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Biomedical subjects

P Conzen

Publications and source records attributed to P Conzen.

44 records · Page 3Linked to original sources

Modulation of resynthesis of 1-alkyl-2-arachidonyl-glycero-3-phosphocholine and phosphatidylinositols for interception in vivo of free arachidonic acid, lyso-PAF, diacyl-glycerols, and phosphoinositides.

Thermal injury causes directly a liberation of inositolphosphates, diacylglycerols, free arachidonic acid, and lyso PAF from eukaryotic cells. From lyso PAF derivates PAF, from free arachidonic acid are derivating PG, LT, and TX. These "soluble mediators" are stimulating inflammatory cell populations in a feedback mechanism: the stimulus activates the inflammatory cells to produce the same soluble mediators (Fig.1). The arising soluble mediators are the take off for the inflammation cascade causing as later step the activation of kinin, clotting, and complement systems. The pure biochemical lesions at the onset results in the clinical manifestation of oedema, increased dermal temperature, and pains. The possibilities for prevention and allevation of early pain, due to the acute burn, lie in the inhibition of the spreading out of inflammatory mediators (Bauer 1987a) (Fig.2).

Animals↗

[Effect of inhalation anesthetics on the myocardium].

A review of the myocardial effects of the volatile anesthetics halothane (HAL), enflurane (ENF) and isoflurane (ISO) is presented. In the first part the effects on cardiac rhythm, myocardial contractility and oxygen supply are discussed. In the second part the pathophysiology of myocardial ischemia during anesthesia and surgery is summarized. Finally the role of inhalation anesthetics in inducing or preventing myocardial ischemia is considered, with special regard to the "coronary steal" phenomenon.

Anesthesia, Inhalation↗

[Liver perfusion and oxygenation with isoflurane].

The influence of 0.7, 1.4 or 2.1 vol % isoflurane on hepatic blood flow and hepatic tissue oxygenation was studied in 12 dogs under basal anaesthesia with i.v. piritramid. Blood flow was measured by the microsphere method (phi = 15 micron). Tissue pO2 was determined by a platinum multiwire electrode and by measuring hepatic venous pO2. Isoflurane effected a marked fall in arterial blood pressure in these surgically not stimulated animals. However, cardiac output fell only moderately due to a considerable reduction in systemic vascular resistance. Both local tissue pO2 and venous pO2 were decreased with isoflurane. A potentially hazardous reduction in hepatic tissue pO2 was found predominantly with high isoflurane concentrations. The decrease in hepatic tissue pO2 results from disadvantageous effects on hepatic O2-balance: total hepatic blood flow decreases, whereas splanchnic O2 consumption increases. The lower blood flow is due to a reduction of portal blood flow whereas arterial perfusion remains unchanged. The increase in splanchnic O2 consumption possibly results from an elevated O2 consumption of the liver. Further studies have to clarify whether the disadvantageous effects of high isoflurane concentrations fail to appear when pain-induced stimulation of the sympathico-adrenergic system counteracts the fall in arterial blood pressure.

Animals↗

[Animal experiment studies on hemodynamics following partial and total blood exchange with a pyridoxalated polyhemoglobin solution].

The effects of a pyridoxalated polyhaemoglobin (SFH-PLP)n-solution on haemodynamics were investigated in a model of partial (hct = 12%) and total blood exchange (hct less than 1%) in 7 dogs. Partial blood exchange resulted in a slight increase in right atrial pressure (RAP) and pulmonary capillary wedge pressure (PCWP) and in a marked decrease in heart rate (HR). Cardiac output (CO) did not increase as would be expected from haemodilution. After total blood exchange, arterial pressure, HR, RAP, PCWP and CO were unchanged compared to the pre-exchange values during the 90 minutes of observation. However, pronounced pulmonary vasoconstriction was observed in 4 dogs. The beneficial effects on haemodynamics are due to the long intravascular persistance of the polymerized haemoglobin molecules (plasma half-disappearance time = 36 hours) and the addition of albumin supplying a sufficient colloid-osmotic pressure of the solution. These characteristics and the good oxygen unloading capacity of the pyridoxalated polyhaemoglobin resulted in longterm survival of three dogs. These results demonstrate a better haemodynamic efficacy of the (SFH-PLP)n-solution compared to previous investigations with unmodified haemoglobin solutions. However, there are still many problems, which have to be clarified prior to its clinical application.

Animals↗

Hypoxic pulmonary vasoconstriction and endogenous prostaglandin (PG) and thromboxane (TX) release in anesthetized pigs.

Products of the arachidonate cascade are known to be released from pulmonary tissue in normal and abnormal states, contributing to the regulation of pulmonary vascular resistance. To what extent hypoxic pulmonary vasoconstriction is affected by prostaglandin imbalances is still controversial. To evaluate PG and TX release, we measured plasma levels of TXA2, PGI2, PGF2a, and 13,14-dihydro-15-keto-PGF2a in healthy pigs undergoing normobaric hypoxic ventilation. Plasma levels of TXA2, PGI2, and PGF2a did not change during 10 minutes of hypoxia, whereas 13,14-dihydro-15-keto-PGF2a, the stable metabolite of PGF2a, was significantly elevated after 2, 5 and 10 minutes. Hemodynamic parameters showed an increase in heart rate and pulmonary vascular resistance. Our results suggest that alveolar hypoxia releases PGF2a from lung tissue, being rapidly metabolized to 13,14-dihydro-15-keto-PGF2a and that prostaglandins, at least in part, contribute to hypoxic pulmonary vasoconstriction.

Anesthesia, General↗

The effect of PEEP ventilation on hemodynamics and regional blood flow with special regard to coronary blood flow.

An experimental study was performed to evaluate the effects of positive end-expiratory pressure (PEEP) on central hemodynamics and on regional blood flow (RBF) using the radioactive microsphere (MS) method. Ten dogs with intact lungs and 10 dogs with oleic acid-induced pulmonary edema were ventilated with PEEP 10 and PEEP 20 (cmH2O). PEEP significantly reduced cardiac output (CO) by 25% at PEEP 10 and 40--50% at PEEP 20 despite volume expansion with dextran 60. RV afterload rose markedly due to a significant increase of pulmonary vascular resistance. PEEP tended to redistribute CO in favor of brain, heart and adrenals, at the expense of stomach, pancreas and thyroid glands. Hepatic artery flow was moderately reduced; renal RBF was seriously affected only when PEEP caused an extreme low-output state. RBF to the RV remained essentially unchanged, whereas RBF to the LV decreased, roughly paralleling the respective ventricular work. Nevertheless, the RV may suffer from underperfusion during PEEP, since its tension-time-index rises; this may indicate increased oxygen needs exceeding actual oxygen delivery.

Adrenal Glands↗

[Regional blood flow in splanchnic organs during positive end-expiratory pressure ventilation (author's transl)].

An experimental study was performed on 10 dogs to evaluate the effect of positive end-expiratory pressure ventilation (PEEP) on hemodynamics and regional blood flow (RBF). The following conclusions can be drawn from the results of this study: 1) PEEP leads to a significant reduction of cardiac output (CO). 2) Total blood flow to the preportal splanchnic organs, and consequently the portal venous flow, decreases in proportion to the reduction of CO. Within the splanchnic area, there is a redistribution of RBF in favour of the small and large intestines, at the expense of stomach and pancreas. 3) The arterial blood flow to the liver is only moderately affected. 4) The observed changes of RBF may in part contribute to the complications of the splanchnic organs occurring in PEEP-ventilated patients. 5) PEEP should be used only when strictly indicated; close monitoring of organ function appears mandatory in these patients.

Animals↗