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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After reviewing the characteristics of neurogenic pulmonary edema, Theodore and Robin suggested that it was probably due to rupture of lung vessels by marked but transitory pulmonary hypertension. In this study, we have determined the effects of increased intracranial pressure in a sheep model in which we could measure the flow rate and protein content of lung lymph, and thus detect changes in pulmonary vascular permeability. We found that increasing intracranial pressure to amounts near systemic arterial pressure produced a 3-fold increase in the flow of protein-rich lymph, which indicates increased lung vascular permeability. The high permeability often developed, and always persisted, without extraordinary increases in pulmonary vascular pressure. We conclude that increased lung vascular permeability may follow intracranial hypertension and that extreme pulmonary hypertension is not a prerequisite. Our data do not permit us to exclude barotrauma to exchanging vessels as a cause of capillary damage, but do suggest that other factors, perhaps local release of permeability mediators, may be involved.
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PMID:Increased pulmonary vascular permeability follows intracranial hypertension in sheep. 44 34

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.
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PMID:Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats. 50 48

The intravenous injection of purified scorpion toxin (tityustoxin, TsTX) into unanesthetized rats induces a severe systemic hypertension followed by a hemorrhagic edema of the lungs. The edema is focal or diffuse, whereas the hemorrhage is always focal and less prominent than the edema. Anesthesia of the rats prevents the appearance of pulmonary edema. It seems likely that this protective action of the anesthesia is due, at least in part, to an interference with the hypertension induced by TsTX. The pulmonary edema is prevented by bilateral adrenalectomy, guanethidine or phenoxybenzamine. It is suggested that the edema depends on a sympathetic-adrenal discharge and that catecholamines released by TsTX act on alpha adrenergic receptors. The mean kininogen content of the rat plasma, 1 h after TsTX injection, is not significantly different from that found in the control animals. The possible role played by kinins and other mediators in the early phases of the pulmonary edema induced by TsTX is under investigation.
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PMID:Mechanism of the pulmonary edema induced by intravenous injection of scorpion toxin in the rat. 63 35

In an attempt to assess cardiac risk in non-cardiac surgery, 1001 patients over 40 years of age who underwent major operative procedures were examined preoperatively, observed through surgery, studied with at least one postoperative electrocardiogram, and followed until hospital discharge or death. Documented postoperative myocardial infarction occurred in only 18 patients; though most of these patients had some pre-existing heart disease, there were few preoperative factors which were statistically correlated with postoperative infarction. Postoperative pulmonary edema was strongly correlated with preoperative heart failure, but 21 of the 36 patients who developed pulmonary edema did not have any prior history of heart failure. Nearly all of these 21 patients were elderly, had abnormal preoperative electrocardiograms, and had intraabdominal or intrathoracic surgery. In the absence of an acute infarction, bifascicular conduction defects, with or without PR interval prolongation, never progressed to complete heart block. Spinal anesthesia protected against postoperative heart failure but not against other cardiac complication. By multivariate regression analysis, postoperative cardiac death was significantly correlated with (a) myocardial infarction in the previous 6 months; (b) third heart sound or jugular venous distention immediately preoperatively; (c) more than five premature ventricular contractions per minute documented at any time preoperatively; (d) rhythm other than sinus, or premature atrial contractions on preoperative electrocardiogram; (e) age over 70 years; (f) significant valvular aortic stenosis; (g) emergency operation; (h) a 33% or greater fall in systolic blood pressure for more than 10 minutes intraoperatively. Notably unimportant factors included smoking, glucose intolerance, hyperlipidemia, hypertension, peripheral atherosclerotic vascular disease, angina, and distant myocardial infarction.
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PMID:Cardiac risk factors and complications in non-cardiac surgery. 66 58

