Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the formulae of Fazio and coworkers, the regional extravascular lung water per blood volume and flow was calculated in normal volunteers, in patients with left heart failure, sarcoidosis, allergic alveolitis and pneumonia. The double-isotope technique was used. 113mIn-chloride was intravascular tracer and 123I-antipyrine extravascular tracer. They were injected intravenously as rapid bolus. The activity in the lungs was detected with gamma camera and the time-activity curves were generated with PDP-Gamma-11 computer system. Mean transit times were calculated using two different mathematical handlings of the dilution curves, with gamma fitting parameters and by the area-per-height method. The latter method gave mean transit times about double those calculated with gamma fitting parameters, because the peripheral injection decreased the peak height. Therefore, the area per height method to calculate mean transit times by peripheral injection was found to be inaccurate. The control group consisted of 16 healthy adults. In two subjects repeated studies were made in one week. Their individual, regional extravascular lung water values varied somewhat, but were on second examination found to be between the range of the values found from the first examination. The regional extravascular lung water values in patient groups were correlated with corresponding clinical, laboratory and roentgenographic findings. The values for extravascular water discussed on the next page are calculated only by means of transit times with gamma fitting parameters, although the extravascular water values determined by the area-per-height method also significantly increased in patients compared to the control group. The cardiac group consisted of 52 patients, of whom 23 had clinically compensated and 29 decompensated left heart failure. Regional extravascular lung water significantly increased in patients with decompensated heart failure when compared to patients with compensated heart failure. The cardiac group was also divided into three subgroups after radiological grading of pulmonary venous hypertension. Between GR I (n = 17) without signs of venous hypertension and GR II (n = 18) with signs of venous congestion no significant differences in regional extravascular lung water were found. However, in GR I and GR II the values for regional extravascular water increased when compared to the control group, which is probably due to increased perfusion of vessels or increased blood volume in these cardiac patients.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Measurement of regional extravascular lung water using the double indicator-dilution isotope technique. 391 68

On occasion, blood pressure rises so precipitously and severily, or the clinical setting in which hypertension occurs is so critical, that prompt pressure lowering becomes crucial to prevent disabling, or even lethal complications. Such hypertensive emergencies more commonly complicate the accelerated phase of untreated or poorly treated hypertension of various etiologies. There is also a group of conditions that qualify as hypertensive emergencies not so much because of the actual height of the pressure, but rather because of complicating disorders that make even moderate pressure elevation harmful. These include aortic dissection, intracranial bleeding and acute left ventricular failure. Two fundamental concepts in the management of hypertensive emergencies are: immediate and effective therapy is required and takes precedence over time-consuming diagnostic procedures; the choice of the drugs will depend on how their time course of action and hemodynamic and metabolic effects meet the needs of the clinical situation. It is well proven that nifedipine reduces Ca-dependent vascular smooth muscle tone by direct interference with transmembrane Ca supply and thereby counteracts every kind of contractile tension development of the vascular wall: the higher the wall tension, the easier relaxation in induced by a given concentration of the compound. Because of this, it has become quite clear from recent studies that: nifedipine is a potent antihypertensive agent.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Nifedipine as a vasodilator antihypertensive with a rapid action]. 393 8

Closed-chest trauma in a young man was followed by rupture of a right ventricular papillary muscle and bifascicular block. This produced signs and symptoms of tricuspid regurgitation and recurrent syncope. Treatment by valve replacement and pacemaker implantation was successful. Review of 30 cases of traumatic tricuspid regurgitation reveals that this patient had characteristic findings: adult onset of isolated tricuspid regurgitation, a history of trauma, right bundle branch block, and cardiomegaly without signs of left ventricular failure. In addition, right atrial hypertension of longstanding may produce cyanosis because of right-left shunting through a patent foramen ovale.
 ...
PMID:Chronic tricuspid regurgitation and bifascicular block due to blunt chest trauma. 394 68

The prevalence of coronary heart disease, left ventricular failure and hypertension was examined in a representative group of 133 newly diagnosed Type 2 (non-insulin-dependent) diabetic subjects (70 men, 63 women), aged 45 to 64 years, and in a group of 144 randomly selected non-diabetic control subjects (62 men, 82 women) of the same age group. The prevalence of previous myocardial infarction (major Q-QS abnormalities in resting ECG and/or myocardial infarction verified at hospital) was increased 1.7-fold in male (NS) and 4.4-fold in female (p = 0.007) diabetic patients compared with that found in non-diabetic subjects. Chest pain symptoms and ischaemic ECG abnormalities were about twice as common among diabetic than among non-diabetic subjects. The frequency of coronary heart disease defined by chest pain symptoms and ECG abnormalities was 3.5 times higher in male (p = 0.001) and 3.1 times higher in female (p = 0.001) diabetic patients than in the respective non-diabetic subjects. The frequency of current digitalis therapy was increased 3.3-fold in male (p = 0.006) and 3.9-fold in female (p = 0.001) diabetic patients suggesting an increased frequency of left ventricular failure among diabetic subjects. The prevalence of hypertension, based on the elevated blood pressure levels and/or current use of antihypertensive drugs, was increased 1.6-1.7-fold among the diabetic patients.
 ...
PMID:Prevalence of coronary heart disease, left ventricular failure and hypertension in middle-aged, newly diagnosed type 2 (non-insulin-dependent) diabetic subjects. 397 84

