4s valence level of adsorbed K atoms probed by metastable-He deexcitation spectroscopy.
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Biomedical subjects
Publications and source records attributed to G Ertl.
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The effect of hypoxia and the renin-angiotensin system on metabolic coronary regulation in hemorrhagic shock was studied in 22 anesthetized open-chest dogs. Left circumflex coronary blood flow was measured with an electromagnetic flowmeter. Dogs were ventilated with room air (n = 8) or 100% oxygen (n = 7). A third group of dogs was ventilated with room air and bilaterally nephrectomized 5 h prior to starting the experimental protocol (n = 7). After control data had been obtained, dogs were bled from the femoral arteries into a pressurized reservoir which maintained blood pressure at 45 +/- 1 mmHg. The angiotensin II receptor blocker, saralasin, was then infused i.v. (0.1, 1.0, 10.0 micrograms/kg per min). Coronary blood flow was reduced by hemorrhage, and no significant difference existed in coronary flow during hemorrhage among the three groups. Coronary sinus oxygen saturation was diminished in control animals during hemorrhage from 26% +/- 1% to 17% +/- 1% (P less than 0.05) but normal in 100% oxygen ventilated animals (30% +/- 3%) and in nephrectomized dogs (34% +/- 4%). Coronary oxygen extraction was reduced by saralasin in intact but not in nephrectomized dogs. In six additional experiments, in which blood pressure was not artificially held constant during saralasin infusion, saralasin still significantly improved coronary sinus oxygen saturation and thus reduced coronary oxygen extraction. The data suggest that both hypoxia and the renin-angiotensin system participate in the restriction of metabolic coronary regulation in hemorrhagic shock.
An increase in plasma renin activity (PRA) following experimental coronary occlusion has previously been demonstrated in anaesthetized and conscious dogs. The purpose of the present study was to analyse the mechanism of this renin release. In two distinct models of myocardial ischaemia in anaesthetized dogs--i.e. occlusion of the left-anterior descending coronary artery (model A, n = 21) and atrial pacing in the presence of stenosis of the left-anterior descending coronary artery (model B, n = 23), an increase in arterial PRA was found from 1.68 +/- 0.43 to 3.06 +/- 0.63 ng ml-1 h-1 (model A, mean +/- SEM, P less than 0.025) and from 9.87 +/- 3.59 to 14.96 +/- 4.06 ng ml-1 h-1 (model B, P less than 0.05), respectively. The increase in PRA following coronary occlusion was not blunted by adrenergic beta-receptor blockade with propranolol (3 mg kg-1 i.v.; n = 4). Coronary sinus PRA was lower than arterial PRA and the increase in PRA did not occur in nephrectomized dogs (n = 5). The data suggest that myocardial ischaemia induces a release of renin from the kidney which is not mediated by adrenergic beta receptors.
A 71-year-old woman was admitted after partial removal of an infected pacemaker system. Septicemia and subclavian vein thrombosis were present. With combined use of a pigtail catheter and a wire loop originally developed for endoscopic polypectomy, the infected catheter was pulled into the inferior vena cava. Counterclockwise rotation of the pigtail catheter following its fixation to the electrode by the wire loop allowed removal of the tip of the endocardial screw-in electrode from the myocardium and its extraction. Open heart surgery was avoided and the source of chronic infection was removed.
Eight patients suffering from congestive heart failure (NYHA III-IV) and pretreated with digoxin received muzolimine over 14 days in an open clinical study. The muzolimine dose was adjusted to 3/4 of the daily furosemide dose necessary to keep the body weight constant at least three days prior to the onset of muzolimine treatment. Plasma concentrations of epinephrine, norepinephrine, aldosterone, renin and digoxin were determined on the last day of the furosemide treatment period and on the last day of the muzolimine period. No significant changes were observed in plasma concentrations of epinephrine, aldosterone, renin, creatinine, and potassium. After muzolimine treatment, however, body weight and sonographically determined liver size decreased further and plasma norepinephrine concentrations were significantly lower. The digoxin concentrations did not change after muzolimine treatment. The results demonstrate the beneficial effect of muzolimine in heart failure patients. Since plasma concentration of digoxin does not change despite marked diuretic effects of muzolimine no relevant interaction between both substances has to be expected.
