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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure induced in Charles River rats by right nephrectomy and left renal artery clamping for 70 min, constantly produced high blood urea and serum creatinine levels 24 h following the experimental procedure. The intravascular administration of propranolol in different doses persistently alleviated the severity of uremia seen on the following day. The optimum dose in this experimental set-up was 1 mg/kg/h. The mean blood urea level was 237 +/- 15.5 (SEM) mg% in the saline-treated controls and 116 +/- 16 mg% in the group treated with propranolol 1 mg/kg/h. P113 alone and prostaglandin A1 alone were not effective in alleviating the ARF. The combination of P113 and propranolol produced the same amount of alleviation in uremia as propranolol alone. The PRA was low in the propranolol-treated rats and high in the group which received both P113 and propranolol, even though alleivation of ARF was produced in both of these groups. The mechanism by which the beta-adrenergic blockade produced by propranolol alleviates the anoxic type of acute renal failure is unknown. However, it does not seem to act through the suppression of renin release from the kidney.
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PMID:Alleviation of anoxic experimental acute renal failure in rats by beta-adrenergic blockade. 89 66

The subject of left ventricular involvement in chronic obstructive airways disease is controversial. We measured left ventricular ejection fraction (LVEF) in 120 patients with severe chronic obstructive airways disease, 92 of them acutely decompensated and 28 stable. A bedside radionuclide technic using a scintillation probe was used to measure LVEF. Of the 28 patients with acute respiratory failure, LVEF was normal (larger than or equal to 55 per cent) in 60 and subnormal in 32. Of the 28 patients with stable chronic obstructive airways disease, LVEF was normal in 12 and low in 16. Coronary artery disease could be demonstrated clinically or at autopsy in 13 of the patients with acute and in 7 of the patients with stable chronic obstructive airways disease. LVEF was 28 plus or minus 10.4 per cent (average plus or minus SEM) in the patients with acute chronic obstructive airways disease and coronary artery disease which was significantly different (P smaller than 0.001) from LVEF in patients without coronary artery disease (61 plus or minus 1.9 per cent). In the patients stable with chronic obstructive airways disease and coronary artery disease, LVEF was (42 plus or minus 3.5 per cent), significantly different (P smaller than 0.001) from LVEF in those without coronary artery disease (55 plus or minus 2.1 per cent). There was no relationship between LVEF and arterial oxygen, or carbon dioxide tension, or pH. Results suggest that LVEF is normal in patients with severe lung disease alone and that reduced LVEF in patients with chronic obstructive airways disease can reasonably be ascribed to coronary artery disease.
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PMID:Left ventricular ejection fraction in severe chronic obstructive airways disease. 113 48

Acute respiratory failure is followed by decreased left ventricular performance probably due to the right ventricle dilatation induced by pulmonary hypertension and intraventricular septal shift to the left. An anacrotic notch on the upstroke slope of the carotid curve was detected in 22 of 36 hemodynamic studies with simultaneous ECG, PCG and external pulse carotid curve recording in 7 burned patients with acute respiratory failure. Comparing the values (x +/- SEM) obtained in group with notch and in group without notch, PAPs, PAPm, PVRI were higher (56 +/- 2.30 mmHg; 32 +/- 0.99 mm Hg; 543 +/- 56.8 dyn x s/cm5/m2 versus 32 +/- 1.08 mm Hg; 20 +/- 0.9 mm Hg; 173 +/- 14.7 dyn x s/cm5/m2) and CI and LVSWI were lower (2.6 +/- 0.17 l/min/m2; 25.8 +/- 2.41 g x m/m2; versus 3.8 +/- 0.26 l/min/m2; 38.3 +/- 2.82 g x m/m2) in group with notch. As it is shown by 11 paired measurements where the notch disappeared immediately after starting vasodilator therapy PAPs, PAPm, PVRI decreased (from 54 +/- 3.1, 35 +/- 0.8 mm Hg, 498 +/- 64.1 dyn x s/cm5/m2 to 35 +/- 0.8, 21 +/- 1.1 mmHg, 189 +/- 18.4 dyn x s/cm5/m2 respectively) and heart performance improved. Since the left ventricle contractility (characterized by EF, PCWP, ICT) was normal in both groups, our findings suggest that critically high PAPs values (over 40 mmHg) cause a septal bulging at the beginning of the systole which in turn narrows the left ventricle outflow tract. Regarding to the clinical importance of the deteriorated biventricular function at the critically high PAPs evidenced by notch phenomenon on carotid curve but measurable only by indwelling pulmonary arterial catheterization always being a source of infection, the noninvasive parameters as independent variables were entered into canonical discriminant analysis. The ratio of the correctly classified cases was 89%.
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PMID:Anacrotic "notch" on the upstroke of external carotid curve may indicate a critically high systolic pulmonary arterial pressure value. 184 11

