Search PubMed⌕ Search

Biomedical subjects

G A Klassen

Publications and source records attributed to G A Klassen.

At least 55 records · Page 3Linked to original sources
PubMed1986

Autonomic nervous system regulation of epicardial coronary vein systolic and diastolic blood velocity as measured by a laser Doppler velocimeter.

The velocity of blood in a major epicardial coronary vein accompanying the left anterior descending coronary artery of dogs was measured by means of a 140-micron fiber optic probe connected to a laser Doppler velocimeter. Right atrial pressure, left ventricular intramyocardial and cavity pressures, aortic pressure, as well as peripheral and central coronary venous pressures were compared with the velocity of blood measured in the epicardial coronary vein midway between the sites of the catheters measuring proximal and distal coronary vein pressures. During control conditions, coronary vein velocity was 14-18 cm/s during systole and 1.0-2.1 cm/s during diastole. Right stellate ganglion stimulation, norepinephrine or isoproterenol increased diastolic coronary vein velocity significantly, whereas left stellate ganglion stimulation did not. Average peak systolic velocity was not affected by these interventions. During these positive inotropic interventions, the peak coronary vein velocity usually occurred later in the cardiac cycle than during control conditions. Positive inotropic interventions appeared to decrease coronary vein velocity during systole and increase it during diastole. Left vagosympathetic trunk stimulation decreased diastolic but not systolic coronary vein velocity and usually caused peak coronary vein velocity to occur earlier in the cardiac cycle than during control states. Changes induced by vagosympathetic trunk stimulation usually occurred within one cardiac cycle. It is concluded that coronary vein blood velocity can be influenced by the autonomic nervous system.

Animals↗
PubMed1985

Model of calcium movements in the mammalian myocardium: interval-strength relationship.

A model is proposed to describe the interval-strength relationship in mammalian cardiac muscle in terms of "discrete" calcium movements associated with each cycle. The sarcoplasmic reticulum is assumed to be comprised of three functional sub-compartments: (1) The "main calcium store" which contains most of the calcium (predominantly bound) and is considered, due to its large buffering capacity, to account for the "long-term memory" lasting 7-10 beats. (2) The "releasable terminal" which contains the calcium readily available for release (all or most of it free) and accounts for the "short-term memory" which affects the subsequent beat. (3) The longitudinal network of the SR recirculating the myofibrillar calcium to the "main calcium store". The total content of calcium in the main store is determined by the transsarcolemmal influx and efflux. While influx occurs only during depolarization, efflux occurs during the whole cardiac cycle. The amount of free calcium in the main store is determined by an equilibrium equation. The release of calcium from the "releasable terminal" is governed by a "concentration-dependent" mechanism. This implies that when the concentration in the "releasable terminal" increases, the fraction released increases and the residual calcium left for the subsequent contraction decreases. The model predicts the following interval-strength relationships: steady state peak tension; changes from one steady rate to another; restitution curves; post-stimulation potentiation; paired stimulation; premature beats; post-extrasystolic potentiation following interpolated, basal or complimentary interval.

Animals↗
PubMed1984

The dynamics of the coronary venous system in the dog.

The coronary vascular system is characterised by a small blood-volume, high resistance arterial system, in which flow is primarily diastolic, a capillary-venule exchange system and a large blood volume, low resistance venous system with predominantly systolic flow. In order to understand the venous component we measured intramyocardial pressure (IMP), peripheral (PVP) and central (CVP) coronary venous pressure, as well as phasic coronary sinus outflow. Based on the experimental data, a model is proposed to describe the hemodynamics of the coronary venous system. This model consists of an intramyocardial vascular storage region into which the arterial blood flows during diastole. During systole, the pressure in the storage vessels increases, pushing the peripheral and epicardial venous system. Blocking the inflow tends to empty the 'storage' and the peripheral regions, reducing venous pressures. Occlusion of the outflow increases the blood volume in these regions, elevating venous pressures. The observations of peak (IMP-PVP) vs peak venous flow during vagal, right abd left stellate stimulation conform satisfactorily with the model.

Animals↗
PubMed1984

QT interval variability on the body surface.