Bovine testicular hyaluronidase (BTH) reduces experimental myocardial infarct size and ameliorates electrocardiographic signs of ischemia. This study was done to determine if heparin, an in vitro inhibitor of hyaluronidase activity, blocks the action of BTH in the myocardium of dogs after coronary artery occlusion. BTH was administered intravenously as 5,000 NF units/kg at 0.5 and 2.5 hours after coronary occlusion. Heparin was administered intravenously as a 150-unit/kg loading dose, followed by 10 units/kg per hour i.v., beginning 15 minutes before coronary occlusion. The area of myocardial ischemia at risk was assessed by a radiolabeled microsphere technique; the area that developed necrosis was assessed by a histochemical technique. In vivo activity of BTH was assessed by a colorimetric analysis of the BTH substrate, i.e., hyaluronic acid (HA), extracted from myocardial tissue. For biochemical analysis of HA, the heart was divided into anterior myocardium, which included ischemic tissue and posterior nonischemic myocardium. The myocardial HA content of dogs treated with BTH plus heparin (anterior, 3.44 +/- 0.40 micrograms HA/mg protein; posterior, 3.69 +/- 0.33 micrograms HA/mg protein) was not significantly different from control (anterior, 3.61 +/- 0.29 micrograms HA/mg protein; posterior, 3.55 +/- 0.23 micrograms HA/mg protein). In contrast, BTH lowered myocardial HA content (anterior, 2.16 +/- 0.21 micrograms HA/mg protein; posterior, 2.08 +/- 0.14 micrograms HA/mg protein) compared with either BTH plus heparin or control groups in both anterior myocardium (p = 0.006) and posterior myocardium (p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of atrial fibrillation (AF) on coronary circulation before and after alpha-receptor blockade were studied in 14 anesthetized, open-chest dogs. AF was induced by electrical stimulation of the left atrial appendage; identical rhythmic heart rates were adjusted by left atrial pacing. During atrial pacing, coronary vascular resistance (CVR) was 0.97 +/- 0.10 mm Hg X min X 100 g/ml (resistance units [RU]), coronary blood flow (CBF) 125 +/- 14 ml/min X 100 g, and oxygen saturation 30 +/- 2%; plasma epinephrine was 193 +/- 42 pg/ml and norepinephrine 584 +/- 111 pg/ml. During AF, CVR was higher (1.16 +/- 0.11 RU, p less than 0.0005), whereas CBF (92 +/- 9 ml/min X 100 g, p less than 0.001) and coronary sinus oxygen saturation (24 +/- 2%, p less than 0.0025) were lower than during atrial pacing. When AF was induced, epinephrine increased to 333 +/- 98 pg/ml (p less than 0.05) and norepinephrine to 1,005 +/- 214 pg/ml (p less than 0.005). The large increase in plasma catecholamines suggested an activation of the sympathoadrenal system during AF. In addition, the alpha-receptor blocker phenoxybenzamine (10 mg/kg, intravenously) abolished the differences in CVR, CBF and oxygen saturation between AF and atrial pacing. The data suggest that the decrease in CBF and increase in CVR during experimentally induced AF are caused by coronary vasoconstriction, mediated by sympathetic activation of alpha receptors in the coronary vascular bed.
