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Query: UMLS:C0034063 (
pulmonary edema
)
10,665
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial
hypertension
, tachycardia, hyperthermia, and increased locomotor activity, often leading to
pulmonary edema
and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial
hypertension
was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial
hypertension
, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial
hypertension
and
pulmonary edema
as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial
hypertension
following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that
pulmonary edema
is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.
...
PMID:Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat. 114 97
A previously unreported combination of critical pulmonary valve stenosis and mitral stenosis is described. The initial clinical presentation was one of right ventricular failure that obscured the evidence of pulmonary venous
hypertension
. Following pulmonary valvulotomy,
pulmonary edema
ensued because of the increased pulmonary blood flow. The importance of urgent cardiac catheterization postoperatively following an operation that increases pulmonary blood flow is discussed.
...
PMID:Pulmonary edema following pulmonary valvulotomy. 119 Aug 90
Hemodynamic data were collected in 42 patients with
pulmonary edema
(P.E.) due to altered permeability of various causes. Pulmonary artery wedge pressure (PWP) was normal, whatever the time of the study and the severity of the P.E. Pulmonary artery
hypertension
was present in the cases with severe hypoxemia, but disappeared with hypoxemia correction. In some cases, a hyperkinetic or a hypovolemic syndrome was found, being induced by the cause of P.E. Although within normal limits, PWP was significantly higher at the first hours of P.E. than after the 6th hour. Perfusion of colloid solutes worsened P.E., although increasing PWP by only a few mmHg. Dehydration using diuretics markedly improved the venous admixture, although PWP was previously normal. These data document the production of P.E. in many causes-such as severe sepsis, drowning, fat embolism, barbiturate overdose-by impaired alveolo-capillary permeability, PWP and blood protein content remaining within normal limits. They also demonstrate the noxious effects of overperfusion and the efficiency of dehydration in such pulmonary edemas.
...
PMID:[Hemodynamic study of pulmonary edemas due to the increase of alveolo-capillary permeability]. 119 58
A traumatic transection of the upper descending thoracic aorta, undiagnosed, was complicated on the tenth day by an acute obstruction of the descending thoracic aorta. The upper body
hypertension
resulted in generalised convulsions and cardiac failure with
pulmonary oedema
. The lower body ischemia resulted in paraplegia, acute ischemia of the lower limbs, liver failure and anuria. An emergency revascularisation of the lower body was achieved by axillary-bifemoral bypass. The improvement of the clinical status allowed complete repair of the aortic transection two days after the extra-anatomic revascularisation. This case emphasizes the severity of the cases with impaired blood flow to the lower body and the benefit of the extra-anatomic bypass in pathology of the upper descending thoracic aorta when complete repair of the aortic transection is associated with an extremely high risk.
...
PMID:[Traumatic rupture of the aortic isthmus revealed by acute obstruction of the descending thoracic aorta]. 128 8
In the postoperative period the alterations of blood pressure are the main hemodynamic complications. Hypotension or
hypertension
may compromise the coronary circulation and increase the metabolic demand of the myocardium.
Pulmonary oedema
is the most frequent manifestation of heart failure. The aim of its treatment is to increase myocardial contractility and decrease the metabolic demand. Myocardial ischemia is mostly silent and is an important correlate of adverse cardiac outcomes. The treatment of these hemodynamic events starts during the peroperative period by prevention of their risk factors.
...
PMID:[Hemodynamic complications during the recovery period after anesthesia]. 130 45
Injection of ibotenic acid (IA), a glutamate agonist, into the ventral medullary raphe (VMR; especially the nucleus raphe magnus) of the rat produced respiratory failure and death following a predictable course of events. The response to the IA injection was characterized initially by increased respiratory frequency and was followed by pulmonary arterial
hypertension
, systemic arterial hypoxemia, acidosis, and hypothermia. Within 90 min apnea occurred as a terminal event in all animals. Gravimetric, bronchoalveolar lavage protein, and histological analyses revealed no evidence of
pulmonary edema
. Intracerebral (VMR) pretreatment with PPP, a sigma receptor agonist, or scopolamine, a muscarinic cholinergic antagonist, prevented pulmonary failure and death even though postmortem histological analysis showed VMR cell loss and gliosis consequent to the cytotoxic IA injection. Based on the results of the study, it is suggested that the VMR has a role in regulation of pulmonary blood flow. Preliminary pharmacological studies suggested that a disruption of glutamatergic and cholinergic mechanisms mediates the lethal pulmonary phenomenon.
