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Biomedical subjects

W M Vogel

Publications and source records attributed to W M Vogel.

31 records · Page 2Linked to original sources
PubMed1982

Movement of necrotic wavefront after coronary artery occlusion in rabbit.

Movement of the necrotic wavefront after coronary artery occlusion (CAO) was defined in rabbits by comparing transient CAO (15, 30, or 60 min) and reperfusion to permanent CAO (n = 5-9/group). At 24 h after CAO the area of necrosis was determined by nitro-blue tetrazolium staining, and the transmural and circumferential extent of necrosis was evaluated at four levels from ligation to apex. Infarct size after permanent CAO for 24 h was 27 +/- 2 (SE) % of the left ventricle. Reperfusion at 60, 30, or 15 min after CAO reduced the infarct size to 24 +/- 3 (P = NS vs. 24 h), 14 +/- 2, and 8 +/- 1% (P less than 0.05 vs. 60 min), respectively. Reperfusion at 15 and 30 min after CAO decreased transmural extent by 49 and 38% (P less than 0.001 vs. 24 h), whereas the circumferential extent was reduced by only 10 and 12%, respectively (P = NS). After 60 min of CAO, reperfusion did not significantly reduce either transmural or circumferential necrosis. Thus early reperfusion reduced infarct size by converting potentially transmural infarcts into subendocardial infarcts but did not significantly reduce the lateral or circumferential extent of necrosis.

Animals↗
PubMed1982

Coronary arterial vasodilator effect of ibuprofen.

The effect of ibuprofen, a nonsteroidal anti-inflammatory agent, on coronary vascular resistance in isolated perfused rabbit heart was studied. Ibuprofen had coronary arterial vasodilatory activity. An arterial concentration of 50 microgram/ml produced a half-maximal coronary vasodilator response. An ibuprofen concentration of 140 microgram/ml produced a coronary vasodilation, equal to that caused by hypoxia. A level of 280 microgram/ml depressed contractile function. The change in coronary vascular resistance did not appear to be physiologic autoregulation of coronary tone because determinants of myocardial oxygen demand were not significantly affected and myocardial oxidative metabolism was not significantly impaired, as reflected by myocardial lactate extraction, which was not significantly affected during the ibuprofen-induced coronary dilation. These results suggest a direct effect of ibuprofen on coronary vascular resistance.

Adenosine↗
PubMed1982

[Osmolarity parameter and kidney function of polytraumatized intensive care patients].

Improved possibilities in prediction of renal failure after polytrauma would possibly improve the survival rate of this severe posttraumatic complication. Our clinical investigation was carried out in 27 patients suffering from severe trauma. We intended to achieve early recognition of acute renal failure by osmolality measurements after polytrauma. Thus we investigated the daily concentration of blood urea, serum and urine creatinine, daily urine output, creatinine clearance, plasma and urine osmolality and the serum colloid osmotic pressure. Additional to important informations for fluid and electrolyte replacement the follow-up of osmolality changes in plasma and urine proved general and renal prognostic value. Early and clear decreases in urine-plasma ration, osmolar clearance and negative free water clearance were found in case of later reduction of renal function and acute renal failure. Consequently we advise regular osmolality measurements in the postoperative management of the polytraumatic patient.

Acute Kidney Injury↗
PubMed1981

Comparison of acute alterations in left ventricular relaxation and diastolic chamber stiffness induced by hypoxia and ischemia. Role of myocardial oxygen supply-demand imbalance.

