The effect of diltiazem on systemic and cerebral hemodynamics and on the blood rheological properties in patients with ischemic stroke and atherosclerotic involvement of the major cerebral arteries]

Overall thirty-five patients with ischemic insult against the background of occlusive lesions of major arteries of the head were evaluated for effects of cardil on systemic and cerebral hemodynamics and rheologic properties of blood. It has been shown that cardil increases significantly cerebral bloodflow predominantly on the side of the stenosis, does not cause intracerebral "stealing" in the acute phase of insult, improves bloodflow to the brain and collateral blood supply in the residual phase due to selectivity of its influence on cerebral vessels, lowers arterial pressure, decreases frequency of contractions, as well as cardial and stroke indices, and volume of circulating blood. The drug suppresses aggregatory properties of thrombocytes and erythrocytes during different stages of ischemic insult, and makes blood viscosity somewhat less.     

Long-term survival of patients with hypertension treated in general practice or at a specialized hypertension clinic. A 21-year observation study of 831 patients with hypertension

This article is based on a study first published in Blood Pressure. After an initial diagnostic and therapeutic assessment at a specialized hypertension clinic, 831 patients with primary hypertension were during a 15-year period allocated to continuing managing care either by their general practitioner or by the hypertension clinic. Survival was assessed in the two groups: general practice (n = 437, 223 males, 214 females) and specialized hypertension clinic (n = 394, 208 males, 186 females). Median observation times for both groups were 11 years. There were no significant differences between the groups concerning age at entry, pretreatment clinical status, pretreatment blood pressure or treated blood pressure level before allocation. Judged by a Cox' regression model, no difference in survival between the two groups could be registered. The leading cause of death in both groups was ischemic heart disease. Our results indicate that after the initial diagnostic assessment and adjustment of treatment, managing care in a specialized hypertension clinic offers no advantage concerning survival compared to managing care in general practice.     

Antihypertensive therapy in stroke: acute therapy, primary and secondary prevention

Arterial hypertension represents the single most important treatable risk factor for stroke, therefore antihypertensive treatment is crucial. Observational studies have shown that in the acute phase of an ischemic stroke blood pressure is elevated during the first few days and helps to restore cerebral perfusion, activates collateral arterial supply and enhances the treatment goal of minimizing infarct size. Especially for acute ischemic strokes with stable deficits drug treatment of hypertension therefore is recommended only at systolic pressures of > or = 220 mm Hg or with diastolic pressures of > or = 120 mm Hg except when heart, lung or renal failure are also present. In primary prevention of stroke there is a large potential for hypertension treatment which reduces the relative risk by 42%. Especially elderly people with moderate hypertension should be treated. One vascular event per year can be avoided in 100 patient treatment years. Only scarce data exist on secondary prevention of stroke which show that hypertension treatment has a major importance for the modification of risk factors.     

Correlations between blood pressure, blood volume and plasma renin during therapy with diuretics in essential hypertension. Comparison between the mineralocorticoid antagonist spironolactone and the "loop" diuretic mefruside

35 patients with benign essential hypertension were treated for 6 weeks with high doses of the mineralocorticoid-antagonist spironolactone (400 mg/day), or with the "loop-diuretic" mefruside (mean maximal dose 110 mg/day). Spironolactone caused greater reductions in blood pressure and blood volume and a more marked increase in plasma renin activity (PRA) than mefruside (p less than 0.05). It appears possible that he weaker antihypertensive effect of mefruside may relate partly to its lesser influence on circulatory volume. With both diuretics, mean decreases in blood pressure were greater in patients with low pre-therapeutic PRA than in patients with normal or high PRA. However, the diuretic-induced changes in blood pressure did not correlate with the associated variations in blood volume or PRA. Thus, the increased blood pressure sensitivity to diuretics in patients with low-renin essential hypertension did not appear to be volume or renin-dependent. Under normal conditions, the maintenance of a constant blood pressure during volume depletion may partly depend on compensatory activation of the sympathetic nervous system. Moreover, patients with low-renin essential hypertension have been found to have decreased adrenergic activity. It seems possible, therefore, that the marked blood pressure sensitivity to diuretic treatment in such patients may be the result of an impaired compensatory sympathetic response to sodium and volume depletion. Analysis of the literature suggests that the diuretic furosemide, a structural relative of mefruside, may also have less blood pressure lowering efficacy in patients with essential hypertension than the distally-acting thiazides, chlorthalidone or spironolactone. Consideration of possible differences in the blood pressure reducing potential of certain diuretics thus appears to be necessary in planning the pharmacotherapy of essential hypertension.     

