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

1. Endothelin, a novel vasoconstrictor 21-residue peptide isolated from the supernatant of cultured porcine endothelial cells, has been shown to be increased in plasma in a variety of cardiovascular disease states, including acute myocardial infarction, acute renal failure and essential hypertension. We determined the time course of plasma and pulmonary lymph endothelin-like immunoreactivity in relation to the progressive deterioration of cardiopulmonary function in an ovine septic shock model leading to multi-organ failure syndrome and death within 42 h of a continuous intravenous infusion of Escherichia coli endotoxin (40 ng min-1kg-1). 2. Plasma and pulmonary lymph endothelin-like immunoreactivity were measured by r.i.a. using a specific antiserum raised in rabbits against porcine endothelin-1. Endothelin-like immunoreactivity was further determined in lung tissue and the thoracic duct lymph of endotoxin-treated sheep by reversed-phase h.p.l.c. In control instrumented conscious sheep not infused with endotoxin, there were no significant changes in any of the measured cardiopulmonary and biochemical variables, with plasma and pulmonary lymph endothelin-like immunoreactivity remaining below the detection limit (less than 1 pg/tube) throughout the 72 h study period. 3. Conscious sheep receiving endotoxin showed a major hypotensive septic syndrome, including persistently decreased systemic blood pressure, systemic vascular resistance, stroke volume, left ventricular stroke work, associated with sustained pulmonary vasoconstriction and protein-rich pulmonary oedema (greater than five-fold increase in pulmonary lymph flow and protein clearance), and marked lactic acidosis, leading to the death of animals within 14-42 h despite institution of mechanical ventilation and adequate intravascular volume replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time course of plasma and pulmonary lymph endothelin-like immunoreactivity during sustained endotoxaemia in chronically instrumented sheep. 165 37

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

The central autonomic network (CAN) is an integral component of an internal regulation system through which the brain controls visceromotor, neuroendocrine, pain, and behavioral responses essential for survival. It includes the insular cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial complex, nucleus of the tractus solitarius, and ventrolateral medulla. Inputs to the CAN are multiple, including viscerosensory inputs relayed on the nucleus of the tractus solitarius and humoral inputs relayed through the circumventricular organs. The CAN controls preganglionic sympathetic and parasympathetic, neuroendocrine, respiratory, and sphincter motoneurons. The CAN is characterized by reciprocal interconnections, parallel organization, state-dependent activity, and neurochemical complexity. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. The paraventricular and other hypothalamic nuclei contain mixed neuronal populations that control specific subsets of preganglionic sympathetic and parasympathetic neurons. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions.
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PMID:The central autonomic network: functional organization, dysfunction, and perspective. 841 66

Data on 40 patients (21 men, 19 women) who died in hospital of influenza in 1975-1990 are analysed. The age of the patients ranged from 47 to 92 years, 37 patients were over 60. 31 deceased had ischemic heart disease (IHD), of them 13 survived myocardial infarction; 11 patients had essential hypertension, 1--lymphoid leukemia, 1--pollenosis. Influenza caused by virus of A type (H3N2) was diagnosed in 27 patients. Influenza virus type B was detected in 13 patients. The disease ran a hypertoxic, severe and moderate course in 3, 20 and 17 patients, respectively. Influenza complicated with pneumonia in 23 cases, with hemorrhagic edema in 4 patients. The lethal outcome was caused by acute cardiovascular failure (n = 20) including acute myocardial infarction (n = 9), pulmonary edema (n = 9), pulmonary artery thromboembolism (n = 8). Influenza remains a serious disease especially for the elderly with IHD.
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PMID:[Clinico-anatomic parallels of cardiac lesion in sporadic influenza]. 1164 39

