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The National Institutes of Health Consensus Development Conference on Optimal Calcium Intake brought together experts from many different fields including osteoporosis and bone and dental health, nursing, dietetics, epidemiology, endocrinology, gastroenterology, nephrology, rheumatology, oncology, hypertension, nutrition and public education, and biostatistics, as well as the public, to address the following questions: (1) What is the optimal amount of calcium intake? (2) What are the important cofactors for achieving optimal calcium intake? (3) What are the risks associated with increased levels of calcium intake? (4) What are the best ways to attain optimal calcium intake? (5) What public health strategies are available and needed to implement optimal calcium intake recommendations? and (6) What are the recommendations for future research on calcium intake? The consensus panel concluded that: A large percentage of Americans fail to meet currently recommended guidelines for optimal calcium intake. On the basis of the most current information available, optimal calcium intake is estimated to be 400 mg/day (birth-6 months) to 600 mg/day (6-12 months) in infants; 800 mg/day in young children (1-5 years) and 800-1,200 mg/day for older children (6-10 years); 1,200-1,500 mg/day for adolescents and young adults (11-24 years); 1,000 mg/day for women between 25 and 50 years; 1,200-1,500 mg/day for pregnant or lactating women; and 1,000 mg/day for postmenopausal women on estrogen replacement therapy and 1,500 mg/day for postmenopausal women not on estrogen therapy. Recommended daily intake for men is 1,000 mg/day (25-65 years). For all women and men over 65, daily intake is recommended to be 1,500 mg/day, although further research is needed for this age group. These guidelines are based on calcium from the diet plus any calcium taken in supplemental form. Adequate vitamin D is essential for optimal calcium absorption. Dietary constituents, hormones, drugs, age, and genetic factors influence the amount of calcium required for optimal skeletal health. Calcium intake, up to a total intake of 2,000 mg/day, appears to be safe in most individuals. The preferred source of calcium is through calcium-rich foods such as dairy products. Calcium-fortified foods and calcium supplements are other means by which optimal calcium intake can be reached in those who cannot meet this need by ingesting conventional foods. A unified public health strategy is needed to ensure optimal calcium intake in the American population. The full text of the consensus panel's statement follows.
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PMID:Optimal calcium intake. 759 55

Only 53%-58% of patients with a subarachnoid haemorrhage (SAB) following the rupture of a cerebral aneurysm survive without neurological damage. Morbidity and mortality are closely related to the delayed ischaemic neurological deficit due to cerebral vasospasm. The following review gives an account of pathophysiological mechanisms; the importance of treatment with calcium antagonists, hypervolaemic haemodilution, and induced arterial hypertension is discussed in light of the current literature. PATHOPHYSIOLOGY. In addition to other vasoactive substances in the blood, haemoglobin, which is released from lysed erythrocytes on the 2nd to 4th day after the haemorrhage, plays an important role in inducing vasospasm. An inflammatory angiopathy ensues, with complete resolution after 6-12 weeks. The cerebral blood flow (CBF) is reduced depending on the extent of vasospasm. Irreversible infarction may follow the decrease of CBF below a critical value. Severe vasospasm causes autoregulatory disturbances and reduced responsiveness of cerebral vessels to CO2. CALCIUM ANTAGONISTS. The calcium blocker nimodipine causes dilatation of small pial vessels with increased CBF. However, systemic vasodilation with the subsequent fall in blood pressure may limit the increase in CBF. Furthermore, it is known that nimodipine decreases intracellular calcium concentrations resulting in some protection against ischaemic cellular injury. Seven placebo-controlled clinical studies have shown that nimodipine improves the outcome of patients with severe neurological damage due to cerebral vasospasm. HYPERVOLAEMIC HAEMODILUTION. Volume expansion and haemodilution to a hematocrit of 30%-33% is suggested to improve cerebral perfusion during vasospasm. The central venous and pulmonary capillary wedge pressures should be 10-12 mm Hg and 15-18 mm Hg, respectively. But there is no evidence of improved outcome with this measure, and pulmonary edema is a frequent side effect. However, impairment of cerebral perfusion and increased neurological damage can be demonstrated with hypovolaemia and haemoconcentration. INDUCED ARTERIAL HYPERTENSION. In the presence of cerebral vasospasm and resulting autoregulatory disturbances, cerebral perfusion can be increased by raising systemic arterial pressure. This measure, too, fails to improve neurological outcome. CONCLUSION. Treatment of cerebral vasospasm following a SAB aims to avoid any impairment of cerebral perfusion. Hypovolaemia and haemoconcentration have to be corrected. Normoventilation should be established to avoid hypocapnic vasoconstriction. Nimodipine should be administered continuously after a SAB. In view of the autoregulatory disturbances, systemic hypotension with its danger of decreased CBF must be prevented. The importance of hypervolaemic haemodilution and/or induced arterial hypertension is not clear. Despite therapeutic efforts, the number of patients who have survived a SAB without a substantial neurological deficit has not increased.
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PMID:[Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Therapeutic value of treatment with calcium antagonists, hypervolemic hemodilution and induced arterial hypertension]. 778 50