GABA and glutamate levels in the substantia nigra reticulata following repetitive cerebral ischemia in gerbils

Repetitive cerebral ischemia produces more severe damage than a similar single duration insult. We have previously shown that, in gerbils, damage in the substantia nigra reticulata (SNr) is seen with repetitive insults rather than a single insult. We have also shown that there is a progressive decrease in the extracellular GABA in the striatum in the days preceding such damage, speculating that a loss of GABA may be in part responsible for this damage. This study evaluates the GABA levels in the SNr in animals exposed to repetitive ischemic insults. Each animal received a total of three ischemic insults of 3-min duration at hourly intervals. In vivo microdialysis was carried out to analyze the GABA and glutamate dialysate levels on Days 1, 3, 5, 7, and 14 following the ischemic insult. In the control and treated (ischemic) animals, there was a significant increase in the GABA levels with the introduction of nipecotic acid on Days 1, 3, 5, and 14. However, on Day 7 there was a significant attenuation in the GABA response to nipecotic acid in the treated animals in comparison to the controls. The glutamate levels in the treated animals were similar to the control animals on Days 1, 3, 5, and 7. However, on Day 14 the glutamate levels were significantly lower than on previous days. Our experiments for the first time measure extracellular glutamate and GABA responses in the SNr in animals exposed to repetitive ischemic insults. Our experiments show that there is a significant decrease in the GABA concentrations at a time when ischemic damage is developing in this region. This confirms our hypothesis that a decrease in GABA may be one factor contributing to neuronal damage during the period following repetitive ischemic insults. Further, the rebound increase in GABA levels on Day 14 with a concomitant fall in glutamate levels would indicate that reparative processes are still active in the 2 weeks following the insult.     

Arterial hypertension: its impact on perioperative morbidity and mortality

Chronic hypertension is associated with structural as well as functional changes of the vasculature, in particular of the coronary, cerebral and renal circulation. It is important to realise that [1] functional changes are often the result of structural changes, [2] the longer lasting the hypertension, the slower and less complete the regression of structural changes, and [3] acute "normalisation" of arterial pressure in long-standing hypertension may initially induce functionally subnormal smooth muscle and/or cardiac activity because the structure of the cardiovascular system is adapted to function at elevated pressures. Despite a multitude of studies, the impact of hypertension on peri-operative morbidity and mortality remains controversial. There are as many studies seeming to suggest that preoperative hypertension correlates with adverse outcome as there are studies that fail to establish such a relationship. When looking at the combined evidence, one is inclined to conclude that hypertension is a predictor of "soft" outcomes (e.g. peri-operative myocardial ischaemia and transient post-operative neurologic deficit) rather than an independent predictor of "hard" outcomes (e.g. unstable angina, myocardial infarction and cardiac death). In view of lack of convincing outcome data, it is impossible to recommend a generally acceptable management strategy for the hypertensive patient. Although, in general, a gradual reduction of blood pressure over a period of weeks to months is the optimal therapeutic approach, we will be hard-pressed delaying surgery for the sole purpose of "better blood pressure control". With full appreciation and detailed knowledge of the pathophysiology of hypertension, combined with sophisticated haemodynamic monitoring and interventions in the peri-operative period, acutely anaesthetising an inadequately treated hypertensive patient will probably not adversely affect his outcome. Delaying surgery for additional work-up may possibly improve outcome in patients with target organ disease, evidence of secondary hypertension, in the most severe forms of hypertension or sudden-onset hypertension.     

