Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A reproducible noninvasive monkey model for global brain ischemia with exact insult (no flow x 16 min) to the brain, with survival and with standardized preischemic, ischemic and postischemic variables is described. This model allowed us to demonstrate for the first time: 1) that a substantial part of brain damage early postischemia is reversible and amenable especially to barbiturate treatment; 2) that the postischemic brain shows increased vulnerability for additional insults. Optimal postischemic intensive monitoring and immobilization for 24-48 hours is important for improved outcome; 3) that immediate postischemic reperfusion pressure (MAP 110-150 mm Hg) significantly improves the outcome; 4) that heparinisation during ischemia has no protective effect and 5) that postischemic heparinisation and intravenous hemodilution does not ameliorate the outcome. The protective effect of trimetaphan against neurogenic pulmonary edema can be explained by the prevention of pulmonary hypertension but its protective effect on the development of secondary cerebral edema has to be elucidated.
 ...
PMID:[Pathogenesis and treatment of anoxic encephalopathy. Definition and importance of experimental animal models (author's transl)]. 746 71

The haemodynamic and gas exchange abnormalities occurring in neurogenic pulmonary oedema (NPO) were examined retrospectively in 20 patients admitted to the Intensive Therapy Unit (ITU) over a 45-month period (February 1992 to November 1995). In 12 patients, where vasoactive therapy with dobutamine was employed, its effect on haemodynamics was examined. Cardiac index (CI median 2.2 l min-1 m-2) and left ventricular stroke work index (LVSWI 20 g.m.m-2) were markedly depressed, while pulmonary artery wedge pressure (PAWP 17 mmHg), mean pulmonary artery pressure (MPAP 30.5 mmHg), systemic vascular resistance index (SVRI 2852 dyne.s.cm-5.m2) and pulmonary vascular resistance index (PVRI 393 dyne.s.cm-5.m2) were substantially elevated above normal values. Mean arterial pressure (MAP 82.5 mmHg) and heart rate (HR 102 bpm) were within normal limits. The poor oxygenation is indicated by a median PaO2/fiO2 ratio of 18.0 kPa. Patients treated with dobutamine showed significant increases in CI and LVSWI and significant falls in SVRI and PAWP at 2 and 6 h after institution of therapy, and there was a significant rise in PaO2/fiO2 ratio to 27.8 kPa at 6 h. NPO was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine.
 ...
PMID:Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. 884 33

We investigated whether use of labetalol, a beta adrenoreceptor blocking antihypertensive agent commonly employed as an alternative to hydralazine, is independently associated with pulmonary edema in women with severe preeclampsia. We retrospectively evaluated women with severe preeclampsia who were given labetalol by intravenous bolus for MAP > 120 mm Hg. Outcome variables included: achieving MAP < 120 mm Hg with < 300 mg of labetalol, incidence of adverse effects of the drug, including pulmonary edema, hypotension, and maternal bradycardia. Total intravenous fluid intake exceeding output (+ delta I/O) and presence or absence of preeclamptic liver involvement were noted. Statistical analysis included unpaired t-tests and Fisher's exact test. Fifty-one women were studied, 7 (13.7%) of whom developed pulmonary edema. Demographic and pregnancy characteristics were not different between patients who did or did not develop pulmonary edema. No patient had detectable underlying heart disease. Patients with or without pulmonary edema did not differ as regards entry MAP (130 +/- 14 vs. 129 +/- 18 mm Hg), total dose of labetalol (209 +/- 83 vs. 193 +/- 39 mg/24 hours), incidence of bradycardia or hypotension (0/7 vs. 8/44), or presence of hepatic involvement (1/7 vs. 9/44). However, there was a significant difference in degree of positive fluid balance. Patients developing pulmonary edema had a net gain of 1,466 +/- 429 mL of fluid in the 24 hours in which they received labetalol than those who did not (659 +/- 1152 mL, P = .003). Initial central hemodynamic monitoring data revealed no impairment of cardiac performance (mean cardiac output 7.7 +/- 1.8 L/min, cardiac index 4.0 +/- 0.8 L/min/m2, left ventricular stroke work index 73 +/- 9 g.m.m-2) despite high pulmonary capillary wedge pressures (22 +/- 4 mm Hg). We conclude that the incidence of pulmonary edema in patients with severe preeclampsia who are treated with labetalol appears to be a result of an increase in third space fluid accumulation as a manifestation of the severity of their disease, not a direct effect of the drug on cardiac performance.
 ...
PMID:Does labetalol predispose to pulmonary edema in severe pregnancy-induced hypertensive disease? 964 12

Hemorrhagic shock (HS) elicits an inflammatory response characterized by increased cytokine production and recruitment of PMN which we previously found to be iNOS dependent. In this study we attempted to remove excess induced-NO by administration of the NO scavenger, NOX, with the goal of suppressing proinflammatory signaling and reducing organ damage. Rats subjected to HS (MAP = 40 mmHg for 100 min) followed by resuscitation and examined 24 h later demonstrated histological signs of lung injury including pulmonary edema as well as an 8.6-fold increase in MPO-positive PMN. These events were accompanied by a 3.9-fold increase in mRNA levels for IL-6, 3.7-fold for ICAM-1, 3.5-fold for IL-1beta, and 7.3-fold for TNFalpha compared to sham animals. Immunostaining of the lungs of shock animals demonstrated IL-6 protein localized to cells lining the luminal sides of bronchiols. These animals also demonstrated a 2-fold and 5.5-fold increase in activation of NF-kappaB and Stat3 (an IL-6 signaling intermediate), respectively. Administration of NOX (30 mg/kg/h beginning at 60 min of shock for total of 4.5 h) resulted in reduced lung injury as measured by a 46% reduction in PMN infiltration, a 20% decrease in wet-to-dry ratio, and improved arterial blood gases. NOX reduced proinflammatory signaling in the lung as demonstrated by a 62% decrease in NF-kappaB binding, 47% reduction in Stat3 binding, a reduction in mRNA expression of 48% for IL-6, 57% for ICAM-1, 67% for IL-1beta, and 64% for TNFalpha, as well as a marked reduction in the intensity of IL-6 protein staining. These data indicate that NOX prevents lung injury in this HS model, possibly through downmodulation of proinflammatory signaling and the shock-induced inflammatory response.
 ...
PMID:A nitric oxide scavenger protects against pulmonary inflammation following hemorrhagic shock. 1183 96