Our previous studies have shown that sustained hyperinsulinemia increases blood pressure in rats. The precise mechanism is still unclear. The present study was conducted to assess if hyperinsulinemia could interact with angiotensin II and other pressor stimuli to increase blood pressure in renovascular hypertensive rats. Intact and uninephrectomized Sprague-Dawley rats with unilateral renal arterial constriction (2-kidney, 1 clip and 1-kidney, 1 clip Goldblatt rats) were administered insulin (3 mU/kg/min) for 6-12 weeks. The clipped rats without insulin infusion and normal rats served as controls. Changes in blood pressure were measured by tailcuff method without preheating. Results showed that either sustained infusion of insulin or renal arterial clipping alone in normal rats significantly increased the blood pressure. Superimposed infusion of insulin for 6-7 weeks into rats with unilateral renal artery constriction in either 2-kidney or 1-kidney model did not accelerate nor exacerbate the development of hypertension. There were no significant differences in body weight and plasma levels of glucose, triglycerides, sodium and potassium between 2-kidney, 1 clip Goldblatt hypertensive rats with and without insulin infusion. These data suggest that chronic hyperinsulinemia and angiotensin II do not act synergistically to increase the blood pressure in rats.
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PMID:The absence of influence of chronic hyperinsulinemia on the development of renovascular hypertension in rats. 795 11

At the acute stage of cerebral ischemia, the "therapeutic window" probably does not last more than 6-12 hours. Despite similar treatments, patients admitted in stroke specialist units are more likely to survive and to have a good functional outcome than patients treated in general wards. In most cases acute arterial hypertension should not be treated. Thrombolytic agents given within 6 hours after onset, are now under evaluation in several clinical trials. There is no scientific evidence to support the use of anti-coagulation as a curative treatment of acute cerebral ischemia; however, clinical trials remain necessary, especially in progressing stroke. Neuroprotective drugs protect neurons against the consequences of hypoxia in animals: most clinical trials with oral nimodipine led to negative results but the meta-analysis suggests that patients receiving nimodipine within 12 hours after stroke onset might have a lower mortality rate and a better functional outcome. Other clinical trials with neuroprotective drugs are currently running: anti-NMDA drugs, chlomethiazol, tirilazad, ganglioside GM 1, etc Most therapeutic agents are now under evaluation. An early admission of patients with acute stroke is required to evaluate therapeutics agents which probably cannot be effective if started more than 6-12 hours after stroke onset.
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PMID:[Treatment of cerebral ischemia in its acute phase and prospectives]. 805 63

