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Biomedical subjects

M Giesler

Publications and source records attributed to M Giesler.

28 records · Page 2Linked to original sources
PubMed1993

Color Doppler echocardiographic determination of mitral regurgitant flow from the proximal velocity profile of the flow convergence region.

Flow rate across an orifice can be determined from color Doppler echocardiographic maps of the flow convergence region proximal to the orifice. Different methods have been developed in vitro. The proximal velocity profile method was prospectively evaluated in patients with mitral regurgitation. Color Doppler echocardiography was performed in 74 patients before cardiac catheterization. The increasing velocities within the flow convergence region were determined in an apical plane on the straight line from the transducer to the leak; thus the proximal velocity profile was established and plotted on a nomogram. Instantaneous regurgitant flow rate was derived from the position of the resulting curve in relation to the nomogram's reference curves, which were derived from in vitro measurements. Regurgitant stroke volume was calculated as regurgitant flow rate.regurgitant velocity-time integral/regurgitant peak velocity, using additional continuous-wave Doppler. The 55 patients with angiographic regurgitation had a close association between regurgitant flow rate (0 to 600 ml/s) and angiographic grade (Spearman's rank correlation coefficient = 0.91; p < 0.0001). Regurgitant flow rate did not overlap between grades < or = 2+, 3+ and 4+. In 16 patients, regurgitant stroke volume by echocardiography correlated well with that by the angiography/Fick method (r = 0.88; SEE = 17.1 ml), with a regression line close to identity (y = 0.89x + 12.7 ml). The proximal velocity profile method enables determination of mitral regurgitant flow and estimation of regurgitant volume.

Blood Flow Velocity↗
PubMed1990

Biochemical manifestations of oxygen toxicity in the newborn lamb.

The purpose of this project was to study the role of lipid peroxidation in oxygen-induced lung injury in the newborn lamb. It was our hypothesis that injury to the microvascular bed of the lung by oxygen would coincide with a burst of peroxidative activity and would be accompanied by an increased rate of excretion of ethane and pentane in expired gas. We measured vascular pressures, the rate of lung lymph flow and concentrations of ethane and pentane in exhaled gas in 10 newborn lambs that breathed greater than 95% oxygen continuously. Our marker for oxygen-induced lung injury was an increase in the permeability of the microvascular bed of the lung to protein (an increase in the rate of lung lymph flow accompanied by an increase in the protein concentration in lymph). Although all 10 lambs demonstrated an abrupt increase in microvascular permeability to protein within 48 to 96 h of exposure to greater than 95% oxygen, the rates of ethane and pentane excretion remained unchanged throughout the entire experimental period. Lung tissue concentrations of glutathione decreased by 40% in the oxygen-exposed lambs and the concentrations of glutathione disulfide increased 85% relative to air-breathing controls. Activities of glutathione reductase and superoxide dismutase were lower in the lungs of the oxygen-exposed lambs than in controls, whereas the activities of glutathione peroxidase and catalase were not changed. We conclude that, in the lamb, changes in the rates of excretion of ethane and pentane do not correlate with the timing of injury to the microvascular bed of the lung.

Animals↗
PubMed1986

Effects of antidotes on soman-induced brain changes.

Rats were pretreated with either diazepam, atropine or benactyzine 10 min prior to soman injection. Local cerebral glucose use (LCGU) was determined during the seizure phase (15 min post soman) or pathology phase (72 h post soman). Diazepam and benactyzine pretreatment prevented convulsive activity, whereas atropine pretreatment only reduced the duration of convulsive activity after soman exposure. Each pretreatment agent had a unique impact on LCGU pattern during the seizure phase. During the pathology phase, the marked reduction in LCGU and the conspicuous brain damage associated with soman-induced seizures was minimized by all three pretreatments.

Animals↗
PubMed1985

Changes in local cerebral glucose utilization induced by convulsants.

With the six convulsants studied (Soman, intrahippocampal penicillin, bicuculline, pentylenetetrazol, picrotoxin and strychnine), the anatomical distribution of changes in local cerebral glucose utilization was related to the type of seizure observed. Strychnine induced a few very intense motor convulsions during the 2-deoxyglucose experimental period without having a major effect on brain local cerebral glucose utilization, in support of the view that its actions are predominantly in the spinal cord. Pentylenetetrazol and picrotoxin induced intermittent intense seizures and marked increases in local cerebral glucose utilization in the globus pallidus and substantia nigra. Soman, intrahippocampal penicillin and bicuculline all induced persistent status epilepticus associated with increases in local cerebral glucose utilization in many brain areas; those with striking increases in glucose use include: cortical areas, the limbic system, basal ganglia and substantia nigra. The glucose use changes produced by Soman, penicillin and bicuculline greatly exceeded those induced by pentylenetetrazol and picrotoxin. Activation of the substantia nigra and basal ganglia occurred with all centrally mediated convulsions and with status epilepticus there was also marked activation of cortical and limbic structures.

Animals↗
PubMed1985

Effect of outflow pressure on lung lymph flow in unanesthetized sheep.

