability, proteinuria, and iopamidol clearance were determined in an additional group of 40 diabetic animals studied at 24, 72, 96, and 120 h after induction. RESULTS: Albumin permeability increased steadily from induction in streptozotocin-treated animals, reaching a plateau at approximately 120 h. Glomerular filtration rate was shown to increase significantly at approximately 7 days and proteinuria correlated with it. Glomerular hypertrophy was observed both in streptozotocin-treated animals and in streptozotocin-treated rats with insulin pellet implants. Strict blood glucose control delayed the appearance of the permeability defect in isolated glomeruli and inhibited the increase in glomerular filtration in intact animals. It did not prevent glomerular hypertrophy. CONCLUSION/INTERPRETATION: An albumin permeability defect exists early in isolated non-perfused glomeruli from streptozotocin-treated rats and seems to be independent of glomerular filtration rate alterations.

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives.

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37+/-8 years) with mild untreated hypertension (mean 163+/-8/ 95+/-12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37 degrees C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR' interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95+/-12 vs. 100+/-12 mmHg: P < 0.02), whereas the heart rate decreased (RR= 873+/-70 vs. 926+/-80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84+/-9 vs. 83+/-8 mmHg and 914+/-158 vs. 913+/-140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7+/-4.6 vs. 9.4+/-2.7 ms/mmHg; P < 0.05 and 423+/-99 vs. 356+/-102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 +/- 3.6 vs. 8.3 +/- 2.8 ms/mmHg; P < 0.03, and 332 +/- 86 vs. 381+/-97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2+/-5.4 vs. 15.2+/-7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate.

Controlled study of the effect of angiotensin converting enzyme inhibition versus calcium-entry blockade on insulin sensitivity in overweight hypertensive patients: Trandolapril Italian Study (TRIS).

OBJECTIVE: The aim of this study was to evaluate the effect of trandolapril, an angiotensin converting enzyme inhibitor, on blood pressure, forearm blood flow and insulin sensitivity in comparison with nifedipine gastrointestinal therapeutic system. PATIENTS AND METHODS: This is a multicentre, two-way parallel-group, open-label comparative study in 90 overweight hypertensive patients, who were randomly assigned to treatment for 8 weeks with either trandolapril or nifedipine. At baseline and after treatment, all patients underwent an oral glucose tolerance test, an evaluation of their metabolic profiles and a euglycaemic hyperinsulinaemic clamp test. In a subgroup of 18 patients, a forearm study was carried out. RESULTS: Blood pressure fell by the second week of treatment and remained significantly reduced compared with baseline in both treatment groups. Plasma triglyceride levels were also significantly reduced after trandolapril therapy, but no significant changes occurred in the other metabolic parameters during treatment with either drug. During the euglycaemic hyperinsulinaemic clamp, whole-body glucose use was similar in the two treatment groups at baseline, and a moderate but statistically significant increase in insulin sensitivity was observed after trandolapril treatment (trandolapril: 5.0 +/- 0.2 versus 4.5 +/- 0.2 mg/kg per min; nifedipine: 4.1 +/- 0.3 versus 4.2 +/- 0.3 mg/kg per min; P < 0.05, versus baseline and trandolapril versus nifedipine treatment). Skeletal muscle glucose uptake was significantly higher after trandolapril than after nifedipine therapy (5.0 +/- 0.7 and 3.0 +/- 0.4 mg/min, respectively; P < 0.01). As forearm blood flow was similar in the two treatment groups at baseline and was unchanged after 8 weeks of therapy, skeletal muscle glucose extraction was significantly greater in the ACE inhibitor treated-group than in the nifedipine comparative group (trandolapril: baseline 21 +/- 2, treatment 24 +/- 3 mg/dl; nifedipine: baseline 18 +/- 3, treatment 16 +/- 2 mg/dl; P < 0.05, trandolapril versus nifedipine treatment). CONCLUSIONS: During short-term treatment, ACE inhibition with trandolapril was able to moderately improve insulin sensitivity, in comparison with calcium blockade, and this effect appeared to be independent of the haemodynamic action of the drug.

Optimizing images of acute deep-vein thrombosis using technetium-99m-apcitide.