The clinical diagnosis of renal artery stenosis relies on a high index of suspicion and confirmation by noninvasive imaging modalities. There are three distinct clinical syndromes associated with renal artery stenosis: renin-dependent hypertension, essential hypertension, and ischemic nephropathy. Clinical features that should heighten suspicion for renal artery stenosis include abrupt-onset or accelerated hypertension at any age, unexplained acute or chronic azotemia, azotemia induced by angiotensin-converting enzyme (ACE) inhibitors, asymmetric renal dimensions, and congestive heart failure with normal ventricular function. Patients with true renin-dependent (renovascular) hypertension are typically young or middle-age women with renal fibromuscular dysplasia (FMD). Initial therapy for renovascular hypertension associated with FMD is an ACE inhibitor; refractory hypertension responds readily to balloon angioplasty without stenting. Elderly patients with generalized atherosclerosis and hypertension often have atherosclerotic renal artery stenosis (ARAS); hypertension in these patients is usually not renin dependent (ie, essential hypertension). Hypertension alone, even if treated with multiple medications, is not a compelling indication for renal artery revascularization; these patients should be treated aggressively with antihypertensive medical therapy. Renal artery revascularization with stenting may be considered for refractory severe hypertension, and would be expected to improve blood control and modestly reduce medication requirements. Renal revascularization rarely cures hypertension in patients with ARAS. Patients with ARAS, hypertension, and end-organ injury should be considered for renal revascularization. Manifestations of end-organ injury include nonischemic pulmonary edema; hypertensive crisis associated with acute coronary syndrome, aortic dissection, or neurologic impairment; and renal insufficiency. Ischemic nephropathy is best treated before the development of advanced renal failure. The best candidates for revascularization are those with baseline serum creatinine less than 2.0 mg/dL, bilateral renal artery stenosis, normal renal resistive indices, no proteinuria, and one or more manifestations of end-organ injury. In these patients, renal revascularization is best accomplished by stenting, although surgical revascularization may be considered in patients with concomitant severe aortic aneurysmal or occlusive disease.
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PMID:Atherosclerotic Renal Artery Stenosis. 1268 6

Essential hypertension accounts for 95% of all cases of hypertension. A small number of patients (between 2% and 5%) have a reversible disease as the cause for raised blood pressure. Unilateral and bilateral renal artery stenosis may be responsible for secondary hypertension. Diagnosis and treatment of renal artery stenosis are of a great importance. Revascularization of ischemic kidney may correct blood pressure control and preserve renal function. Much data suggest close pathophysiological relation between renal artery stenosis, ischemic nephropathy and development of hypertension. However, it should be stressed that not every renal artery stenosis leads to hypertension and ischemic nephropathy. Therefore diagnosis of renal artery stenosis in hypertensive patient is not always equivalent with renovascular hypertension. The true prevalence of renal artery stenosis is unknown. In unselected population it accounts for less than 1% of hypertensive patients. Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. Physical examination may reveal bruits over major vessels, including the abdominal aorta and renal arteries. The principle aim of the renal artery stenosis investigation is to confirm presence and size of vessel obstruction and its association with hypertension. Typical evaluation is based on imaging techniques and physiological studies. Former include: doppler duplex ultrasonography, conventional angiography, intraarterial and intravenous digital subtraction angiography, computed axial tomography, magnetic resonance angiography and intravascular ultrasonography. Functional studies are occasionally used. These are renal scintigraphy, evaluation of plasma renin activity in renal veins and evaluation of plasma rennin activity after ACE inhibition. Treatment of patients with renal artery stenosis and hypertension should restore vessel patency and inhibit its occlusion. Revascularization should elicit an improvement in or normalization of blood pressure control and renal function. Therapeutic approach include percutaneous renal artery angioplasty (PTRA), with or without stenting, revascularization by surgery and pharmacotherapy. PTRA is currently the first choice option. In general, it is simpler and similarly effective as surgical reconstruction. In some cases PTRA is completed with stent placement. It prevents immediate recoil but does not completely eliminate restenosis of revascularized artery. Surgical bypass is currently reserved for patients in whom PTRA and stenting fail and in patients with extensive atherosclerotic lesions. Patients with renal artery stenosis and hypertension should be provided with pharmacological treatment according to current recommendations. Specific procedures to limit associated risk factors of atherosclerosis should also be introduced.
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PMID:[Renovascular hypertension: is it only the top of the iceberg?]. 1497 69

Fibromuscular dysplasia (FMD) and aortoarteritis are the most frequent causes of secondary hypertension induced by renal artery stenosis (RAS). Revascularization of this disease entity usually cures arterial hypertension. Demographic evolution leads to an increasing incidence of atherosclerotic RAS, one of the major causes of end-stage renal failure. Furthermore, atherosclerotic RAS leads to deterioration of primary hypertension, progression of atherosclerosis manifestation such as occlusive and aneurysmatic peripheral artery disease, and chronic or acute organ damage such as left ventricular hypertrophy and recurrent flash pulmonary edema. Despite the lack of sufficiently powered randomized controlled trials, each hemodynamically relevant RAS (eg, > or = 70%) should be considered for stent angioplasty in patients without end-stage ischemic nephropathy or limited life expectancy due to concomitant disease (eg, cancer). Drug-eluting stents will probably reduce the overall low in-stent restenosis rate of 10% to 20%. Interventions in patients with dialysis-dependent end-stage nephropathy are left to appropriate clinical study protocols.
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PMID:Renal artery stenosis. 1748 11