Positive end expiratory pressure (PEEP) is an accepted treatment for children with acute respiratory failure secondary to restrictive lung diseases. Using a simple technique based on open circuit nitrogen washout, we determined the functional residual capacity (FRC) in 25 ventilated children (age 3 wk-10 y) with acute respiratory failure secondary to restrictive lung disease (pulmonary edema, bilateral pneumonia). FRC measured at a physiologic level of PEEP (2-4 cm H2O) was 45.0 +/- 3.6% (mean +/- SEM; range 12-80%) lower than normal predicted values. At the PEEP level chosen clinically (4-10 cm H2O, mean = 6.0), the FRC was below normal predicted values for nonintubated children by a mean of 31.8% (range 0-73%) (p = 0.0001) and only seven patients (28%) had FRC within 20% below predicted normal values. FRC normalized at PEEP levels of 6-18 cm H2O (mean = 11.6), which was up to 200% above the clinically chosen PEEP level. In six children without lung disease who were ventilated at a PEEP level of 2-4 cm H2O, the FRC was within normal range in two, but significantly higher (by 45%) in the other four. We conclude that FRC in ventilated children with acute restrictive lung disease is significantly lower than normal and the clinically chosen PEEP fails to normalize the FRC in most of the cases.
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PMID:Functional residual capacity in ventilated infants and children. 225 67

Using the multiple inert gas elimination technique, we studied ventilation-perfusion (VA/Q) relationships in eight patients with chronic obstructive pulmonary disease (COPD) during mechanical ventilation (MV) and again during weaning (spontaneous ventilation [SV] through an endotracheal tube) from MV needed for acute respiratory failure. The patients, seven men and one woman with a mean age of 63 +/- 2.8 (SEM) yr (FEV1 33 +/- 5.2% of predicted), required MV for 9.0 +/- 2.4 days prior to the study. The patients were studied at maintenance FIO2 (0.28 to 0.40) while breathing 100% O2, both during MV and SV. After 30 min of SV, PaCO2 increased from 48.9 +/- 3.4 to 58.3 +/- 3.1 mm Hg (p = 0.003) and pH decreased from 7.42 +/- 0.01 to 7.36 +/- 0.01 (p = 0.001) without significant changes in PaO2. Despite a decrease in tidal volume (VT) from 700.0 +/- 41.1 during MV to 313.0 +/- 39.6 ml during SV (p = 0.001), minute ventilation remained unchanged (from 8.2 +/- 0.7 during MV to 7.4 +/- 0.6 L/min during SV). Furthermore, cardiac output (QT), oxygen delivery (QO2), and mixed venous PO2 (PVO2) significantly rose during SV when compared with the MV (QT: from 4.7 +/- 0.4 to 6.7 +/- 0.7 L/min, p = 0.011; QO2: from 857.3 +/- 113.0 to 1078.5 +/- 158.9 ml/min, p = 0.0074; PVO2: from 36.7 +/- 1.1 to 42.3 +/- 2.2 mm Hg, p = 0.041). Overall VA/Q inequality worsened as blood flow was redistributed to low VA/Q areas (from 9.4 +/- 4.4 to 19.6 +/- 5.3% of QT, p = 0.05). The dispersion of the ventilation distribution (log SDV) significantly worsened during SV (from 1.0 +/- 0.08 during MV to 1.2 +/- 0.08 during SV, p = 0.044). No changes were observed in either series dead space or ventilation of high VA/Q ratio units.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilation-perfusion mismatching in chronic obstructive pulmonary disease during ventilator weaning. 255 65