This study evaluates 33 patients suffering from mild-moderate arterial hypertension (systolic blood pressure over 160 mmHg; diastolic blood pressure over 95 mmHg) and with concomitant indications of concentric left ventricular hypertrophy at echocardiography. Twenty patients completed the trial according to the criteria established in the protocol and were found suitable for evaluation of the results at the end of the study. Ten patients were treated with 40 mg of nifedipine retard tablets, administered twice (1 x 20 mg tablet twice daily) and 10 patients were treated with a single administration of 20 mg quinapril (1 x 20 mg tablet per day). Total follow-up was performed for one year (variability 12-14 months) with evaluation of the pressure response at 1-3-6-12 months and clinical evaluation and echocardiographic control for comparison with the baseline at the end of the study. The left ventricular mass values measured at the end of the study presented a statistically significant reduction (p < 0.001) with respect to the baseline in both groups. In the patients treated with quinapril the percentage regression of left ventricular hypertrophy was 19.39%, and slightly higher (19.5%) in the patients treated with nifedipine. Finally, although the series is perhaps too limited to draw conclusions, the finding that the indicators of diastolic filling of the left ventricle improved, and, in particular, were correlated with an increase in the speed of the first fast filling phase, and thus that there was a partial improvement in left ventricular compliance, is important.
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PMID:[Evaluation of regression of left ventricular hypertrophy after antihypertensive therapy. Comparative echo-Doppler study of ace inhibitors and calcium antagonists]. 836 9

Hypertension is the most common complication of r-HuEPO therapy in dialysis patients. The aim of this study was to test the hypothesis that hypertension develops in patients who fail to autoregulate adequately their hemodynamic response to correction of anemia. Twenty-five dialysis patients (17-71 yrs, 13 male, 13 CAPD) initially received r-HuEPO 50 U/kg 3 times/week intravenously or subcutaneously. Hypertension, defined as a rise in mean blood pressure (BP) of greater than 15 mmHg during therapy developed in 44% (Group 1: stable BP; Group 2: rise in BP). There was no difference in sex, age, mode of dialysis or route of administration of r-HuEPO between the groups. Before commencement and after 6-12 months of r-HuEPO therapy, assessment of the baroreflex arc was performed using the Valsalva ratio and orthostatic BP testing, sympathetic efferent nerve function was assessed by the cold pressor test and afferent parasympathetic function by the 30:15 ratio and heart rate variation (HRV). No difference was detected prior to r-HuEPO therapy between the two groups in Valsalva ratio (Group 1: 1.26 +/- 0.06 vs Group 2: 1.23 +/- 0.06, mean +/- SEM); 30:15 ratio (1.06 +/- 0.02 vs 1.03 +/- 0.01), or systolic, diastolic, mean BP or pulse rate after standing for 3 minutes or following hand immersion in ice slush. Both groups had a fall in systolic and diastolic BP (p < 0.05) and a rise in pulse rate (p < 0.05) on standing. HRV during deep respiration between the 2 groups was not different (9.6 +/- 2.3 vs 7.1 +/- 1.4 beats/minute).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autonomic dysfunction and the development of hypertension in patients treated with recombinant human erythropoietin (r-HuEPO). 844 12