Systemic venous hypertension (SVH) is a frequent finding in pulmonary edema. To study the possible contributory or even causal role of SVH in pulmonary edema, a dog model was developed in which balloon catheters were placed in the left and right atria. Inflation of the left atrial balloon produced a tendency to pulmonary edema by causing pulmonary venous hypertension (PVH) (pulmonary artery wedge pressure of 20 mmHg). Inflation of the right atrial balloon produced SVH (central venous pressure of 15 mm Hg). After 2 hours, dogs with SVH with or without PVH demonstrated a greater amount of lung fluid accumulation (P less than 0.01) compared to controls or PVH alone. There was no significant difference in lung water in SVH dogs with or without PVH. Pulmonary blood flow was not significantly different between the experimental groups, each of which was less than control. Impairment of pulmonary lymphatic flow is one possible mechanism producing the worsening edema; however, bronchial venous hypertension or neurogenic reflexes cannot be excluded. We conclude that the contribution of systemic venous hypertension to the development of pulmonary edema may have therapeutic implications.
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PMID:Contribution of systemic venous hypertension to the development of pulmonary edema in dogs. 68 59

A 25-year-old man died after an intravenous injection of 100 mg of methedrine. Postmortem studies showed visceral congestion, lung edema, pericardial petechiae, centrolobular necrosis of the liver, and diffuse subarachnoid blood, intracranial vasculitis and cerebritis in the absence of aneurysms, arteriovenous malformations or chronic hypertension. A review of the English-language literature produced 3 other cases of fatal amphetamine-induced intracranial hemorrhage and seven nonfatal cases. Some were the result of overdose, others of hypersensitivity. Angiographic evidence suggests that such hemorrhages result from the development of fibrinoid necrosis and the formation of microaneurysms in the small intracerebral vessels.
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PMID:Intracranial hemorrhage and amphetamine usage. Review of the effects of amphetamines on the central nervous system. 90 May 66

Pulmonary venoocclusive disease has been established as a definite clinical entity characterized by congestive cardiac failure with pulmonary arterial hypertension, chronic interstitial pulmonary edema, and normal wedge pressure on cardiac catheterization. This disease was diagnosed and confirmed in a patient during life. A review of the 32 patients reported earlier has been done in an attempt to fine possible etiological agents. Early recognition and treatment with anticoagulants, methylprednisolone, aspirin, and dipyridamole may improve the prognosis.
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PMID:Pulmonary venoocclusive disease. 96 9

Among 909 patients with acute myocardial inarction treated in an intensive care unit between 1970 and 1974, atrial flutter and (or) fibrillation occurred in 124 (13.6%). The incidence of these arrhythmias rose with increasing age and predominantly in paroxysmal form (78%). The clinic mortality of patients with arrhythmias was 42%, while in the remaining 785 it was only 26% (P less than 0.001). Patients with atrial fibrillation and (or) flutter had a higher mean age, more frequently cardiac failure (P less than 0.001) - especially in the prognostically unfavourable severe forms with pulmonary oedema (P less than 0.05) and combined right and left heart failure (P less than 0.001) - and other disorders of impulse conduction or formation and chronic arterial hypertension (P less than 0.01).
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PMID:[Atrial fibrillation and flutter as a complication of acute myocardial infarction (author's transl)]. 97

The effect of lymphatic ligation on relative lung water (g H2O/g dry lung) was studied in dogs. Raising left atrial pressure to 20 mmHg for 2 h in chronically lymphatic-ligated dogs (4 days) caused a significantly greater increase in relative lung water than the same hemodynamic challenge did in sham-operated and acutely lymphatic-ligated dogs. There was no significant difference in relative lung water between the acutely lymphatic-ligated and sham-operated dogs. At normal left atrial pressures, there was no significant difference in relative lung water between the sham-operated and chronically lymphatic-ligated dogs. Since the combined effects of chronic lymphatic ligation and left atrial hypertension is greater than the sum of the individual effects, it appears that chronic lymphatic ligation increases the susceptibility of the lung to hemodynamic edema, we suggest that chronic lymphatic ligation may have produced increases in the interstitial volume and protein mass that are undetectable by our technique. These increases, in turn, could lead to a reduction in tissue safety factors against hemodynamic pulmonary edema.
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PMID:Hemodynamic pulmonary edema in dogs with acute and chronic lymphatic ligation. 99 Jan 16

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.
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PMID:Hypoxemia and lung water in acute myocardial infarction. 99 75


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