As manifest by tubular collapse and the virtual absence of flow into the glomerulotubular junction (GTJ), filtration in most nephrons (SNGFR) of rats poisoned with 9 mg/kg body wt HgCl2 16 to 28 hours earlier was virtually absent. Arterial colloid osmotic pressure (COPA) and Bowman's space pressure (PBS) were modestly depressed (P less than 0.05 or below), and mean blood pressure was reduced from 115 +/- 2 mm Hg (SEM) to 97 +/- 1 mm Hg (P less than 0.001). Glomerular capillary hydraulic pressure (Pg), 25.6 +/- 1.3 mm Hg was some 24 mm Hg lower than control (P less than 0.001) and yielded a net afferent effective filtration pressure (Pnet) of 4.1 +/- 1.2 mm Hg. Excluding three rats with values greater than 10 mm Hg, Pnet averaged 2.0 +/- 0.9 mm Hg (N = 17 rats) versus 20.0 +/- 1.8 mm Hg in controls (N = 10, P less than 0.001), the former being statistically almost indistinguishable from 0 mm Hg and barely able to support any filtration. This decrease in Pg was caused by a major increase in preglomerular resistance (RA) and a reciprocal fall in efferent arteriolar resistance (RE), the RA/RE ratio of 7.2 +/- 0.8 being fourfold higher than control (P less than 0.001). Renocortical blood flow was not different from control (P greater than 0.2). A wide spread of Pg values in individual glomeruli and the absence of tubular flow despite the appearance of i.v. injected lissamine green in a quadrant of surface glomeruli suggested the possibility of a greatly increased, glomerular capillary resistance. It is concluded that reciprocal changes in RA and RE are the immediate cause of filtration failure in this form of ARF and that, in the virtual absence of filtration, tubular leakage can play no important role. Since PBS was depressed in both the developmental and established phases of ARF, tubular obstruction appears to play no direct role in the pathogenesis of this particular model of murine acute renal failure.
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PMID:Glomerular hemodynamics in mercury-induced acute renal failure. 365 37

Neonatal pulmonary manifestations of prolonged (2-8 weeks) amniotic fluid leak (PAL) were evaluated in 22 neonates. The severity of respiratory insufficiency was evaluated by a profile scoring system based on arterial blood gases, ventilatory support, and evidence of "fetal compression". The spectrum included acute respiratory failure with pulmonary hypoplasia (3), pulmonary hemorrhage (2), severe bronchopulmonary dysplasia (3), subacute lung disease (5), and transient respiratory disease (2). Seven neonates were completely asymptomatic. Clinical manifestations were correlated to age of onset and duration of PAL. The onset of PAL in the asymptomatic babies had occurred after 32 weeks gestation (mean +/- SEM, 33.5 +/- 1.1 wk; duration was 4.4 +/- 1.1 wk). In symptomatic neonates the onset of PAL was 24.0 +/- 1.0 weeks; duration being 6.0 +/- 0.6 weeks. When PAL occurred before 22 weeks and the duration of leak was longer than 6 weeks, the pulmonary profile score was less than 3 and associated with severe respiratory sequelae. These manifestations culminated in neonatal demise despite aggressive conventional ventilatory techniques. Onset of PAL between 23 and 28 weeks gestation and continuing longer than 8 weeks also was associated with a similar outcome. Duration of PAL between 2 and 7 weeks in this group was associated with less severe pulmonary manifestations and higher scores. Pulmonary morbidity was significantly correlated to the initial profile score (P less than .05) and was influenced by the prenatal reduction in thoracic volume.
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PMID:Neonatal pulmonary manifestations due to prolonged amniotic leak. 371 44

Sepsis remains the most common associated factor in acute respiratory failure (ARF). Endogenous opiates are known to have both respiratory and cardiovascular depressant effects. Because there is a high level of circulating endogenous opiates in sepsis, the possible role of opioids in the ARF syndrome seen in sepsis was studied. Sixteen piglets were infused with an LD100 dose (7.5 X 10(10) organisms/kg) of live Escherichia coli (Type 09-41). The pigs were hemodynamically monitored. Serial blood samples were taken for arterial blood gases and lactate. Serial lung biopsies were taken for determining wet/dry lung weight ratios and for histology. Group I (n = 8): septic shock controls without naloxone; group II (n = 8): naloxone treated, given as 2 mg/kg/hr intravenous boluses, starting within 1 min of E. coli infusion. All animals died of septic shock. Survivors at 150 min in group II had a higher blood pressure than group I (67.7 +/- 5.33 SEM vs 39.0 +/- 9.39) and cardiac output was also greater (1.07 +/- 0.23 vs 0.25 +/- 0.25). By 210 min, group I had no survivors (0/8) while 3/8 in group II survived. Pulmonary vascular resistance in group II at 90 and 120 min (870.8 +/- 274.1 and 942.5 +/- 12.9, respectively) was lower than in group I (2868.3 +/- 843.6 and 4156 +/- 1067). The PO2 was markedly better in group II and at 90 min; controls had a PO2 70.7 +/- 13.0, while group II had a PO2 111.4 +/- 8.4 (P less than 0.05). PCO2 levels showed a progressive rise in group I from 39.25 +/- 1.4 to 49.4 +/- 8.57.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pulmonary effects of opiate blockade in septic shock. 637 93