Diuretics, especially thiazide-type diuretics, are widely used in the treatment of essential hypertension. The most frequent adverse reactions are hypotension, photosensitivity, hypokalaemia, anorexia and epigastric distress. Life-threatening adverse reactions are rare. We report a case of pulmonary oedema associated with low left ventricular filling pressures and hypotension, occurring in a patient shortly after ingestion of 12.5 mg of hydrochlorothiazide (HCTZ). By reviewing the literature (Medline search) 49 similar cases were found. We compared the findings of all these patients in an attempt to reveal the underlying mechanism of this non-cardiogenic pulmonary oedema and shock. We believe that an allergic type III reaction is most likely the underlying mechanism of this adverse drug reaction to HCTZ. It is important to recognize the causality of the symptoms of this rare but life-threatening side effect of thiazide-type diuretics, in order to stop the drug intake immediately and to prevent any unthoughtful reinitiation of this treatment.
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PMID:Hydrochlorothiazide-associated noncardiogenic pulmonary oedema and shock: a case report and review of the literature. 1753 14

During normal pregnancy, renal blood flow and GFR increase gradually until they reach a peak of about 150% of their normal values by the end of the 1(st) trimester. This increase in GFR is secondary to the extra-cellular compartment expansion caused by a positive sodium balance of about 500-900 mmol which is in turn associated with a water retention amounting 6 to 8 liters. Blood pressure decreases during a normal pregnancy because of the decrease in peripheral vascular resistance. This drop in blood pressure is limited by the renin-angiotensin system. Blood pressure gradually recovers during the 3(rd) trimester. Systemic hypertension, proteinuria >0.3 g/day and edema are the usual signs leading to the diagnosis of PE. However, any of the above listed signs found in isolation can be a tell tale sign of PE and must therefore prompt for the identification of a possible fetal effect The differential diagnosis of PE includes essential hypertension and hypertension secondary to a pre-existing renal failure. In the latter, signs of renal impairment early in the pregnancy, or (and) renal failure prior to the pregnancy are of important diagnostic clues. Causes of acute renal failure during pregnancy are numerous. PE associated acute renal failure presents in 5-10% of severe forms of PE. This is always a bad prognostic sign with a predicted mortality of 10%. Histological features are those of acute tubular necrosis with "endotheliosis" an inflammation of the glomerular endothelium. This renal impairment is frequently complicated by pulmonary edema. Passed the acute phase, the recovery of the renal function is usually complete. An acute renal failure during pregnancy can also be secondary to a pre-existing renal impairment suddenly aggravated by PE. In this setting, the probability of these patients requiring long term dialysis is high. Post-partum Haemolytic-Uremic Syndrome (HUS), although rare, is a serious condition which, following delivery, will require an early diagnosis (haemolysis, hypertension, acute renal failure) and urgently require symptomatic, perhaps specific, treatment (Plasma exchange transfusion).
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PMID:[Kidney and preeclampsia]. 2035 4

Renovascular hypertension is due to reduced renal parenchymal perfusion. The correct diagnosis can be difficult. It is important to note that the demonstration of renal artery stenosis in a patient with hypertension does not necessarily constitute renovascular hypertension. Often, clinically nonsignificant and asymptomatic renal artery stenosis are found in patients with essential hypertension, or renal failure of other origin. Renovascular disease is a complex disorder with various clinical presentations. In patients with significant renovascular hypertension plasma renin is increased. For this reason the therapy aims to block the renin-angiotensin-aldosterone system. Bilateral renal artery stenosis causes renal sodium retention. In this situation a diuretic drug has to be added to the therapy. Endovascular or surgical therapy has to be considered in patients with flash pulmonary edema or fibromuscular dysplasia. The control of cardiovascular risk factors is important.
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PMID:[Hypertension therapy in patients with renal artery stenosis]. 2254 59


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