We reviewed cardiac catheterization data and the medical records of 30 patients with systemic hypertension to establish their pulmonary hemodynamic profiles and the relationship between certain clinical and demographic variables and increased pulmonary vascular resistance. Mean systemic arterial pressure ranged from 110 to 210 mm Hg, and systemic vascular resistance ranged from 17.6 to 47.0 units. Seven patients had normal pulmonary wedge pressure and normal pulmonary vascular resistance, one had elevated pulmonary wedge pressure and normal pulmonary vascular resistance, five had elevated pulmonary wedge pressure and increased pulmonary vascular resistance, and 17 had normal pulmonary wedge pressure and increased pulmonary vascular resistance. There were significant positive correlations between systemic vascular resistance and pulmonary vascular resistance and between mean systemic arterial pressure and mean pulmonary artery pressure, but there was no correlation between mean pulmonary wedge pressure and pulmonary vascular resistance. Of the 17 patients with normal pulmonary wedge pressure and increased pulmonary vascular resistance, seven had clinical or radiologic evidence of prior left ventricular failure. We conclude that increased pulmonary vascular resistance occurs commonly in patients with systemic hypertension. Although some cases of increased pulmonary vascular resistance relate to active or preexistent left ventricular failure, the majority remain unexplained, suggesting that neurohumoral or other factors may produce a hypertensive response in both the systemic and pulmonary arterial circuit.
 ...
PMID:Pulmonary hemodynamics in systemic hypertension. 401 75

Calcium channel blockers are assuming increasingly important roles in the practice of emergency medicine. Two cases and a review of the literature relating to treatment of hypertensive emergencies with nifedipine are presented. Nifedipine has a rapid onset of action (buccal, 10-15 minutes; oral, 30-45 minutes) and peak effect (buccal, 30 minutes, oral, 60 minutes). The duration of effects is four to six hours regardless of the route of administration, with a mean arterial pressure reduction of 21.6% (248/134 mm Hg to 165/87 mm Hg). In patients with severe hypertension and left ventricular failure, a consistent reduction in systemic vascular resistance (2,088 dynes/sec/cm-5 to 1242 dynes/sec/cm-5) and cardiac index (2.76 l/min/m2 to 3.77 l/min/m2) has been reported. The patients in this study had severe hypertension (systolic blood pressure greater than 180 mm Hg, diastolic blood pressure greater than 120 mm Hg) and end organ involvement (including heart failure, left ventricular strain, headache, confusion, dizziness, and shortness of breath). Nifedipine (10 mg) was administered buccally with prompt reduction of blood pressure and resolution of the patients' symptoms. Nifedipine appears to be a safe, effective agent for the management of hypertensive emergencies. Its pharmacokinetic profile and routes of administration make it particularly valuable in the practice of emergency medicine.
 ...
PMID:Nifedipine in the management of hypertensive emergencies: report of two cases and review of the literature. 406 18

Semantic difficulties arise when hypertrophic obstructive cardiomyopathy is seen without obstruction and with congestive failure, and also when congestive cardiomyopathy is seen with gross hypertrophy but without heart failure. Retention of a small left ventricular cavity and a normal ejection fraction characterizes hypertrophic cardiomyopathy at all stages of the disorder. Congestive cardiomyopathy is recognized by the presence of a dilated left ventricular cavity and reduced ejection fraction regardless of the amount of hypertrophy and the presence or not of heart failure. Longevity in congestive cardiomyopathy seems to be promoted when hypertrophy is great relative to the amount of pump failure as measured by increase in cavity size. Conversely, death in hypertrophic cardiomyopathy is most likely when hypertrophy is greatest at a time when outflow tract obstruction has been replaced by inflow restriction caused by diminishing ventricular distensibility. Hypertrophy is thus beneficial and compensatory in congestive cardiomyopathy, whereas it may be the primary disorder and eventual cause of death in hypertrophic cardiomyopathy. Reasons are given for believing that hypertension may have been the original cause of left ventricular dilatation in some case of congestive cardiomyopathy in which loss of stroke output thenceforward is followed by normotension. Development of severe hypertension in these patients after recovery from a prolonged period of left ventricular failure with normotension lends weight to this hypothesis. No fault has been found in the large or small coronary arteries in either hypertrophic cardiomyopathy or congestive cardiomyopathy when they have been examined in life by selective coronary angiography, or by histological methods in biopsy or post-mortem material. Coronary blood supply may be a limiting factor in the compensatory hypertrophy of congestive cardiomyopathy, and the ability to hypertrophy may explain the better prognosis of some patients. In hypertrophic cardiomyopathy excessive metabolic demand may not be met, and inadequacy of blood flow may contribute both to sudden death and to progressive replacement fibrosis in this disease. Histochemical and ultrastructural methods have failed to show any fundamental differences between hypertrophic cardiomyopathy and congestive cardiomyopathy, whereas conventional histology permits recognition of hypertrophic cardiomyopathy and distinction both from congestive cardiomyopathy and from ;normal' secondary hypertrophy in organic aortic stenosis.
 ...
PMID:Ventricular hypertrophy in cardiomyopathy. 425 44