Acute respiratory failure in humans often follows extrathoracic sepsis. The purpose of this study was to determine the effect of repeated episodes of intra-abdominal sepsis over several weeks on the structure and function of rat lung. Intermittent peritonitis and a bacteremia of Escherichia coli and Bacteroides fragilis were produced by weekly intra-abdominal implants of gelatin capsules containing these organisms (3.0 +/- 1.0 X 10(7) and 5.0 +/- 1.0 X 10(7) colony-forming units/ml, respectively; mean +/- SEM). After 4 weeks alveolar walls were thickened and cellular with focal areas of alveolar space consolidation: circulating polymorphonuclear leukocytes were increased (12.2 +/- 1.2 to 19.9 +/- 2.0 X 10(3)/mm3; p less than 0.05), as were plasma levels of 6-keto-PGF1 alpha (0.56 +/- 0.08 to 1.02 +/- 0.18 ng/ml; p less than 0.01). After 8 weeks the capillary bed was dilated and the alveolar walls and ducts appeared less cellular but showed fibrosis: The WBC count had increased to 25.5 +/- 1.0 X 10(3) (p less than 0.01). After 4 or 8 weeks of intermittent sepsis there was no increase in the pulmonary artery pressure or vascular resistance or any change in arterial oxygen tension, plasma thromboxane beta 2 level, or platelet count. We conclude that repeated bouts of sepsis and bacteremia in the rat cause progressive injury to lung alveoli without evidence of altered blood gas tensions or pulmonary hemodynamics.
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PMID:The development of a model of subacute lung injury after intra-abdominal infection. 637 62

An early event in the evolution of acute respiratory failure (ARF) is thought to be the activation of platelets, their pulmonary entrapment and subsequent release of the smooth muscle constrictor serotonin (5HT). This study tests the thesis that inhibition of 5HT will improve lung function. The etiology of ARF in the 18 study patients was sepsis (N = 10), aspiration (N = 3), pancreatitis (N = 1), embolism (N = 2), and abdominal aortic aneurysm surgery (N = 2). Patients were divided into two groups determined by whether their period of endotracheal intubation was less than or equal to 4 days (early ARF, N = 12) or greater than 4 days (late ARF, N = 6). Transpulmonary platelet counts in the early group showed entrapment of 26,300 +/- 5900 platelets/mm3 in contrast to the late group where there was no entrapment (p less than 0.05). The platelet 5HT levels in the early group were 55 +/- 5 ng/10(9) platelets, values lower than 95 +/- 15 ng/10(9) platelets in the late ARF group (p less than 0.05), and 290 +/- 70 ng/10(9) platelets in normals. The selective 5HT receptor antagonist, ketanserin was given as an intravenous bolus over 3 minutes in a dose of 0.1 mg/kg, followed by a 30-minute infusion of 0.08 mg/kg. During this period mean arterial pressure (MAP) fell from 87 +/- 5 to 74 +/- 6 mmHg (mean +/- SEM) (p less than 0.05). One and one-half hours following the start of therapy, MAP returned to baseline. At this time, patients with early ARF showed decreases in: physiologic shunt (Qs/QT) from 26 +/- 3 to 19 +/- 3 (p less than 0.05); peak inspiratory pressure from 35 +/- 2 to 32 +/- 2 cmH2O (p less than 0.05) and in mean pulmonary arterial pressure from 32 +/- 2 to 29 +/- 1 mmHg (p less than 0.05). At 4 hours all changes returned to baseline levels. In early ARF ketanserin did not alter pretreatment values of: pulmonary arterial wedge pressure, 17 +/- 3 mmHg; cardiac index, 2.8 +/- 0.3 L/min X m2; platelet count, 219,000 +/- 45,000/mm3; platelet 5HT, 55 +/- 5 ng/10(9) platelets; plasma 5HT, 142 +/- 21 ng/ml; plasma thromboxane B2, 190 +/- 30 pg/ml; or plasma 6-keto-PGF1 alpha, 40 +/- 10 pg/ml. Ketanserin infusion in patients with late ARF yielded no benefit. In both ARF groups the decreases in QS/QT were inversely related to the duration of intubation (r = 0.70; p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of serotonin in patients with acute respiratory failure. 654 16


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