Changes of collateral perfusion pressure (CPP) and segmental coronary resistances during reactive hyperemia were studied in nine chloralose-urethan-morphine anesthetized open-chest dogs. Coronary perfusion pressure was controlled by a cannula in the left main coronary artery and inflow measured by an electromagnetic flowmeter. The first or second diagonal branch of the left anterior descending coronary artery was cannulated and perfused from a carotid artery; inflow was abolished by embolization with latex microspheres (diameter: 25 +/- 5 mu) and peripheral coronary pressure was assumed to represent CPP. Segmental coronary resistances were defined as follows: Proximal coronary resistance (R1) was calculated from the difference between coronary perfusion pressure and CPP divided by coronary inflow. Distal coronary resistance (R2) was calculated from CPP divided by coronary inflow. Reactive hyperemia was produced by interruption of coronary inflow for 15 s and analysed at 30 s and 60 s of reperfusion when cardiac function had recovered. At baseline, R1 was 0.52 +/- 0.04 mm Hg X min X 100 g/ml (RU) and R2 0.63 +/- 0.07 RU. At 30 s, R1 was reduced by 19 +/- 3% (P less than 0.01) this was less (P less than 0.05) than R2 which was reduced by 32 +/- 3% (P less than 0.01). At 60 s R1 and R2 were reduced by 11 +/- 2% and 13 +/- 2%, respectively; this was not significantly different. Accordingly, CPP (baseline: 59 +/- 4 mm Hg) at 30 s was reduced by 7 +/- 2% (P less than 0.03), at 60 s the reduction was not significant. The data suggest that reactive hyperemia, as a model of metabolic coronary dilatation, may reduce CPP equivalent to a coronary steal phenomenon.
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A method was applied in anesthetized dogs enabling the measurement of regional resistances up to and behind the start of collaterals and the collateral resistance. The studies show that peripheral coronary pressure, i.e. perfusion pressure of the collaterals, can change when the ratio of pre- and post-collateral resistance alters. Drugs can influence collateral blood flow not only by directly effecting the collaterals but also by altering collateral perfusion pressure. Glyceryl trinitrate given in minor doses improved collateral blood flow by directly dilating the collaterals and also by increasing collateral perfusion pressure. Higher doses did not improve collateral flow due to a decrease of collateral perfusion pressure. A steal-phenomenon occurred in some cases. Adenosine and verapamil had no direct influence on the collateral resistance. Verapamil given in small doses increased perfusion pressure slightly but not enough to improve collateral blood flow. High doses of verapamil, like low doses of adenosine, had no significant influence on collateral perfusion pressure and collateral blood flow. Adenosine given in high dosage led to a diminution of collateral flow by decreasing collateral perfusion pressure, i.e. a steal-phenomenon.
Incidence and type of arrhythmia, using continuous ECG monitoring, were examined in 79 patients six weeks to 24 months after acute myocardial infarction, the findings being compared with arrhythmias at rest and on exercise, and correlated with signs of heart failure and coronary insufficiency. Arrhythmias were revealed in 16% (n = 13 at rest) and 19% (n = 10 of 52) on exercise. But continuous ECG monitoring revealed it in 86% (n = 68). On the other hand, arrhythmias may occur in the resting ECG but be rare on continuous monitoring. Ventricular extrasystoles were the most common arrhythmia, often multifocal and giving rise to bigeminy, only rarely as a result of exercise. Such extrasystoles usually showed right or right and left bundle conduction delays. Their frequency increased with increasing age of the patient. They were particularly frequent in patient who already had cardiac symptoms at rest, in patients with a large heart, and those who could not easily be exercised. Arrhythmias were more frequent a year after infarction than shortly before discharge from hospital or six months after infarction.
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The purpose of this work was to visualize the whole three-dimensional coronary artery tree of the perfused beating rat heart using three-dimensional MRI. The spatial resolution amounts to 140 microns. Also, vessels having smaller diameters could be detected. Different strategies for the visualization of the three-dimensional coronary angiograms including maximum intensity projection, data thresholding, and segmentation, were shown. The coronary artery tree was best visualized by hysteresis threshold segmentation and subsequent surface reconstruction.