Neuroprotective effects of lamotrigine in global ischemia in gerbils. A histological, in vivo microdialysis and behavioral study

A sudden surge in the release of glutamate is currently believed to be an important initiating step in neuronal damage due to an ischemic insult. In this experiment, we tested the efficacy of neuroprotection with lamotrigine, a novel antiepileptic drug that blocks voltage gated sodium channels and inhibits the ischemia-induced release of glutamate in the gerbil forebrain model of cerebral ischemia. The medication was administered 30 min before and 30 min after the insult in two groups of animals. Histological assessment of neuronal damage was evaluated at 7 and 28 days after the ischemic insult. Animals evaluated at 28 days also underwent behavioral testing. Microdialysis was used in the same model to study the response of ischemia-induced glutamate in saline treated controls versus animals treated with lamotrigine 20 min before the insult. There was highly significant neuronal protection in animals who were treated with lamotrigine either before or after the insult. Protection was seen both at 7 and 28 days after the insult. Behavioral testing also showed significantly better recovery in both sets of animals in comparison to the saline-treated group. Microdialysis confirmed a significant attenuation of the ischemia-induced glutamate surge when compared to the saline-treated animals. Our morphological, behavioral and microdialysis experiments show that lamotrigine offers significant neuroprotection from the effects of transient forebrain ischemia in gerbils. Neuroprotection with post-ischemic therapy probably depends on preserving the capacity of the sodium/calcium exchanger to reduce intracellular calcium concentrations or persistent 'toxicity' of glutamate in the reperfusion period on the already 'primed' injured neurons. These concepts need further study.     

Clinical profile of arterial hypertension in patients with cerebrovascular diseases

The aim this work was to assess retrospectively the history of hypertension in patients admitted for cerebrovascular diseases. Two hundred and forty eight patients were studied (69% with ischemic strokes, 24% with hemorrhagic strokes and 7% with transient ischemic attacks. 76% of cases had a history hypertension with an evolution of ten years or more in 81% of cases. No differences in the prevalence of hypertension was observed among the different types of strokes. Of the 139 patients in whom the severity of hypertension was registered, 37% had mild, 45% moderate, 15% severe and 3% systolic hypertension. Those with severe hypertension had a higher incidence of hemorrhagic stroke. Fundoscopic examination was abnormal in 81% of the 64 patients in whom it was performed, left ventricular hypertrophy was found in 62% of the 146 patients in whom it was investigated. 51% of patients were receiving anti hypertensive treatment and it was effective in 26% of them. Thirty one percent of subjects had old lesions in the CAT scan; these subjects had a similar prevalence of hypertension and effectiveness of treatment than patients without old lesions. It is concluded that a history of more than ten years of hypertension is a risk factor for cerebrovascular disease, that severe hypertension is mostly associated to hemorrhagic strokes and that only 26% of patients with stroke had and adequate anti hypertensive treatment.     

Current status of antihypertensive therapy for elderly patients in Japan

To assess how elderly Japanese hypertensive patients are treated by specialists, we conducted a cross-sectional survey. A total of 1,163 outpatients aged 50 years or older were studied. Hypertension was diagnosed in 939 of these patients, and 827 were receiving drug therapy. The average blood pressure during therapy was 143 +/- 16/81 +/- 10 mmHg. In patients aged 70 years or older, systolic blood pressure during antihypertensive therapy was significantly higher (p < 0.01) and diastolic blood pressure was significantly lower (p < 0.01) than the corresponding values in those aged 50 to 59 years or 60 to 69 years. The calculated mean blood pressures were similar in the different age groups. The rate of monotherapy in the patients aged 70 years or older was 58.8%, which was significantly higher (p < 0.01) than the rates of monotherapy in the other age groups. Calcium channel blockers were prescribed in about 80% of patients, irrespective of age or comorbidity. Of the patients receiving calcium channel blockers, 43.5% were treated with monotherapy. This rate significantly (p < 0.01) increased with advancing age. Diastolic blood pressures were significantly lower (p < 0.05) in patients with stroke and in those with ischemic heart disease, diabetes mellitus, or dyslipidemia, as compared with patients with no comorbidity. Among patients aged 70 years or older, the difference in systolic blood pressure between those with ischemic heart disease and those with no comorbidity was not significant. Blood pressure in elderly hypertensive patients was reduced to a level similar to that in younger patients. The target blood pressure was influenced by the presence of comorbidity. Furthermore, specialists showed a high preference for the use of calcium channel blockers in the management of hypertension.     

Pathophysiology and treatment of cerebral ischemia

This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused "penumbra" tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6-12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative.     

