[Clinical aspects of AIDS: early neuropsychiatric symptoms].
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AIDS-Related Complex↗
Biomedical subjects
U Schick
Publications and source records attributed to U Schick.
[Fatal hepatic failure in a normally developed 5-year-old boy caused by VPA monotherapy].
A five-year-old, normally developed boy who had been healthy except for an absence epilepsy prior to valproate (VPA) treatment died 16 weeks after the introduction of VPA-monotherapy due to liver failure and intractable bleeding disorder. This case emphasizes that the restriction of VPA-therapy to children of more than two years of age, on monotherapy, and without evidence of other diseases or retardation does not exclude fatal complications. Until today world-wide about 100 patients have died during VPA-treatment.
Chemical and Drug Induced Liver Injury↗
Pulmonary vascular pressure-flow relationship in canine oleic acid pulmonary edema.
We tested the hypothesis that the increased impedance to flow in canine oleic acid (OA) lung injury is predominantly due to an increase in effective downstream pressure (EDP), obtained by extrapolating to zero flow the linear portion of the pulmonary artery pressure (PAP)/flow (Q) relationship. PAP-Q coordinates were obtained in eight anesthetized, O2-ventilated dogs by varying Q through systemic arteriovenous fistulae. PAP-Q lines were obtained before and approximately 5 h after injection of OA. A second group of six dogs served as a time control (TC) group. There was a linear relationship between PAP and Q in both experimental and control groups (mean r value 0.948). The presence of pulmonary edema in the OA group caused the EDP to almost double, from 7 to 12 mmHg (P less than 0.01). In contrast, EDP remained constant in TCs. Incremental vascular conductance (IVC), slope of the PAP/Q line, decreased (P less than 0.05) a similar amount in both groups. The above findings are consistent with the modeling of the pulmonary circulation according to a Starling resistor in that large amounts of edema changed EDP but not incremental conductance.
Animals↗
Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism.
Pulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear. Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8.8 +/- 2.1 (SD) mm Hg. Emboli increased PAP (15.1 +/- 1.6 to 36.5 +/- 3.5 mm Hg; p less than .001) and decreased CO (3.8 +/- 0.6 to 2.4 +/- 0.8 liters X min-1; p less than .001). Incremental resistance (the slope of the PAP-CO line) only increased slightly. On the other hand, the marked increase in PAP was predominantly due to an increase in effective outflow pressure (from 8.8 +/- 2.1 to 28.6 +/- 3.6; p less than .001). Hydralazine was administered in a dose sufficient to double CO. This did not affect PAP and caused an inconsistent and small decrease in incremental resistance. However, a consistently significant decrease in effective outflow pressure, averaging 23%, was observed. In this canine preparation of pulmonary hypertension the predominant effect of hydralazine appears to be a decrease in the mean vascular closing or outflow pressure.
Animals↗
Acute cardiopulmonary effects of nitroglycerin in canine oleic acid pulmonary edema.
In a canine model of acute respiratory failure, the authors investigated acute cardiopulmonary effects of nitroglycerin (TNG) and compared the results with those obtained after phlebotomy. Oleic acid increased intrapulmonary shunt (Qs/Qt) from 7.4 to 31% (P less than 0.001) and decreased (P less than 0.01) cardiac output (CO). In the presence of assumed low-pressure pulmonary edema, TNG was infused to decrease mean blood pressure (BP) by 40%; this was associated with a 26% decrease (P less than 0.05) in CO. Qs/Qt increased from 31 to 42% (P less than 0.01). There was a slight increase (P less than 0.01) in pulmonary vascular resistance (PVR) with TNG, and mean pulmonary artery pressure (PAP) decreased (P less than 0.05). In contrast, when CO was decreased by a similar amount with phlebotomy, mean Qs/Qt did not significantly change. There were similar changes in PVR and PAP and mixed venous O2 tension with TNG and phlebotomy. Accordingly, current results rule out increased flow, increased PVO2, and mechanical alterations in pulmonary vascular pressures as contributory to the increase in Qs/Qt with TNG. Alternatively, the increase in Qs/Qt with TNG may be explained by a direct pharmacologic decrease in pulmonary hypoxic vasoconstriction and/or by nonspecific pharmacologic effects.
Animals↗
Effects of reduced resistive afterload on left ventricular pressure-volume relationship.
In seven anesthetized, beta-blocked dogs, we investigated the effects of a reduction in systemic vascular resistance (SVR) on left ventricular (LV) systolic mechanics. LV pressure and volumes (scintigraphic techniques) were measured in base-line condition, after opening one and then two arteriovenous fistulas (AVF). Volume was infused to maintain LV end-systolic pressure (LVESP). Despite a constant ESP, the mean end-systolic volume (LVESV) fell from 42 to 31 ml (P less than 0.025) when the SVR fell from 81 to 48 units (P less than 0.0025), and the LVESV fell further to 24 ml (P less than 0.0025) when the SVR was decreased to 30 units (P less than 0.025). In six similarly prepared dogs, aortic flow was measured, and when resistive afterload decreased, instantaneous flow increased. Since end-diastolic volume was not significantly changed when resistive afterload decreased, instantaneous LV volume decreased despite constant systolic LV pressure. In two of these dogs, LV pressure-volume (PV) trajectories were drawn for the ejection period. When SVR decreased there was a marked leftward shift of the PV trajectory as the end of ejection was approached. It is concluded that at a given contractile state and ventricular pressure, alterations in resistive load directly affect rate and extent of ventricular shortening.
Animals↗
Direct effects of nitroprusside do not alter gas exchange in canine oleic acid edema.
The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange.
Analysis of Variance↗
Treatment of shock in a canine model of pulmonary embolism.
Despite the high mortality (greater than 30%) associated with hypotension complicating pulmonary embolism, previous studies have not systematically investigated how best to treat shock resulting from pulmonary embolism. In 24 dogs, we measured relevant hemodynamic parameters before and after shock was produced by intravenously injected autologous blood clots. When systemic blood pressure fell to 70 mmHg, dogs were randomly divided into groups and treated blindly for 1 h. All control dogs and all dogs treated with volume and isoproterenol died. In contrast, all dogs treated with noradrenaline were resuscitated and remained hemodynamically stable for 1 h. This effect of noradrenaline was significant (p less than 0.01, Fisher's exact test). Noradrenaline improved right ventricular performance by increasing blood pressure and improving right ventricular perfusion and/or by a direct increase in contractility. We conclude that in a canine model of pulmonary embolism and shock, noradrenaline may be the drug of choice for acute resuscitation.
Animals↗