To clarify conflicting reports concerning the effects of ischemia on left ventricular chamber stiffness, we compared the effects of hypoxia at constant coronary perfusion with those of global ischemia on left ventricular diastolic chamber stiffness using isolated, perfused rabbit hearts in which the left ventricle was contracting isovolumically. Since chamber volume was held constant, increases in left ventricular end diastolic pressure (LVEDP) reflected increases in chamber stiffness. At a control coronary flow rate (30 ml/min), 2 min of hypoxia and pacing tachycardia (4.0 Hz) produced major increases in postpacing LVEDP (10+/-1 to 24+/-3 mm Hg, P < 0.01) and the relaxation time constant, T, (40+/-4 to 224+/-37 ms, P < 0.001), while percent lactate extraction ratio became negative (+ 18+/-2 to -48+/-15%, P < 0.001). Coronary perfusion pressure decreased (72+/-5 to 52+/-3 mm Hg, P < 0.01), and since coronary flow was held constant, the fall in coronary perfusion pressure reflected coronary dilation and a decrease in coronary vascular resistance. Following an average of 71+/-6s reoxygenation and initial heart rate (2.0 Hz), LVEDP and relaxation time constant T returned to control. Hypoxia alone (without pacing tachycardia) produced similar although less marked changes (LVEDP, 10+/-1 to 20+/-3 mm Hg; and T, 32+/-3 to 119+/-22 ms; P < 0.01 for both) and there was a strong correlation between LVEDP and T (r = 0.82, P < 0.001). When a similar degree of coronary vasodilatation was induced with adenosine, no change in LVEDP occurred, indicating that the increase in end diastolic pressure observed during hypoxia was not secondary to vascular engorgement, but due to an acute effect of hypoxia on the diastolic behavior of the ventricular myocardium. In contrast, global ischemia produced by low coronary flow (12-15 ml/min) resulted in a decrease in LVEDP, as well as a marked fall in left ventricular systolic pressure. In 14 global ischemia experiments, pacing tachycardia led to a further decline in left ventricular systolic pressure, and no increase was noted in postpacing LVEDP. Changes in lactate extraction ratio were much smaller in magnitude than with hypoxia and constant coronary perfusion. In two experiments (one at normal coronary flow and one at 15 ml/min), left ventricular systolic pressure did not change markedly from control when tachycardia was superimposed, and postpacing LVEDP showed a marked rise (to > 25 mm Hg), which gradually recovered over 1-2 min at the control heart rate. From these results, we conclude that left ventricular chamber stiffness increases when myocardial O(2) demand exceeds supply. This change is usually masked in ischemic (reduced coronary flow) preparations, perhaps because of reduced turgor of the coronary vascular bed, marked reductions in systolic work (and therefore myocardial O(2) requirements), and local accumulation of hydrogen ion and metabolites following acute severe reduction of coronary flow. The increased chamber stiffness during hypoxia is accompanied by marked slowing of relaxation, with increased diastolic pressure relative to volume persisting throughout diastole.

Animals↗
PubMed1980

An isolated, blood-perfused, feline heart preparation for evaluating pharmacological interventions during myocardial ischemia.

A preparation is described in which feline hearts were perfused with arterial blood drawn from a blood-donor cat. Ventricular function was measured with a fluid-filled latex balloon within the left ventricle. Left ventricular developed pressure, maximum left ventricular dP/dt, ventricular compliance, and coronary blood flow changed only slightly during two hours of perfusion at a constant pressure of 75 mmHg. Water, sodium, potassium, and calcium contents, and creatine kinase activity of isolated hearts did not differ from the values obtained for intact hearts from the blood-donor cats. Isolated hearts subjected to 40 minutes of normothermic global ischemia with one hour of reperfusion exhibited significantly decreased contractility, but no change in ventricular compliance. Myocardial water and sodium contents were increased after 40 minutes of ischemia and reperfusion. Hearts subjected to 60 minutes of ischemia with reperfusion exhibited decreases in both contractility and compliance. A prolonged reactive hyperemic response was maintained throughout the hour of reperfusion. Myocardial sodium content increased more than could be accounted for by edema formation; decreases were observed in potassium content and creatine kinase activity while calcium content was increased. The applicability of this model for evaluating the effects of pharmacological interventions on myocardial ischemic injury are discussed.

Animals↗
PubMed1980

Protective effects of dimethyl-propranolol (UM-272) during global ischemia of isolated feline hearts.

This study was designed to determine the effects of dimethyl-propranolol (UM-272) on myocardial injury after global ischemia of isolated feline hearts. Untreated ischemic hearts developed contracture, resulting in a leftward shift of the diastolic pressure-volume curve. Active pressure development in perfused ischemic hearts was significantly depressed compared to preischemic values. Untreated ischemic hearts exhibited increased water, sodium (Na+) and calcium (Ca++) contents and depletion of potassium (K+). The Ca++ accumulating ability of cardiac microsomal fractions isolated from untreated ischemic hearts was severely depressed. In hearts treated with UM-272, active ventricular pressure development after ischemia declined to the same extent as in untreated hearts, but ischemic contracture in treated hearts was delayed and completely reversed by reperfusion. Treated hearts were not depleted of K+ and changes in Na+ and Ca++ were significantly less than in untreated hearts. Microsomal Ca++ accumulation in the treated group was well preserved compared to that in untreated hearts. Experiments in which hearts were paced during UM-272 administration suggest that decreased myocardial oxygen consumption contributes substantially to the protective effects of UM-272. In addition, UM-272 may protect the ischemic heart through direct effects on myocardial Ca++ regulating mechanisms.