Metabotropic glutamate receptors are involved in calcium-induced LTP of AMPA and NMDA receptor-mediated responses in the rat hippocampus

INTRODUCTION: Previous studies have demonstrated a high prevalence of "white coat" hypertension (20%), but it is still controversial if it implies an increase in cardiovascular risk. PATIENTS: Between 1992 and 95 we prospectively studied 175 untreated hypertensive patients aged over 18 years (V Joint National Committee's stage I-II), and 91 controls. DESIGN AND METHODS: The subjects were submitted to clinical evaluation, ambulatory blood pressure monitoring, 24-hour Holter monitoring, signal-averaged ECG, echocardiography/Doppler and ergometry. "White coat" hypertension was defined as mean daytime (6.00-22.00 H) ambulatory blood pressure < 136/87 mm Hg (males) and < 131/86 mm Hg (females). RESULTS: "White coat" hypertension was present in 29 patients (18%). "White coat" hypertension patients had an identical prevalence of smoking, family history of cardiovascular disease, abnormal ECG and retinopathy (> Keith-Wagener II) as patients with daytime hypertension. Ambulatory blood pressure values (24 hour, 6.00-22.00 h, 22.00-6.00 h, sleep, blood pressure load, heart rate) were all significantly different from controls (p < 0.03 to 0.0007). In patients with daytime hypertension, only 24 hour and daytime diastolic ambulatory blood pressure (p < 0.005) were different from "white coat" hypertension patients. Exercise testing blood pressure values (6 min exercise, maximal, 3 min recovery) were significantly different between "white coat" hypertension patients and the control group (n = 70) (p varying from 0.05 to 0.005) but not between "white coat" hypertension and daytime hypertension (n = 33) patients. Diastolic function was studied only in 39 daytime hypertension patients, 10 individuals with "white coat" hypertension and 34 controls (for technical reasons and because we only analyzed individuals younger than 55 years). E velocity and E/A ratio were similar in "white coat" hypertension and daytime hypertension, but only in daytime hypertension patients they reached a significant difference from controls (p = 0.04; p = 0.01), probably due to the small number of patients. CONCLUSIONS: These data (clinical, ambulatory blood pressure, ergometric, diastolic function) suggest that "white coat" hypertension might not be a benign entity.     

The pathophysiology of ischemic neuronal injury: an overview

Despite the enormous scientific efforts that have been made to clarify the pathophysiology of ischemic neuronal injury, the mechanism responsible for neuronal cell death after ischemia remains unclear. Neuronal injury can be roughly classified into three categories: acute ischemic injury, delayed neuronal death and neuronal injury in the penumbra. Flow disturbance known as the noreflow phenomenon and postischemic hypoperfusion is the first limiting factor for neuronal resuscitation after an ischemic insult. Extracorporeal circulation has been tried in an attempt to prevent this blood flow disturbance, but it has become apparent that this is no more effective than conventional resuscitation. Delayed neuronal death seems to be triggered by short exposure to ischemia. Although a molecular mechanism including "glutamate excitotoxicity" has been proposed to explain this phenomenon, the details are still uncertain. The interventional point underlying the protective effect of hypothermia against delayed neuronal death may be the key to understanding its pathophysiology. Neuronal death in the penumbra seems to show deterioration through a mechanism of repeated depolarization "spreading depression", although spreading depression itself has no harmful effect on neurons. The pathophysiological mechanism of spreading depression in combination with flow restriction and other relevant factors related to ischemia remains to be investigated.     

A general practice-based study examining the absolute risk of cardiovascular disease in treated hypertensive patients

BACKGROUND: When managing hypertension, the assessment of the absolute risk of a cardiovascular' event is now advocated as the most accurate way in which the risks and benefits of anti-hypertensive therapy should be judged. Most studies that have examined control of hypertension have relied solely on the blood pressure level attained after treatment, with no measurement of the likely absolute risk in individual patients. AIM: To assess control of hypertension by quantifying the 10-year absolute risk of cardiovascular disease in patients treated by their general practitioners, and to assess which risk factors are associated with uncontrolled hypertension in this group of patients. METHOD: A cross-sectional study was made of patients on drug treatment for hypertension in 18 Oxfordshire general practices subscribing to the VAMP (value-added medical products) computer system. The absolute risk of suffering a cardiovascular event in the following 10 years was measured according to each individual's risk factor profile. Factors associated with uncontrolled hypertension were ascertained using multiple logistic regression analysis. RESULTS: Overall, 40.9% (37.6% to 44.1%) of the hypertensive population had an absolute risk exceeding 20% of having a cardiovascular event in the following 10 years. The distribution of risk factors varies throughout the population. A higher blood pressure reading was strongly associated with an increased likelihood of high absolute risk, but high blood pressure readings in individual patients did not necessarily equate to a high absolute risk. The factors independently associated with uncontrolled hypertension were age, sex, past history of stroke, ischaemic heart disease and transient ischaemic attack, a body mass index greater than 30, diabetes, and current smoking. CONCLUSIONS: Absolute risk assessment maximizes the risk-benefit ratio in treated hypertensive patients. Individual control and management requires multifactorial assessment and management. Treatment of hypertension according to blood pressure reading alone is not a reliable way of reducing the absolute risk of cardiovascular disease.     