Contrasting information has been reported concerning the course of renal function in NIDDM with hypertension alone or in association with renal damage. The aim of the present study was to elucidate the course of the glomerular filtration rate (GFR) in hypertensive NIDDM patients during antihypertensive therapy. Furthermore, we compared the effects of ACE inhibitors (cilazapril, Inibace, Roche, Milan, Italy) and Ca(2+)-channel blockers (amlodipine, Norvasc, Pfizer, Rome, Italy). Of the hypertensive NIDDM patients attending the outpatient's clinic of the internal medicine departments of the University of Padova and Sassari, 44 participated in the present study. Of these patients, 26 were normoalbuminuric and 18 microalbuminuric. They were randomly treated with either cilazapril or amlodipine. The target of antihypertensive treatment was a value < 140 mmHg for systolic and 85 mmHg for diastolic blood pressure (BP). Microalbuminuria was defined as an albumin excretion rate (AER) between 20 and 200 micrograms/min. GFR was measured by plasma clearance of 51Cr-labeled EDTA at baseline and every 6-12 months during a 3-year follow-up interval. A significant decrease was observed in the values of GFR, AER, and systolic and diastolic BP in normoalbuminuric and microalbuminuric patients during antihypertensive therapy. The GFR fall in the overall population of NIDDM patients was significantly and inversely related to the decrease of mean BP (diastolic + 1/3 pulse pressure) (r = -0.80, P < 0.0001) but not to that of HbA1c, triglycerides, and BMI. The GFR decline (mean +/- SE) per year in the normoalbuminuric patient was 2.03 +/- 0.66 ml.min-1 x 1.73 m-2 (95% CI 0.92-3.17) during cilazapril and 2.01 +/- 0.71 ml.min-1 x 1.73 m-2 (95% CI 0.82-3.11) during amlodipine therapy. The GFR decline per year in the microalbuminuric patient was 2.15 +/- 0.69 ml.min-1 x 1.73 m-2 (95% CI 0.86-3.89) during cilazapril and 2.33 +/- 0.83 ml.min-1 x 1.73 m-2 per year (95% CI 1.03-3.67) during amlodipine therapy. Cilazapril and amlodipine lowered AER to a similar extent in normoalbuminuric and microalbuminuric patients. No significant changes were observed concerning other clinical and biochemical features between the two antihypertensive therapies and particularly HbA1c, BMI, triglycerides, and cholesterol plasma values. These results support the tenet that arterial hypertension plays a pivotal role in contributing to renal damage in NIDDM, even when AER is normal. However, the degree of BP control, with both cilazapril and amlodipine, can successfully delay the slope of GFR decline in hypertensive NIDDM patients with or without incipient nephropathy.
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PMID:Effects of cilazapril and amlodipine on kidney function in hypertensive NIDDM patients. 854 68

The National Institutes of Health Consensus Development Conference on Optimal Calcium Intake brought together experts from many different fields including osteoporosis and bone and dental health, nursing, dietetics, epidemiology, endocrinology, gastroenterology, nephrology, rheumatology, oncology, hypertension, nutrition and public education, and biostatistics, as well as the public, to address the following questions: 1) What is the optimal amount of calcium intake? 2) What are the important cofactors for achieving optimal calcium intake? 3) What are the risks associated with increased levels of calcium intake? 4) What are the best ways to attain optimal calcium intake? 5) What public health strategies are available and needed to implement optimal calcium intake recommendations? and 6) What are the recommendations for future research on calcium intake? The consensus panel concluded that: A large percentage of Americans fail to meet currently recommended guidelines for optimal calcium intake. On the basis of the most current information available, optimal calcium intake is estimated to be 400 mg/day (birth-6 months) to 600 mg/day (6-12 months) in infants; 800 mg/day in young children (1-5 years) and 800-1,200 mg/day for older children (6-10 years); 1,200-1,500 mg/day for adolescents and young adults (11-24 years); 1,000 mg/day for women between 25 and 50 years; 1,200-1,500 mg/day for pregnant or lactating women; and 1,000 mg/day for postmenopausal women on estrogen replacement therapy and 1,500 mg/day for postmenopausal women not on estrogen therapy. Recommended daily intake for men is 1,000 mg/day (25-65 years). For all women and men over 65, daily intake is recommended to be 1,500 mg/day, although further research is needed for this age group. These guidelines are based on calcium from the diet plus any calcium taken in supplemental form. Adequate vitamin D is essential for optimal calcium absorption. Dietary constituents, hormones, drugs, age, and genetic factors influence the amount of calcium required for optimal skeletal health. Calcium intake, up to a total intake of 2,000 mg/day, appears to be safe in most individuals. The preferred source of calcium is through calcium-rich foods such as dairy products. Calcium-fortified foods and calcium supplements are other means by which optimal calcium intake can be reached in those who cannot meet this need by ingesting conventional foods. A unified public health strategy is needed to ensure optimal calcium intake in the American population.
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PMID:Optimal calcium intake. Sponsored by National Institutes of Health Continuing Medical Education. 874 90

