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Immunohistochemical and functional studies suggest that opioid peptides are involved in blood pressure regulation. Endorphin and enkephalins contained in the brain seem to exert their effects by mediation of cardiovascular centers in the brain stem. Additional effects on blood pressure may be exhibited by circulating opioid peptides released from the pituitary and adrenal gland which may act at both central and peripheral sites. It is expected that further studies will complete our knowledge about the interaction of opioid peptides and blood pressure regulation and will result in therapeutic applications.

Summary In 2 groups of normovolemic dogs norepinephrine (7.5 µg/kg . min) is infused i.v. by an infusion pump. One group (n = 5) is subjected to a standardized hemorrhagic shock; the infusion of norepinephrine starts 20 min after reinfusion of the withdrawn blood. In the second group of 6 dogs norepinephrine is infused without a preceding hemorrhagic shock.

The purpose of this study was to evaluate the effect of free radical ablation therapy in acute hemorrhagic pancreatitis. Acute pancreatitis was induced in 64 rats by retrograde injection of 5% sodium taurocholate. Thirty animals were pretreated with 100,000 units/kg/hr of superoxide dismutase (SOD) and 400,000 units/kg catalase within the first 3 hr. After 0.5, 3.5, and 12 hr of observation time, serum enzymes and the tissue content of conjugated dienes, malondialdehyde, reduced and oxidized glutathione, as well as ATP, ADP and AMP were measured. In addition, tissue samples were examined by light microscopy. Untreated rats (N=34) developed within 12 hr an acute hemorrhagic necrotizing pancreatitis with a concomitant increase in serum enzyme levels and a decrease in reduced glutathione and ATP. Within the 12-hr observation period, 57% of the animals died. Scavenger treatment improved the tissue damage and attenuated the increase of the serum enzyme levels and the decrease in reduced glutathione and ATP. Moreover, the lethality rate was significantly lower. Oxygen radicals seem to be instrumental for the development of acute hemorrhagic pancreatitis. Thereby, antioxidant treatment reduces tissue damage, biochemical alterations and extrapancreatic complications, thus improving the final outcome.

Summary Sixteen anesthetized foxhounds were instrumented for hemodynamic measurements. The adrenolumbar vein was cannulated, and hemorrhagic hypotension (MAP=40 mmHg for 3 h) was induced by bleeding. The plasma levels ofß-endorphin (ß-END), methionine-enkephalin (M-ENK), and leucine-enkephalin (L-ENK) were determined in systemic and adrenal venous blood by specific RIA. Five dogs received an i.v. bolus of naloxone (2 mg/kg) and a subsequent naloxone infusion of 2 mg/kg per hour 1 h after onset of hypovolemia. Eleven dogs served as controls and received equivalent volumes (1 ml/kg per hour) of saline.

Leukotriene C4 (LTC4) underwent rapid elimination from the circulating blood and was extensively converted to LTD4 within the vascular space of the guinea pig. To mimic the elimination and metabolism of endogenous LTC4 generated during anaphylaxis, 14,15-3H-labeled LTC4 was infused intravenously over a period of 15 min, leading to a recovery in bile of 85% of the infused LT radioactivity within 2 h. Corresponding to the tracer studies, LTD4 and, to a lesser extent, LTC4 were the predominant endogenous cysteinyl LTs in guinea pig bile. The biliary production rate of endogenous LTD4 increased from 0.3 +/- 0.1 to 6.2 +/- 1.8 pmol x min-1 x kg-1 (p less than 0.001) during anaphylactic shock induced by intravenous injection of OVA (0.2 mg/kg) into sensitized guinea pigs. A novel LT biosynthesis inhibitor (MK-886; 10 mg/kg, i.v., 15 min before antigen challenge) suppressed the antigen-induced cysteinyl LT production by greater than 92% (p less than 0.001). This inhibition of systemic LTC4 formation was associated with a complete protection against lethal anaphylactic shock in animals pretreated in addition with the H1 receptor antagonist pyrilamine. Pretreatment with either the inhibitor of LT synthesis or the histamine receptor antagonist reduced the lethality during anaphylactic shock from 100 to 60 and 78%, respectively. In artificially ventilated, pyrilamine-pretreated animals, the antigen-induced decrease in dynamic lung compliance and the rise in hematocrit were significantly reduced (p less than 0.05) by pretreatment with the inhibitor of LT synthesis. Dexamethasone at high doses (10 mg/kg, i.p., once daily for 7 d, or in a single dose of 10 mg/kg, i.v., 3.5 h before challenge) had no inhibitory effect on LT generation during anaphylaxis in vivo. However, in resident peritoneal macrophages, harvested from these dexamethasone-treated sensitized guinea pigs and stimulated with zymosan, both cysteinyl LT and 6-keto-PGF1 alpha formation were strongly suppressed. These studies indicate an important role of cysteinyl LTs in systemic anaphylaxis in vivo and demonstrate the blockade of anaphylactic LT generation by a novel inhibitor of LT biosynthesis (MK-886) but not by dexamethasone.