Prevalence, knowledge, treatment and control of arterial hypertension in Oporto, Portugal

The aim of this study was to assess the prevalence, awareness, treatment and control of hypertension among subjects above the age of 39 years living in the urban area of Oporto, Portugal. One hundred and seventy seven individuals from the community were selected by random digit dialing. Each subject was asked about his/her personal history of hypertension, antihypertensive treatment and had his/her blood pressure measured. The prevalence of hypertension was 57.1%, defined by systolic blood pressure (SBP) > or = 140 mm Hg and/or diastolic blood pressure (DBP) > or = 90 mm Hg and/or administration of current the antihypertensive medication. If the values defining hypertension were SBP > or = 160 mm Hg, and DBP > or = 95 mm Hg the prevalence would be 37.9%. The overall prevalence of hypertension was higher in females, but a slightly higher non significant value was found in males in the fifth and sixth decades. Among hypertensives, 62.7% were aware of their condition, 56.7% were treated, 84.2% of hypertensives treated were controlled (SBP < 160 mm Hg and DBP < 95 mm Hg) and 44.7% were very well controlled (SBP < 140 mm Hg and DBP < 90 mm Hg). The question "Are you hypertensive?" had a sensitivity of 62.7%, a specificity of 83.6% and an accuracy of 75.7%. In the preliminary results of this study of an urban population with a high prevalence of hypertension, the awareness of hypertension is similar to that described in the United States of America twenty years ago, the percentage of hypertensives treated is similar to the American percentage fifteen years ago and the percentage of hypertensives treated and controlled is close to the current American percentage.     

Regulating angiogenesis: a new therapeutic strategy

Angiogenesis is the proliferation of endothelial and smooth muscle cells to form new blood vessels. Largely muted after adolescence, angiogenesis may be reignited by cancerous cells. Neoangiogenesis plays a primary role in tumor growth and metastases. Antiangiogenic therapy to limit and even reverse the growth of tumors are under investigation and showing promise. A derivative of fumagillin, TNP 470, is the first angiogenesis inhibitor to be given to humans. Surprisingly, several potent inhibitors are derived from tumors themselves. Researchers nowc recognize that stimulation of angiogenesis may have a place in the treatment of cardiovascular disease. Reestablishing blood flow to ischemic tissue through angiogenesis may provide a biologic "bypass" for patients with ischemic heart disease. The same applies to the treatment of peripheral vascular disease.     

An attempt at reversibility and increase of the virulence of axenic strains of Entamoeba histolytica

Sequential changes of cerebral autoregulation were studied in 20 cats after recirculation of cerebral ischemia. The cerebral autoregulation was evaluated by autoregulation index (A.I.), calculating % delta cerebral blood flow (CBF)/delta cerebral perfusion pressure (CPP), with changing the mean arterial blood pressure (MABP) within 80-130 mmHg. Duration of ischemic insult was 15 min after disappearance of direct cortical response (DCR). Following recovery of cerebral circulation, MABP, CBF and intracranial pressure (ICP) were observed sequentially for at least 48 hours. In 6 of 20 cats the autoregulation was disturbed early after recirculation, and the ICP was increased, resulting in no cerebral blood flow (early deteriorated group). In the other 14 cats the autoregulation was restored immediately, but in 7 of the 14 cats it was disturbed again after 24 hours following recirculation (delayed deteriorated group), finally the ICP was elevated and the CBF became 0 as same as early deteriorated group. In another 7 cats it was not disturbed until 5 days. The changes in CBF following insult were five patterns. These were classified into type A (Gradual decrease), type B (Transient increase), type C (Constant maintenance), type D (Relatively rapid decrease) and type E (Rapid decrease). The delayed cerebral dysautoregulation occurred in the types except for type A and type E. These results suggested there was close relation between delayed dysautoregulation and delayed neuronal dysfunction that we reported previously. Moreover, we considered the delayed dysautoregulation could be speculated from the value of ICP/CBF immediately after recirculation and the pattern of the changes in CBF during ischemic insult.     

