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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.
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PMID:Renal effects of left atrial distension in dogs with chronic congestive heart failure. 43 20

We investigated the effects of acute hypoxia (10% O2) on plasma level of atrial natriuretic peptide (ANP) and pulmonary hemodynamics in five subjects with a history of high-altitude pulmonary edema (HAPE). Plasma renin activity and plasma levels of aldosterone, epinephrine and norepinephrine were also measured. The plasma ANP levels in HAPE-susceptible subjects rose significantly in response to 10% O2 (from 34.8 +/- 5.4 to 51.4 +/- 7.3 pg.ml-1; P less than 0.05), not associated with any increase in either atrial pressure. Compared with six control subjects, the rise of ANP level was greater in HAPE-susceptible subjects (16.6 +/- 4.4 vs 3.9 +/- 1.2 pg.ml-1; P less than 0.05). There was a significant positive correlation between the rise of ANP level and the increase of pulmonary arterial pressure. No significant difference was observed in any of other hormonal responses to acute hypoxia between the two groups. We interpret these results as indicating that the ANP secretory response to acute hypoxia in HAPE-susceptible subjects, which is not mediated by an increase in atrial pressure, may be greater than that in nonsusceptible subjects in association with a greater pressor response of pulmonary circulation.
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PMID:Hypoxia-induced ANP secretion in subjects susceptible to high-altitude pulmonary edema. 141 Aug 44

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.
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PMID:[Pathophysiology, prevention and therapy of altitude pulmonary edema]. 149 42

Scorpion envenomation is a common medical problem and life hazard in many countries of the world. Scientific investigations have addressed the interrelationship between the stimulatory effects of the venom on the autonomic nervous system and adrenals and the subsequent effects of released transmitters on the cardiovascular system. A number of clinical cardiovascular syndromes may dominate the initial clinical presentation after envenomation: the syndromes usually vary with the age of the victim, the size of the offender and the season. Central nervous system dysfunction is seen in children but rarely observed in adults; if accompanied by severe hypertension the clinical picture is consistent with acute hypertensive encephalopathy. Heart failure, pulmonary edema or a shock-like syndrome has been observed in 25% and hypertension in 30% to 77% of our patients. The electrocardiographic abnormalities recorded in the majority of the patients after envenomation include an "acute myocardial infarction-like pattern." Rhythm disturbances are frequent but conduction abnormalities are rare. Echocardiographic, radionuclide and experimental hemodynamic observations have provided evidence that heart failure and pulmonary edema after envenomation are multifactorial with diminished systolic performance following the initially increased left ventricular contractility and decreased ventricular diastolic compliance. Clinical laboratory data reporting increased catecholamine metabolite excretion and elevated plasma renin and aldosterone are consistent with the stimulatory effects of the venom on the autonomic nervous system. Treatment, including our experience with vasodilators and calcium channel blockers, is reviewed.
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PMID:The cardiovascular system after scorpion envenomation. A review. 158 74

Since acute mountain sickness (AMS) is associated with rapid ascent and with fluid retention, we assessed clinical status and fluid homeostasis in men slowly ascending on foot over 3 d to 4559 m and remaining at this altitude 5 d. We studied 15 male mountaineers, 6 of whom had previously had repeated, severe AMS or high altitude pulmonary edema (HAPE), at 1170 m, 3611 m, and 4559 m. We found that four of the six subjects with previous AMS or HAPE compared with none of nine with no such history, developed these conditions. Those who remained well had a diuresis that could not be overcome by increasing fluid intake and no change in renin activity, plasma aldosterone, or atrial natriuretic peptide (ANP). Those who became ill showed considerable weight gain independent of fluid intake, and a great increase in ANP which correlated with measurements of right atrial cross section. We conclude that mountaineers who have previously experienced repeated AMS or HAPE get fluid retention despite slow ascent and that this is associated with widening of the atrium and an increase in ANP.
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PMID:Effects of slow ascent to 4559 M on fluid homeostasis. 182 79

Plasma renin activity, active renin concentrations, and total renin concentrations were measured serially in 15 women in preterm labor treated with ritodrine. All three parameters showed rapid increases during treatment that depended on ritodrine doses and paralleled changes in maternal pulse rate. The slope of the correlation between plasma renin activity and active renin concentrations suggested an increase in both active renin and renin substrate during ritodrine treatment. In contrast, levels of inactive renin remained unchanged for several hours during ritodrine infusion, showing only a late and much smaller response than that of either total or active renin concentrations. Thus ritodrine treatment results in further activation of an already activated renin-angiotensin system in pregnancy. This activation relates to an increase in both renin enzyme and its substrate. It may be responsible for the disturbance in water balance and the risk of pulmonary edema associated with beta-sympathomimetic drug treatment in preterm labor.
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PMID:Activation of the renin-angiotensin system during ritodrine treatment in preterm labor. 218 11