The antihypertensive effects of intravenous labetalol were evaluated in 59 patients with hypertensive crises or severe hypertension in need of rapid lowering of blood pressure in a multicenter study. Patients appearing with a supine diastolic blood pressure 125 mm Hg or greater, or a supine systolic blood pressure of more than 200 mm Hg received an initial mini-bolus injection (20 mg) of labetalol. This was followed by repeated incremental doses of 20 to 80 mg given at 10 minute intervals to achieve a supine diastolic blood pressure of less than 95 mm Hg or decrease 30 mm Hg or greater, or a satisfactory decrease in systolic blood pressure. Patients were stratified into those who had taken antihypertensive medication within 24 hours and those who had not. The initial mini-bolus injection caused rapid but not abrupt reduction in blood pressure; the baseline mean blood pressure decreased 23/14 mm Hg. Further injections were needed in the majority of patients (mean: 197 mg). The blood pressure reduction after the last dose of labetalol was 55/33 mm Hg. In pretreated patients and in those who had no medication for 24 hours prior to the intravenous labetalol, the response was similar. Heart rate decreased 10 beats per minute in the total population. In patients pretreated with beta-adrenergic blockers, blood pressure response was similar to that in the total group (59/35 versus 55/33 mm Hg), but heart rate remained essentially unchanged. The dose required to achieve the therapeutic effect was less in pretreated patients than in untreated patients, but the duration of action was shorter. No serious adverse effects were encountered even in patients with concomitant diagnoses of acute left ventricular failure, myocardial infarction, stable congestive heart failure, atrial fibrillation, angina pectoris, acute stroke, transient ischemic attack or encephalopathy. Labetalol is a safe and effective treatment for a rapid blood pressure reduction in hypertensive emergencies.
 ...
PMID:Intravenous labetalol in the treatment of severe hypertension and hypertensive emergencies. 613 20

We assessed the effects of labetalol on pulmonary wedge pressure (PWP) and other hemodynamic variables in 18 patients with acute myocardial infarction (AMI) and systemic hypertension (systolic blood pressure greater than 150 mm Hg). According to the initial value of PWP, the patients were separated into two groups of nine patients each: Group 1 (PWP greater than or equal to 15 mm Hg) and Group 2 (PWP less than or equal to 12 mm Hg). Labetalol was infused at increasing rates to lower systolic blood pressure below 130 mm Hg; this optimal rate (mean rates for Groups 1 and 2: 1.8 and 2.1 mg/min, respectively) was maintained for 1 h. Hemodynamic variables were measured before and after 1 h of infusion. Labetalol normalized blood pressure in both groups by a significant decrease in total systemic resistance [22% (p less than 0.001) and 13% (p less than 0.02)] and in cardiac index [17% (p less than 0.005) and 12% (p less than 0.02)]. While the hemodynamic responses were rather similar in both groups, the PWP decreased significantly (from 22 to 15 mm Hg, p less than 0.01) in Group 1, but did not change significantly in Group 2 (from 7 to 10 mm Hg, NS). The possible mechanisms behind these different responses are discussed. We conclude that labetalol is an effective drug for treating systemic hypertension in AMI which acutely decreases total systemic resistance and preload in patients with moderate left ventricular failure.
 ...
PMID:Effect of labetalol on preload in acute myocardial infarction with systemic hypertension. 619 18

Calcium channel blockers have a selective action on the cardiovascular system. They reduce the energy requirement of the heart, reduce vascular smooth muscle tone, and increase systemic blood flow. Vasodilatation occurs in both the systemic and the pulmonary systems to an extent proportional to the baseline level of vascular resistance, and results in reduction of blood pressure when it is elevated. Thus, these blockers are useful in patients with high blood pressure. Clinical experience of calcium channel blockers in hypertension is so far confined almost exclusively to verapamil and nifedipine. This article reviews the advantages and limitations of these two compounds, their acute hemodynamic effects in hypertensive subjects, and their use in the treatment of hypertensive emergencies, hypertensive encephalopathy, and pheochromocytoma, and as ventricular afterload reducing agents in hypertensive left ventricular failure. Similarities in the effects of nifedipine on systemic and pulmonary vascular tone are presented as evidence that altered intracellular Ca++ concentration is involved in the vasoconstriction seen in both systems in systemic high blood pressure. They also provide support for the hypothesis that inappropriate Ca++ handling may be involved in maintaining elevated blood pressure in human hypertension.
Hypertension
PMID:Treatment of hypertension with calcium antagonists. Review. 622 73


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>