OBJECTIVE: The purpose of this paper is to introduce the nuclear medicine technologist to a new radiopharmaceutical, 99mTc-apcitide, for imaging acute venous thrombosis. After reading this paper, the technologist should be able to: (a) describe patient preparation for imaging with 99mTc-apcitide; (b) state the amount of 99mTc-apcitide that is administered to patients for imaging acute venous thrombosis; (c) explain patient positioning for optimal image acquisition; and (d) discuss gamma camera acquisition parameters and their importance in obtaining high-quality images. Clinical cases illustrate both the whole-body distribution and diagnostic value of 99mTc-apcitide in detecting acute deep-vein thrombosis.

Control of glomerular hyperfiltration and renal hypertrophy by an angiotensin converting enzyme inhibitor prevents the progression of renal damage in hypertensive diabetic rats.

OBJECTIVE: Glomerular hyperfiltration and renal hypertrophy are both considered important in the progression of diabetic nephropathy. The aim of this study was to compare the effects of an equivalent reduction in blood pressure produced by the angiotensin-converting enzyme (ACE) inhibitor spirapril (SPI) and an antihypertensive triple drug combination of hydralazine, reserpine and hydrochlorothiazide (HRH) on kidney function, proteinuria and renal structure in hypertensive diabetic rats. DESIGN AND METHODS: Four groups of animals were evaluated in short-term and long-term studies. In both studies one group served as a non-diabetic hypertensive control (H). The other three groups were rendered diabetic and were allocated to one of the following groups: the first diabetic group received no specific therapy (HD), the second diabetic group was treated with SPI (HD-SPI) and the third diabetic group was treated with HRH (HD-HRH). In each of the two studies the systolic blood pressure (SBP), 24 h urinary total protein, glomerular filtration rate (GFR), glomerular area, proximal tubular area and glomerular sclerosis were evaluated. RESULTS: The blood pressure reduction was equal in rats receiving either SPI or HRH. The GFR, proteinuria, glomerular area and tubular area were significantly increased in the HD group, both in the short-term and the long-term study. In the HD-SPI group the diabetic hyperfiltration and renal hypertrophy responses were prevented. In the HD-HRH group the GFR and proteinuria were slightly reduced in the later phases of diabetes, while the glomerular area and tubular area were not affected. Semiquantitative analysis of renal lesions showed that SPI was more effective than HRH in the prevention of the development of glomerulosclerosis. CONCLUSIONS: The results of this study suggest that the control of early adaptive hyperfiltration and renal hypertrophy by SPI may be relevant in the prevention of glomerulosclerosis.

Regional and systemic haemodynamic response to aortography in hypertensives.

OBJECTIVE: To study the effects of aortography and of aortic counterflow bolus injection per se on regional and systemic haemodynamics in hypertensives in comparison to normotensive matched controls. DESIGN AND METHODS: Mean blood velocity (MBV) and pulsatility index (PI)--as an index of regional vascular resistance--by the Doppler technique, at the femoral, common carotid and brachial arteries, finger arterial pressure and electrocardiographic R-R' interval were monitored beat-by-beat, before, during and for 3 min following counterflow bolus injections into the abdominal aorta of 40 ml/2.6 s of iopamidol (I), iso-osmolar mannitol (M) and 0.9 N saline (S), in 11 hypertensive and nine normotensive patients. RESULTS: After bolus injection of iopamidol, MBV increased to a peak at 35+/-5 s, both in normotensive (deltaMBV versus baseline +16.7+/-9.9 cm/s; P < 0.01) and in hypertensive subjects (deltaMBV versus baseline: +13.9+/-6.6 cm/s; P < 0.01). At the same time, the PI decreased both in normotensive (deltaPI versus baseline: -4.05+/-2.49; P < 0.01) and in hypertensive subjects (deltaPI versus baseline: -3.02+/-2.25; P < 0.01). After M boluses, the haemodynamic changes were of the same direction and magnitude as I for both groups, while after S the magnitude was approximately 50% lower. No significant differences were observed between normotensive and hypertensive subjects. In other vascular circulations, a 15% increase of the early diastolic backflow in the brachial artery, in phase with the femoral artery haemodynamic changes, was the only evidence of the procedure. Mean arterial pressure decreased and heart rate increased in phase with flow changes of the femoral artery. CONCLUSIONS: (1) The regional flow and systemic pressure changes observed during aortography seem, at least partially, to be due to the hydrodynamic perturbation induced by bolus injection per se. (2) The physical and chemical properties of the contrast media and therefore the probable different shear-stress modifications induced by the fluid injected could explain why the haemodynamic changes were greater after I compared to S and were more similar to M. (3) Hypertensive subjects did not show a different vasoreactive response in comparison to normotensive subjects during aortography.