Studies in anesthetized animals have shown that the flow rate from lung lymphatics (QL) depends on the pressure at the outflow end of the vessels (Po). We tested this in unanesthetized sheep prepared with chronic lung lymph cannula. We measured QL with the lymph cannula held at various heights above the olecranon and calculated Po as the height + QL X cannula resistance. QL decreased with increases in Po (delta QL/delta Po = -8.2 +/- 6.4 microliter X min-1 X cmH2O-1, mean +/- SD). We increased QL by raising left atrial pressure or infusing Ringer solution or Escherichia coli endotoxin and found that QL was even more sensitive to Po (delta QL/delta Po = -32 +/- 22). Cannula resistance caused a 9-70% reduction in QL. Changes in QL caused by increasing Po were not associated with changes in lymph protein concentration for up to 330 min. This indicates that increases in Po shunt lymph away from cannulated vessels but do not substantially effect microvascular filtration rate. The shunted lymph may flow into other vessels or collect in the lung. We conclude that QL does not accurately represent microvascular filtration rate because it depends on the cannula resistance and position at which the investigator chooses to place the cannula.

Animals↗
PubMed1985

Delayed effects of Soman: brain glucose use and pathology.

The [14C]-2-deoxyglucose (2-DG) technique was used to determine the delayed effects of Soman, a potent anticholinesterase inhibitor, on local cerebral glucose utilization (LCGU). Rats were given 100 micrograms/kg of Soman (0.9 LD50; i.m.) or saline and LCGU was assessed 24, 48 or 72 hours later. All Soman injected rats had strong, continuous seizures which persisted for at least one hour. At 24 hours post-Soman there was greater than a 2-fold reduction in LCGU in the frontal cortex, cingulate gyrus, anterior and ventral thalamic nuclei, lateral habenula, parietal cortex, lateral geniculate and medial geniculate. On the other hand, the hippocampal structures did not show a significant decrease in LCGU until 48 hours post-Soman exposure. Conspicuous neuropathology was obvious in a number of structures upon inspection of the frozen brain sections, hematoxylin and eosin stained sections or the 2-DG autoradiograms, 24 to 72 hours post soman-exposure. Damage was most severe in the piriform cortex and amygdala. The lateral and ventral thalamic nuclei, many cortical regions and variable segments of the hippocampus were also consistently damaged. We suggest that energy deprivation, inadequate perfusion and/or inadequate calcium sequestration may contribute to the delayed effects following Soman-induced seizures. The 2-deoxyglucose method provides information about the dynamic process of cerebral glucose utilization and serves as a "window" for identifying neuroanatomical structures affected by neurotoxins.

Animals↗
PubMed1983

Two dilatory mechanisms of anti-anginal drugs on epicardial coronary arteries in vivo: indirect, flow-dependent, endothelium-mediated dilation and direct smooth muscle relaxation.

Potential mechanisms of antianginal drugs involve preload and afterload reduction and a dilation of large conduit coronary arteries without a substantial concomitant dilation of the coronary resistance vessels. We analyzed the dilatory mechanism. It consists of two independent components: a direct effect on the arterial smooth muscle and an indirect, endothelium-mediated, shear-stress-dependent effect on the arterial vasculature. Therefore, we tested the relative contribution of these two components in the dilatory response of large coronaries to various antianginal drugs. In chronically instrumented dogs, the outer diameters and the flow in two coronary branches (left circumflex and descending) were registered continuously. A pneumatic occluder implanted distally to the site of the diameter measurements was used in one branch to control flow rates or to maintain constant flow, independent of arteriolar dilation. Increments in flow of more than 100% were elicited by i.v. injections of adenosine, dipyridamole, nifedipine, diltiazem, verapamil, nitroglycerin, ISDN, and molsidomine. All these agents induced a slowly developing dilation of the epicardial coronary arteries (by more than 100 microns), which reached its maximum 90 s after the onset of the increase in flow (while arterial pressure fell). When flow in one branch was experimentally kept constant, the epicardial dilation by adenosine and dipyridamole was completely offset, while it remained unaffected in the control branch with unrestricted flow. Thus, the dilation of the coronary artery by these two drugs is based on the indirect component, caused by the flow-dependent mechanism, in contrast to nitroglycerin-, molsidomine-, and ISDN-induced dilations, which were not affected at all by experimentally limiting the flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMedDate not supplied

Flow-dependent, endothelium-mediated dilation of epicardial coronary arteries in conscious dogs: effects of cyclooxygenase inhibition.

Endothelial damage or removal abolishes the dilation of epicardial coronary arteries induced by increments in flow through these arteries in vitro. Therefore, we tested whether or not the release of a cyclooxygenase product from endothelial cells in vivo is the mechanism of this flow-dependent dilation. In eight conscious dogs, instrumented to register the external diameter of two epicardial branches--anterior descending and circumflex--of the left coronary artery, increments in coronary flow increased and reductions in coronary flow decreased the diameter of the left circumflex epicardial artery by 182 +/- 11 micron/100% change in flow. When mean coronary flow in one epicardial branch was kept constant by a distal, flow-limiting stenosis during the application of flow-augmenting stimuli (temporal coronary occlusion or 80-400 micrograms/kg adenosine i.v.), no dilation of this artery was observed. Cyclooxygenase inhibition (suppressing the bradykinin-induced elevation of plasma 6-keto-PGF1 alpha) by indomethacin (5 mg/kg) or by diclofenac (10 mg/kg) increased smooth muscle tone in both epicardial arteries, but did not modify the flow-diameter relation (181 +/- 10 and 179 +/- 9 microns/100% change in flow, respectively). It is concluded that a tonic, instantaneous influence of coronary flow on the smooth muscle tone of the epicardial coronary arteries exists in vivo. It is unlikely that prostacyclin or another prostanoid is a mediator of this endothelium-mediated influence of flow on smooth muscle tone.

6-Ketoprostaglandin F1 alpha↗