Individualized ACTH treatment of the West syndrome (WS) was assessed in a prospective multicenter study, in which each patient's dosage was increased stepwise according to response. Our series included six patients with cryptogenic and 24 with symptomatic infantile spasms. During the treatment period the total ACTH dose ranged from 58 to 373 i.u./kg. In the cryptogenic group one patient responded to pre-ACTH pyridoxine and four to the lowest dosage of ACTH (3 i.u./kg daily) with cessation of spasms and good outcome; one patient needed the highest dosage (12 i.u./kg daily) for cessation of seizures and became developmentally retarded. In the symptomatic group, 21 of the 24 patients needed 6-12 i.u./kg daily; 12 became seizure-free or having infrequent non-IS fits. Complications such as arterial hypertension, cerebral ventricle dilatation, cardiac hypertrophy, and prolonged adrenocortical hyporesponsiveness were related to the dose. The individualization provides all the benefits of ACTH treatment with minimal side effects and cost.
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PMID:West syndrome: individualized ACTH therapy. 898 Aug 46

Reversal of opioid-related respiratory depression is often accompanied by an "acute abstinence like syndrome" with hypertension, tachycardia, and pain. This overshoot was used to investigate the extent at which opioids of high potency but different structure are involved in naloxone-induced abstinence. In 10 awake and trained mongrel dogs two highly mu-selective compounds, alfentanil and fentanyl, were given in cumulative doses and at different occasions (30-60-120-240 micrograms/kg, and 6-12-24-48 micrograms/kg, respectively). Subsequently, a high dose of naloxone (100 micrograms/kg) was given at 5 min intervals while arterial blood gases, blood pressure, heart rate and the somatosensory evoked potential (SEP) were measured continuously. Following a wash-out period, the 19-isoamyl derivative of etorphine (M-140; 10,000 times more potent than normorphine and a 4.5 fold potency of ethylketocyclazocine in a bioessay preparation) was also given in increasing doses (0.2-0.4-0.8-3.2 micrograms/kg). Again, naloxone was given (100 micrograms/kg) at 5 min interval, while cardiovascular parameters, blood gases and SEPs were measured continuously. All three opioids induced a dose-related respiratory depression with hypercarbia and hypoxia, a dose-related bradycardia, and a modest hypotension. This was accompanied by a dose-related depression of the amplitude of the SEP, reflecting the degree of blockade of nociceptive afferents. Naloxone was sufficient to reverse respiratory impairment after fentanyl, alfentanil and M-140. However, in contrast to fentanyl and alfentanil, there was no cardiovascular or evoked potential overshoot following naloxone reversal of M-140. After alfentanil naloxone increased blood pressure, heart rate and amplitude of the SEP by 7%, 41% and 38%, respectively. After fentanyl this increase in blood pressure, heart rate and amplitude of the SEP was 17%, 43% and 96%, respectively. The study indicates that the more potent the opiate mu ligands are the more is naloxone liable to induce a hyperexcitatory state of the cardiovascular system and an increase of nociceptive stimuli to pain modulating centres. After M-140 reversal of mu-related respiratory depression by naloxone was possible. However, no precipitation on an acute abstinence-like syndrome affecting antinociception or inducing cardiovascular overshoot was observed. This may stem from an intense binding and slow dissociation of the ligand from the receptor site or may be due to high binding affinity to both the mu and the kappa receptor site. Opioids which interact with various receptor sites may be of clinical interest for substitution therapy in opioid dependent addicts.
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PMID:Studies on the abstinence-like overshoot following reversal of the potent 19-isoamyl derivative of etorphine with naloxone. A comparison with the opioids fentanyl and alfentanil. 903 35


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