The most important component of the renal-body fluid feedback is renal pressure natriuresis which through sodium and water excretion stabilizes arterial pressure. The chronic effects of angiotensin II in regulating the pressure natriuresis was studied in dogs by the Guyton school. Renal perfusion was either permitted to increase or was maintained constant with a servo-controlled occluder placed on the abdominal aorta just above the kidneys. When the renal pressure was allowed to increase, sodium excretion was reduced for a day and after 4-5 days there was little net change in sodium balance and arterial pressure stabilized at about 30 mm Hg above control. In the servo-controlled renal perfusion, escape from sodium retention did not occur, arterial pressure continued to rise, and pulmonary edema developed. Angiotensin II, by its hemodynamic and tubular effects, modulates renal sodium and water excretion and has an important role in blood pressure regulation. Antibodies to renin and converting enzyme inhibitors showed a causal relationship between the stimulated renin-angiotensin system and the antihypertensive effect of these agents. Chronic effects are observed in hypertensive patients with normal or even low plasma renin activity. This suggests that local angiotensin concentrations in the vascular and renin tissues may be more important in determining sodium and water excretion. Our knowledge of the renin-angiotensin system in regulating blood pressure made the usage of converting enzyme inhibitors a logical and efficacious modality in the therapy of hypertension. In a multicenter study of 202 hypertensive patients, the efficacy and safety of ramipril and enalapril was studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The renin-angiotensin system, the kidney, and hypertension. 247 96

Previous studies have shown that ECG changes following a subarachnoid haemorrhage are associated with increased catecholamine levels, necrotic myocardial lesions, and a poor prognosis. Furthermore, beta-blockade using propranolol reverses some of the ECG changes and prevents necrotic myocardial lesions. This study was established to assess the affects of adrenergic blockade on morbidity and mortality following subarachnoid haemorrhage. Patients were admitted to the randomized double-blind between-patients study if they presented at the neurosurgical unit within 48 hours of a subarachnoid haemorrhage confirmed by lumbar puncture. Of 224 patients, the first 118 received an alpha-blocker, phentolamine 20 mg three-hourly, and either the beta-blocker propranolol 80 mg eight-hourly, or placebo. The last 106 patients received either propranolol or placebo. Treatment was continued for three weeks. Assessment at four weeks revealed significant improvements in the treated group for neurological deficit (p = 0.003) and death (p = 0.02). More treated patients underwent operation and those that did had a better outcome (p = 0.01). Assessment at one year showed that although patients had improved in both groups, patients in the treated group had significantly fewer neurological deficits (p = 0.003). There were fewer deaths in the treated group but this difference was not significant (p = 0.09). Possible mechanisms for this protective effect of propranolol may include a reduction in plasma renin activity, a reduction in pulmonary oedema, prevention of myocardial infarcts, and a reduction in cerebral oxygen requirements. It is concluded that early beta-blockade benefits patients with subarachnoid haemorrhage, in terms of fewer neurological deficits, for up to one year.
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PMID:Beta-blockade benefits patients following a subarachnoid haemorrhage. 286 45

To test the hypothesis that angiotensin II could be a mediator of acute lung injury, we studied the effects of perindopril diacid, a new angiotensin-converting enzyme inhibitor, on hemodynamics, blood gases, lung mechanics, and extravascular lung water (EVLW). Twenty-four dogs were anesthetized, paralyzed and ventilated with a fraction of inspired oxygen of 0.4 in which pulmonary edema was induced by 0.1 ml/kg iv oleic acid. Perindopril diacid (1 mg/kg) was administered iv either before (eight dogs) or 100 min after (eight dogs) oleic acid injection. In the control group (eight dogs) not treated with perindopril diacid, 150 min after oleic acid injection, PaO2 changed from 193 +/- 7 (mean +/- SEM) to 55 +/- 4 torr, venous admixture from 3 +/- 1% to 52 +/- 5%, cardiac index from 4.1 +/- 0.3 to 3.1 +/- 0.3 L/min X m2, mean pulmonary artery pressure from 13 +/- 1 to 17 +/- 1 mm Hg, dynamic compliance from 90 +/- 8 to 46 +/- 7 ml/cm H2O, and EVLW from 165 +/- 25 to 750 +/- 92 ml/m2. Administration of perindopril diacid reduced systemic BP by 20% but did not affect other hemodynamic variables, blood gases, or dynamic compliance. Maximum increases in EVLW were from 169 +/- 16 to 615 +/- 54 ml/m2 in the pretreated group and from 188 +/- 23 to 675 +/- 56 ml/m2 in the treated group (no significant difference from the control group). However, pretreatment with perindopril diacid significantly (p less than .05) slowed the rise in EVLW, which was lower 60 and 90 min after oleic acid injection compared to untreated dogs. Plasma renin activity and angiotensin I concentration increased after oleic acid injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of angiotensin-converting enzyme by perindopril diacid in canine oleic acid pulmonary edema. 303 15

In order to prevent hypovolemia fludrocortisone acetate treatment was started on admission in 39 consecutive patients with CT evidence of subarachnoid hemorrhage. In 28 patients an aneurysm was proven or probable, and in 21 of these the effects of fludrocortisone acetate on sodium balance and on plasma volume could be studied. In the first five days plasma volume decreased more than 10% in four patients, decreased less than 10% in five and increased in 12. The cumulative sodium balance measured over five days was negative in seven of the 21 patients. Plasma renin values were measured in 15 of the 21 patients and also in stored samples of 18 patients who were not treated with fludrocortisone acetate. Plasma renin values were less high in patients treated with fludrocortisone acetate, regardless of the presence of a negative sodium balance. In three of the 39 patients signs of pulmonary edema developed, and low serum potassium values were observed in four of the 21 patients. In comparison with previous studies, these findings suggest that fludrocortisone acetate is an effective method of decreasing the incidence of volume depletion and negative sodium balance.
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PMID:The effect of fludrocortisone acetate on plasma volume and natriuresis in patients with aneurysmal subarachnoid hemorrhage. 319 46


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