Animals↗
PubMed1977

Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog.

Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left anterior descending artery (LAD). Infarct size was determined by dehydrogenase staining after 24 or 96 hours. Heart slices were incubated with nitro-blue tetrazolium and nonstaining infarcted tissue was dissected and weighed. Myocardial depletion of creatine phosphokinase activity (CPK) and lactate dehydrogenase activity (LDH) were determined 24 hours after temporary LCX occlusion. When measured after 24 hours, methylprednisolone sodium succinate treatment did not reduce infarct size or decrease enzyme loss. After temporary LCX occlusion infarct size was 30.4 +/- 3.6% of left ventricular weight in control dogs and 30.0 +/- 2.3% in treated dogs. No significant difference in infarct size was observed in hearts examined 24 or 96 hours after myocardial infarction. After permanent LAD occlusion, infarct size in control dogs was 39.2 +/- 1.6% of left ventricular weight and 33.7 +/- 3.5% in treated dogs. CPK activity in the LCX area decreased by 26.5 +/- 7% in controls and by 28.1% +/- 7% in treated dogs. Treated dogs sustained a significantly greater fall in arterial blood pressure after LCX occlusion than did controls. During LCX occlusion and upon reperfusion, methylprednisolone sodium succinate treated dogs exhibited a significantly greater number of premature ventricular beats. Since infarct size and enzyme depletion were not reduced when measured after 24 hours, methylprednisolone sodium succinate treatment does not appear to have enhanced myocardial cell viability.

Animals↗
PubMed1977

Inactivation of glucocorticoid receptors in cell-free preparations of rat liver.

We have examined the rates of inactivation of glucocorticoid receptors in cell-free preparations from several rat tissues. The t1/2 of inactivation of the glucocorticoid-binding ability of thymus, heart, and kidney cytosols (37,000 X g supernatants) ranges from 2 to 4 hr at 0 degrees, whereas that of liver is much slower (15 to 25 hr). The rate of inactivation of the glucocorticoid-binding capacity of soluble preparations from liver varies roughly according to the g force at which they have been centrifuged. The 100,000 X g supernatant. The ability of the particulate enzyme to inactivate glucocorticoid receptors at 0 degrees is not affected by protease inhibitors but is inhibited by fluoride and molybdate. The rapid inactivation of unbound glucocorticoid receptors that occurs in a high-speed (100,000 X g) supernatant preparation from rat liver at 25 degrees can be completely inhibited by molybdate. These observations suggest that the inactivation of glucocorticoid receptors observed in cell-free liver preparations in vitro is due to a nonproteolytic enzymatic function.

Animals↗
PubMedDate not supplied

Methylprednisolone sodium succinate treatment in global ischemia of the cat isolated heart.

Effects of methylprednisolone were studied on isolated, blood-perfused cat hearts subjected to 1 hr of normothermic ischemic arrest. Untreated hearts sustained decreases in peak ventricular pressure pulse, dP/dt, and ventricular compliance. Ischemic hearts also became edematous, gained sodium, and lost potassium and creatine kinase enzyme activity. Steroid treatment did not significantly alter any of these ischemia-induced changes. Methylprednisolone treatment did increase resting coronary flow and also increased the hyperemic response after reperfusion. These results, in isolated hearts, provide no evidence that steroid treatment exerts a direct protective effect on the globally ischemic myocardium.

Animals↗
PubMedDate not supplied

A system for continuous long-term measurement of respiratory gas exchange in ventilated patients.

A system for continuous long-term measurement of respiratory gas exchange in ventilated patients is presented. The method is noninvasive and may be applied in a clinical setting over a period of several days without adversely affecting the patient's wellbeing. The set-up was designed exclusively as a research tool. It registers oxygen uptake and CO2 elimination at 5 min intervals; breath-averaged measurements are carried out every 30 s. Expired minute volume is measured with a pneumotachograph equipped with an automatic drift compensation. A newly developed gas mixer insures that the inspiratory oxygen concentration remains constant. Expired gases are analysed for O2 and CO2 concentrations by mass spectrometer. The effect of the compressible gas volume is eliminated by segregating the inspiratory gas from the expired gas. The basic accuracy of measurement of the method is +/- 2.5% for oxygen uptake and +/- 2.0% for CO2 elimination. This result is based on a comparison of the individual components of the system with standard methods. The system's time constant (t90) for changes in O2 and CO2 concentrations is about 50 s. Based on the results of a case study, we will discuss oxygen uptake, CO2 elimination and the oxygen uptake profile of a patient measured over a period of seven days.

Adult↗