To assess the effects of measurement methodology on QT determinations and to define the spectrum of QT values, including interlead variability, on the body surface, we measured QT in each of 120 simultaneously-recorded, signal-averaged ECG leads in 10 normal subjects and 14 patients with QT prolongation (lead II QTc greater than 440). Two separate, but related, methods of QT measurement were utilized. Method A was a relatively conventional technique in which ST-T offset was defined as the time instant of return of the T wave to a P-P baseline, or as the point of U-on-T intersection. Method B was a more rigorous method, which defined ST-T offset in a similar manner, and in addition discarded from analysis all QT values from leads with monophasic ST-T waveform in which the QT values were greater than the longest QT from leads with definite U waves. Method B was utilized to minimize factitious prolongation of QT by inapparent U-on-T. By both methods the mean body surface QTc values were significantly greater (p less than 0.001) in the patient group (482 +/- 65 [S.D.] msec, method A; 447 +/- 43 msec, method B), than in the normal subject group (399 +/- 14 msec, method A; 396 +/- 12, method B). Interlead QTc variability (difference between the longest and shortest QT) was considerable with both methods and in both study groups. Expressed as percent of average body surface values, the mean interlead QTc variability in normal subjects averaged 22 percent with method A and 19 percent with method B; in the patient group, however, it averaged 32 percent with method A and only 18 percent with method B. In absolute terms, the mean variability in the patient group with method A (155 +/- 62 msec) was significantly greater (p less than 0.001) than that of the normal group (89 +/- 33 msec); with method B, interlead variability was the same (p = NS) in the normal (76 +/0 27 msec) and patient groups (80 +/- 44 msec). This latter finding suggests the possibility that the repolarization abnormality in patients with QT prolongation may occur relatively uniformly throughout the ventricular myocardium. Thus, measurement techniques are important in multiple-lead QT determinations. Although reduced by techniques designed to minimize factitious QT prolongation, interlead QT variation is considerable over the torso surface, in both normal subjects and patients with repolarization abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Pressure and flow in epicardial coronary veins of the dog heart: responses to positive inotropism.

Peripheral coronary venous pressures and coronary sinus venous flow were measured in the canine heart as well as intramyocardial, intraventricular, aortic, and coronary artery pressures. Maximum coronary venous flow occurred after maximum intramyocardial and peripheral coronary artery pressures had been reached. Maximum venous flow occurred at or following the maximum peripheral coronary vein pressure. Positive inotropic changes induced by stimulation of the right or left stellate ganglia or infusing isoproterenol, norepinephrine, or dobutamine significantly increased intramyocardial pressure, systolic epicardial coronary venous pressure, and systolic coronary venous flow. Mean coronary sinus flow was augmented by all interventions except isoproterenol. The estimated systolic vein resistance was slightly increased following right stellate ganglion stimulation, but not following left stellate ganglion stimulation, isoproterenol, or dobutamine. Norepinephrine reduced this parameter minimally. These data indicate that coronary veins respond differently to a variety of different positive inotropic interventions.

Animals↗
PubMed1984

Hemodynamics of coronary artery stenosis.

A model is proposed to study the hemodynamics of various types of coronary stenosis. The model coronary artery is assumed to be an elastic tapered tube. A progressive degree of concentric and eccentric stenoses are studied. Measured pulsatile coronary pressure, flow, and intramyocardial pressure are used as input data to calculate the pressure and flow velocities at different locations of the artery. The simulation yields results that agree well with published data in dog experiments, and those from human stenotic coronary arteries. The present model shows that in a cardiac cycle, the overall hydraulic resistance owing to a specific stenosis tends to be flow independent at low flow rate but increases linearly with flow at higher coronary flow. This flow independent resistance increases with progressive stenosis. At low flow, the mean coronary flow in a cardiac cycle is relatively constant with stenoses up to 80%, but decreases dramatically with further increase in the degree of narrowing. At high resting flow rate, this mean flow is markedly reduced at much smaller degrees of constriction. The simulated pressure velocity relation of poststenotic dilatation indicates an additional pressure loss at the distal end of the stenosis, but the calculated resistance to flow is actually lessened. While stenosis length increases pressure loss and resistance to flow, its effect on mean flow appears disproportionally insignificant. Eccentric lesions appear to be more detrimental than concentric ones as they produce additional pressure loss and greater resistance across the coronary artery lesion.

Animals↗
PubMed1984

Coronary venous pressure and flow: effects of vagal stimulation, aortic occlusion, and vasodilators.