Summary The significance of pulmonary pressure-flow relation and its correlation to alveolar dead space and histological lesions of the lung were evaluated in ten mongrel dogs, which were subjected to standardized bone trauma and hemorrhagic hypotension at 40 mm Hg for 3 h. These results were compared with those of 5 control dogs without trauma and shock.

Summary The distribution of myocardial blood flow (MBF) was evaluated in pressureinduced LV hypertrophy of foxhounds. At the early stage of developing hypertrophy, i.e., 3 months after aortic banding (+53% LV weight) resting MBF and flow reserve were not significantly different from control hearts. One year after banding (+94% LV weight) myocardial flow reserve had clearly decreased.

Summary The influence of coronary stenosis on resting blood flow (201Tl-uptake) and myocardial flow reserve (bicycle regometry) is studied in 18 patients with coronary disease. Severe coronary stenosis of 75–90% caused a reduced201T-u[pake both at rest and peak exercise. In contrast to this group patients with a 50–60% stenosis have a normal scintigram at rest but focal defects of201Tl-uptake at peak exercise.

Background and Methods. The infusion of dextran solutions is associated with haemodilution and, under some conditions, with a slight increase in plasma viscosity. To clarify the compound effects of simultaneous haemodilution and plasma viscosity increases on macro‐ and microhaemodynamics, we investigated the changes in arterial perfusion (radiolabelled microspheres, 15 μrn Ø) and oxygenation (tissue Po2) of vital organs using an animal model of plasma hyperviscosity. In nine splenectomized beagles plasma viscosity was increased step by step from 1.06 (baseline) to 2.14, and 2.99 mPas by infusion of small amounts (4% of total blood volume) of an ultra‐high‐molecular‐weight dextran (50% w/v, mw: 500,000).

Summary 24 dogs (19.5–31.5 kg) are subjected to traumatic shock by 200 hammer blows on the posterior extremities. After the trauma the blood pressure and cardiac output fall significantly. The resistance in the systemic circulation and in the demaged extremities increases continuously. After 21/2 h the total peripheral resistance decreases because the periphery reacts less to noradrenalintested with 2 µg/kg-and due to central damage, shown by the fall in heart rate. The median pulmonary artery pressure drops only initially after trauma, with simultaneous reduction of cardiac output. This results from the considerable increase of the pulmonary flow resistance, 50% in the first 30 min. The thrombocyte count decreases by 33% immediately after trauma. The increase in resistance is not due to mechanical obstruction of the pulmonary circulation. The falling cardiac output alone suffices to cause a rise in resistance. This is proved also by the decrease of the intrathoracic blood volume. 12 dogs are given treatment. 7 receive 1.5 mg/kg polydextran (mol. weight ca. 2 Mio.) i.v., after which the thrombocyte count falls permanently by 25%. 5 animals receive the aggregation-inhibiting preparation VK 744 (Thomae), after which the thrombocyte count remaines constantly high. Despite treatment with opposite effects on the thrombocyte count, the pulmonary flow resistance rises by 50 % in the first 30 min after trauma, the same as in the control group.

Summary A particular difficulty in angiographic estimation of coronary blood flow is the exact determination of the length of the sector of the coronary vessel to be measured. Considerable perspective foreshortening occurs according to the position of the artery in space. In order to judge the extent of the alteration, an X-ray opaque calibrated ruler, 5 mm long, is introduced from the femoral artery into the descending branch through a Judkins coronary catheter. The pin lying in the artery is compared with a 3-dimensional ruler implanted parallel to the descending branch.—In 7 anaesthetised dogs with electromagnetic flow probes previously implanted on the descending branch the coronary flow is determined angiographically from the parameters of radius and length of the sector of coronary vessel and the velocity of the contrast medium bolus. The velocity of the advance of the contrast medium bolus in the descending branch is recorded with a fast camera at an exposure rate of 80 pictures per sec. For the descending branch of the left coronary artery in dogs the results are 21.93 to 83.05, average 42.69 ml/min. The values found are closely correlated with the electromagnetically measured flow values (r = 0.901). There is no directional deviation between the two measuring methods.