Local immunoglobulin G antibodies in the stomach may contribute to immunity against Helicobacter infection in mice

The central nervous system consumes 20% of the cardiac output for normal function. The neurons are very sensitive to the effects of ischemia. Cessation of cerebral blood flow results in severe damage to neurons and other brain structures. This is secondary to a combination of energy loss, excessive excitation promoting intracellular calcium (Ca2+) buildup, relative lack of inhibitory responses, generation of oxygen free radicals (especially during the reperfusion period) and several other destructive cascades. Medications that antagonize the effects of glutamate at post-synaptic receptors are either ineffective or have serious side-effects. Ca2+ entry blockers have shown disappointing results in clinical trials in patients with acute cerebral infarction. Data with protective effects of oxygen free radical scavengers in the post-ischemic period have shown conflicting results. There is recent interest with the use of agents that increase cerebral inhibitory responses after an ischemic insult. Such agents are effective when used before, during or up to 4 hours after the ischemic insult. Many such medications have few side-effects and are in clinical use for other indications. This review will summarize inhibitory mechanisms that may be important in cerebral ischemia, and provide experimental evidence for their potential efficacy.     

Increase in the resistance of stenotic coronary segment by intravenous infusion of isoproterenol

Curantil intracarotid injection resulted in brain blood supply and in brain oxygen consumption increase as well as in redox processes normalization in 75 cats with main brain arteries occlusion and heart insufficiency induced by chemical necrosis of the myocardium. A single intravenous injection of a higher curantil dose resulted in a significantly less effect. Long-term (3-72 hours) curantil infusion led to the improvement of the functions disturbed (limb movements, speech, vision) in 32 of 42 patients with brain ischemic insult. The greatest therapeutic efficacy was observed in patients with nonobturated brain infarction induced by brain vascular spasm or cardiocerebral vascular insufficiency.     

Ischemic colitis

Colon ischemia is a well-recognized clinical entity that often occurs spontaneously in patients over the age of 50 years. Many previous cases of nonspecific colitis are now felt to have been secondary to an ischemic event. In contrast to patients with acute mesenteric ischemia and extensive necrosis of the small bowel, the majority of patients with isolated colon ischemia follow a benign clinical course. Most patients present days, weeks, or months after the initial ischemic insult, and many may not have any recognizable antecedent episode of colon ischemia. However, some patients develop a fulminant form of the disease that causes colon infarction and death if not treated early. A high index of suspicion is necessary to make the diagnosis in the hospitalized patient. Endoscopy is recommended to confirm the diagnosis and the extent of injury and to monitor progression or resolution of disease. Aggressive management is of paramount importance to minimize the damage to the ischemic colon and reduce the otherwise high in-hospital mortality rate. Surgical intervention is indicated for patients with evidence of peritonitis or transmural infarction or perforation of the colon and for patients with chronic symptomatic colitis or stricture.     

A new technique for determining the denture tooth bond

As we learn more about hypertension, it is becoming increasingly apparent that conventional blood pressure measurements are fraught with potential error. Noninvasive ambulatory blood pressure monitoring is proving to be extremely valuable in both diagnosis and treatment. Advancing medical technology has provided small, noninvasive, reliable systems what are well tolerated by patients. The commercial availability of these systems facilitates their use in both clinical practice and in research. There have been legitimate concerns that continuous blood pressure monitoring may add considerably to the costs of diagnosing and treating hypertension. These worries, however, may be misplaced. If there are indeed as many patients being treated unnecessarily as has been suggested by many studies, then the money saved on drugs may well cover the costs of prolonged blood pressure monitoring. Moreover, many subjects can be spared unnecessary therapy. Although much work needs to be done with larger groups of patients followed over longer periods of time, the early experiences with 24-h ambulatory blood pressure monitoring have been extremely encouraging. These procedures have added to our understanding of hypertension and of the agents used in its treatment and are rapidly assuming an increasing importance in overall management.