Coronary venous pressure and coronary sinus flow in the canine heart were compared with intramyocardial, intraventricular, aortic, and coronary artery pressures. Stimulation of the thoracic vagus augmented coronary venous pressure, mean venous flow per systole, and coronary venous systolic resistance, but decreased the mean venous flow. Partial occlusion of the aorta augmented coronary venous pressure and coronary venous flow, while systolic coronary venous resistance remained unchanged. Adenosine increased peripheral and central coronary venous pressure and venous flow; it reduced peripheral coronary artery pressure. Adenosine augmented flow per systole and reduced venous resistance more than the other interventions. Dipyridamole decreased left ventricular, aortic, and central coronary artery systolic pressures and systolic venous resistance. It increased the venous flow, mean flow per systole, and coronary venous pressure, even though intramyocardial pressure remained unchanged. Nitroglycerine elevated coronary venous pressure and flow, as well as venous flow per systole, even though it decreased left ventricular, aortic, and central coronary artery pressures. Nitroglycerine significantly decreased coronary venous resistance. It is concluded that coronary venous resistance may be an important resistive component to consider when the total coronary circulation is studied.

Adenosine↗
PubMed1984

Flow and pressure responses of coronary arteries and veins to vasodilating agents.

The response to a bolus injection of nitroglycerine, adenosine, nifedipine, and dipyridamole of the canine systemic as well as coronary artery and venous circulations was observed and contrasted. Particular attention was paid to the time of change of pressures and flows and to changes in oxygen extraction by the myocardium induced by the pharmacological agents. The dosages of vasodilators used were selected so that no significant change in aortic blood flow occurred. Nitroglycerine and adenosine caused a rapid and similar vasodilation in the coronary circulation. Oxygen extraction was not altered by nitroglycerine, but was decreased by adenosine. The onset time of the vasodilation produced by either nifedipine or dipyridamole was similar, but the time to peak action was much slower for dipyridamole. As well, the effect of dipyridamole on intramyocardial and left intraventricular pressures was more delayed than that following the injection of the other agents. Oxygen extraction was reduced by nifedipine and dipyridamole. These results indicate that pharmacological vasodilating agents can affect coronary arteries, coronary veins, and myocardial oxygen extraction differently.

Adenosine↗
PubMed1983

Canine coronary venous pressures: responses to positive inotropism and vasodilation.

The epicardial coronary venous pressure in 16 dogs was compared with coronary arterial pressure as well as aortic, intraventricular, and intramyocardial pressures. Partial aortic occlusion augmented intraventricular (IVP), intramyocardial (IMP), aortic (AP), and coronary arterial pressures. Peripheral coronary venous pressure was also elevated. Dobutamine significantly augmented IVP and IMP but not aortic or central coronary artery pressures; this agent significantly elevated coronary venous systolic pressure (28/8 to 84/12 mmHg) (1 mmHg = 133.322 Pa). Nitroglycerine decreased IVP, IMP, and AP significantly. Central coronary arterial pressure also fell significantly, but coronary venous pressures remained unchanged. In contrast dipyridamole resulted in no change in IVP, IMP, AP, or coronary arterial systolic pressures; however, the peripheral coronary venous systolic pressure became significantly elevated. Thus the two vasodilators, nitroglycerine and dipyridamole, had different effects upon coronary venous pressure. These data reinforce the recently expressed view that coronary veins behave in a complex fashion and further suggest that their pressures are dependent upon coronary artery pressure, intramyocardial pressure, and coronary venous tone.

Acetylcholine↗
PubMed1982

Epicardial coronary venous pressures: autonomic responses.

Intramyocardial, ventricular, aortic, and central and peripheral coronary artery as well as peripheral and central coronary venous pressures were measured simultaneously in dog hearts. A gradient of coronary vascular pressures was detected and quantitated. Stellate stimulation increased all pressures. Isoproterenol induced outflow tract obstructions so that aortic and central coronary artery pressures were unchanged while the other pressures increased. Vagal stimulation dissociated the intramyocardial venous pressure relationship in as much as arterial pressures decreased while epicardial coronary venous pressure was increased. These data suggest that coronary venous pressure in response to sympathetic stimulation increases as intramyocardial pressure increases. However, vagal stimulation permits a dissociation of these effects suggesting that coronary venous pressure regulation is complex.

Animals↗
PubMed1982

Coronary artery compliance in the dog.

Measurement of left anterior descending coronary arterial pressure, phasic coronary flow, and intramyocardial pressure in an open-chest dog provided data, which when entered into the computer model of the coronary circulation, permitted calculation of coronary artery compliance and resistance during systole and diastole. Resting in vivo compliance averaged 0.21 x 10(-3) mL/mmHg (1 mmHg = 133.322 Pa) while systolic resistance averaged 4.05 mmHg X min-1 X mL-1 and during diastole 2.06 mmHg X min-1 X mL-1. Left stellate ganglion stimulation or vasodilation caused minimal changes in compliance but glutaraldehyde applied to arterial wall caused a decrease in compliance. Sympathetic stimulation and vasodilation decreased both diastolic and systolic resistance. Transmural distribution of coronary flow was not significantly altered by the experimental changes in compliance and resistance.