...
PMID:Respiratory failure without pulmonary edema following injection of a glutamate agonist into the ventral medullary raphe of the rat. 137 23
Hemodynamic parameters were studied in 80 cases of pregnancy induced
hypertension
(PIH) using noninvasive cardiovascular detector (TP-CBS). Women were categorized into 3 kinds of hemodynamic patterns: (1) normal cardiac output, 45 cases, cardiac index (CI) = 2.5-4 L.min-1/m2; (2) high cardiac output, 10 cases, CI greater than 4 L.min-1/m2; (3) low cardiac output, CI less than 4 L.min-1/m2, 25 cases (31.5%). Ten cases in each category were selected for test after volume expansion therapy. MAP decreased in varying degrees. CI showed marked increase in the low cardiac output group, but decreased to normal in the high output group. The monitoring criteria for protecting against
pulmonary edema
during volume expansion therapy were discussed.
...
PMID:[Hemodynamic surveillance in pregnancy induced hypertension during volume expansion therapy]. 138 Apr 22
Four patients admitted to our hospital with different symptomatology are studied: a 9-years-old boy with hyperhidrosis; a 47-years-old woman with arterial
hypertension
and two young males, 25 and 36-years-old, respectively, with thoracic pain. In all cases, the presence of pheochromocytoma was suspected. One of them died due to left ventricular failure with acute
lung edema
. The other three patients were diagnosed by hormonal determinations, detecting a supra-renal body with abdominal echography and computerized axial tomography and undergoing surgery. Currently, they are asymptomatic.
...
PMID:[Pheochromocytoma: a motley tumor]. 139 82
In vagotomized rats, cerebral compression (CC) produced marked increase in arterial pressure and pulmonary hemorrhagic edema (PHE). We studied the effects of a vasodilator and an oxidant scavenger to delineate the role of hemodynamic and permeability factors in this type of neurogenic PHE. Infusion of sodium nitroprusside at a dose of 5 micrograms/kg/min significantly reduced the CC-induced pressor response by 14% and the
lung edema
by 41%. A dose of 10 micrograms/kg/min blocked the pressor response by 51%, and completely prevented the lung injury. Dimethylthiourea (DMTU), a potent scavenger for oxidants such as hydroxyl radical and hydrogen peroxide, in doses of 300 and 600 mg/kg was pretreated 15 min before CC. Although DMTU was shown to block the permeability lung damage caused by phorbol myristate acetate (a neutrophil activator), this agent did not exert any effect on the CC-induced pressor response and lung injury. The data indicate that granulocyte-mediated oxidants such as hydroxyl radical and hydrogen peroxide do not appear to be involved in this type of neurogenic lung pathology. The results support the concept that PHE induced by intracranial
hypertension
is initiated by hemodynamic changes in the systemic and pulmonary circulation. Hydrostatic effect plays a major role in this type of neurogenic lung pathology.
...
PMID:Vasodilator and oxidant scavenger in the neurogenic pulmonary edema induced by cerebral compression. 145 71
To determine whether nitroglycerin is as effective as nifedipine in lowering the blood pressure in severe
hypertension
and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg nitroglycerin sublingually or a 10-mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mmHg to 171/95 mmHg and after nifedipine from 210/118 to 185/102 mmHg. The greater effect of nitroglycerin may result from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15-20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mmHg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant differences in side effects were determined. Since a hypertensive crisis is usually accompanied by left ventricular failure,
pulmonary edema
, angina pectoris, or infarction, nitroglycerin has been definitively shown positively to influence these conditions, and preference should be given to nitroglycerin in the treatment of hypertensive crises.
...
PMID:Comparison of nitroglycerin with nifedipine in patients with hypertensive crisis or severe hypertension. 146 34
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