Animals↗
PubMed1981

Epicardial coronary venous pressure.

Coronary venous pressure was measured in two sites in the canine heart. Central coronary venous pressure was that pressure recorded by a catheter in an epicardial coronary vein directed antegrade towards the coronary sinus. This pressure was 6 +/- 1/0.2 +/- 0.6 mmHg (1 mmHg = 133.322 Pa). Peripheral coronary venous pressure was recorded by a catheter in an epicardial vein which was directed towards the apex. It was 27 +/- 5/8 +/- 2 mmHg. Simultaneous measurement of peripheral coronary artery and vein pressures demonstrated similar pressure wave forms with peak pressures during systole. Peripheral coronary venous pressure was similar if measured from a side branch leading to the major epicardial veins or via a catheter placed retrograde in a major epicardial vein. Thus artifact of measurement caused by antegrade catheter placement was negligible. During norepinephrine administration, venous pressures were significantly increased. These data suggest that coronary venous pressures are higher than is generally assumed and that intramyocardial pressure has an important effect upon coronary venous pressure.

Animals↗
PubMed1981

Intravenous propranolol therapy for acute myocardial infarction in man: hemodynamic and serial creatine kinase assessment.

Propranolol was administered intravenously to 12 patients with presumed acute myocardial infarction in the attempt to limit infarct size. Patients' conditions were uncomplicated (heart rate greater than or equal to 60/min, systolic blood pressure greater than or equal to 100 mm Hg, mean pulmonary capillary wedge pressure mean [PCWP] less than or equal to 20 mm mercury). The aim was to produce beta-blockade that was early, complete, and continuous. Target loading dose was achieved in seven patients and full maintenance was achieved in six patients. The remaining patients received smaller loading or maintenance doses or both because of varying degrees of bradycardia, hypotension, or elevated mean PCWP. Myocardial CK release in the propranolol group was 2651 mIU/ml +/- 843 (mean +/- SE, n = 12) vs 2987 mIU/ml +/- 422 in 21 comparison patients, a difference not statistically significant. The time to CK plateau (completion of infarction) was related to total CK release in both propranolol and comparison patients.

Adult↗
PubMed1980

Effect of acute sympathectomy by epidural anesthesia on the canine coronary circulation.

The effects of reversible sympathetic neural blockade of the canine myocardium under control conditions and in the presence of decreased coronary blood flow and after myocardial infarction were investigated in 17 dogs. A multiple-microsphere technique was used to measure distribution of blood flow in the myocardium. Epidural blockade was associated with the following changes in the ratio of endocardial to epicardial blood flow: under control conditions, no change; after 50 per cent decrease in coronary flow, 18 per cent increase in endocardial/epicardial ratio; after myocardial infarction at unrestricted coronary flow, 43 per cent ratio increase; after myocardial infarction and 50 per cent decrease in coronary flow, 76 per cent increase of endocardial/epicardial ratio. These effects appear to be independent of systemic factors, and may result from alterations in tone of transmural resistance vessels. In addition, cervicothoracic epidural blockade resulted in a decrease in systemic pressure and an increase in coronary vascular resistance as myocardial oxygen demand decreased. When systemic pressure was restored these effects were abolished. In the presence of myocardial infarction, epidural blockade had less effect on systemic pressure and left ventricular filling pressure was decreased. With decreased coronary flow, sympathetic blockade redistributed coronary blood flow, favoring sympathetic blockade redistributed coronary blood flow, favoring the endocardium in both the normal and the infarcted heart.

Anesthesia, Epidural↗
PubMed1980

Effects of oral perhexiline on canine myocardial flow distribution.

Perhexiline maleate at a dose of 400 mg three times daily for 2 days administered to normal dogs altered the relative regional transmural resistance so that during reduced coronary flow the endocardium:epicardium (endo:epi) ratio is increased. In the presence of acute myocardial infarction heart rate was significantly lower and the endo:epi ratio of perfused areas was increased when coronary flow was normal. A linear relationship was observed between the endo:epi ratio and the concentration of perhexiline in plasma, and its monohydroxyl metabolite in plasma. The results suggest that the mechanism of action of the drug is due to redistribution of a limited coronary flow.

Animals↗