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Biomedical subjects

G A Klassen

Publications and source records attributed to G A Klassen.

At least 73 records · Page 4Linked to original sources
PubMed1979

Autoimmune myocarditis: a clinical entity.

In a case of myocarditis electron microscopic and immunoflourescent studies of a transmural myocardial biopsy specimen indicated an autoimmune process. Extensive inflammatory cell infiltration, immunoglobulin and complement deposition along the sarcolemma and in the interstitium, and capillary endothelial injury were found. After a short course of immunosuppressive therapy the inflammatory process was replaced by collagenous scarring and lymphocytic depletion; the blood vessels were then normal. Earlier therapy in such cases may be lifesaving.

Adult↗
PubMed1979

The effect of myocardial force on coronary transmural flow distribution.

The role of myocardial force as a determinant of transmural coronary flow distribution was examined in the presence and absence of autoregulation by infusing calcium chloride into a segment of the left coronary system. The concentration of calcium used was adequate to increase force but did not alter coronary pressure or endoventricular pressure. No alterations in transmural gradients of flow were observed following increased regional force. These results suggest that increases in regional force are not of importance as a determinant of transmural blood flow.

Adenosine↗
PubMed1978

Redistribution in left ventricular regional flow following acute right ventricular pressure overload.

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.

Animals↗
PubMed1978

Autoregulation of cerebral blood flow during early experimental renal hypertension in the conscious dog.

Using the radioactive microsphere technique, cerebral blood flow (CBF) was measured in six conscious dogs before intervention and again on the 3rd-5th days after inducing hypertension by the one-kidney Goldblatt (1-KGH) procedure. Sham-operated controls were also studied. The normal temporal variability of CBF, as well as the precision of the microsphere technique in measuring CBF were also determined in other normal dogs. A left atrial catheter was used for the microsphere injections (15 micrometer diam spheres) and an aortic catheter was used for cardiac output and blood pressure measurements. On the 3rd-5th days after 1-KGH, mean aortic pressure increased from a control value of 94 +/- 7 mmHg to 135 +/- 20 mmHg (P less than 0.005). CBF did not change significantly from the control flow of 57.1 +/- 7.9 ml/100 g per min. Calculated cerebral vascular resistance increased by 47 percent (P less than 0.025) above the control value. Hence, the early phase of experimental renal hypertension is associated with adequate autoregulation of cerebral blood flow.

Animals↗
PubMed1978

Role of autoregulation in spatial and temporal perfusion heterogeneity of canine myocardium.

Spatial heterogeneity, the region-to-region variation in flow at an instant, and temporal heterogeneity, the time variation of flow in a small region of myocardium, were investigated with radioactive labeled microspheres in 111 regions of left ventricular myocardium. The error of the method was measured by simultaneously injecting four differently labeled microspheres (15 +/- 5 (SD) micron). The coefficient of variation (CV) was 6.5 +/- 1.0%. Spatial variation with autoregulation intact was 21.7 +/- 1.4% (CV); with autoregulation abolished and low perfusion pressure, it was 34.3 +/- 3.7%; and with normal perfusion pressure, 30.8 +/- 6.4% (differences not significantly). This degree of variation was similar in the entire left ventricle and its layers. Forces which tended to cause vessel closure (low perfusion pressure, ventricular systolic pressure, and ventricular diastolic pressure) tended to increase CV. Temporal heterogeneity as measured by 20-s intervals between microsphere injections was 11.1 +/- 1.0% (CV) with autoregulation, 9.8 +/- 1.3% (P less than 0.05) with autoregulation abolished, and 8.4 +/- 0.8% (P less than 0.05) when perfusion pressure was restored. A periodicity of flow cycles of 30-90 s was suggested by the data. These results suggest that spatial heterogeneity is less influenced by autoregulation than by hydraulic considerations, whereas temporal heterogeneity is a component of autoregulation.

Animals↗
PubMed1978

Transmural myocardial deformation in the canine left ventricular wall.

A biplane cineradiographic technique was used to measure deformation of the myocardium as indicated by small lead spheres implanted into the anterior left ventricular wall of anesthetized dogs. Deformation was resolved into nine separate components for each of the epicardial, middle, and endocardial layers. The data illustrate the mechanical effect of myocardial fiber orientation and the ability of muscle layers to deform differentially. In order to present an overview of all the results, the implications of the deformation components are discussed first separately and then in a coordinated fashion.

Animals↗
PubMed1977

Myocardial infarction after aortocoronary saphenous vein bypass. Vectorcardiographic study.

Vectorcardiograms and scalar electrocardiograms were recorded in 30 patients before and after aortocoronary saphenous vein bypass surgery to determine whether vectorcardiograms are helpful in making the diagnosis of perioperative transmural infarction. The vectorcardiogram indicated inferior infarction in 2 cases and anterior infarction in 1 case when the diagnosis was not apparent on the electrocardiogram. In the solitary case of anterior infarction diagnosed by the electrocardiogram, anterior infarction was already present on the preoperative vectorcardiogram. The study indicates that the recording of vectorcardiograms before and after aortocoronary bypass surgery facilitates the diagnosis of perioperative anterior and inferior infarction and may reveal perioperative infarction about a previously infarcted area.

Adult↗
PubMed1977

The role of coronary flow and pressure as determinants of myocardial oxygen consumption in the presence or absence of vasomotor tone.

When coronary flow was kept constant and coronary pressure increased by angiotensin or decreased by dipyridamole, myocardial oxygen consumption (MVO2) remained unchanged. When vasomotor tone was abolished by dipyridamole or was intact, changing coronary flow resulted in a change in MVO2 in the same direction as flow; this change in MVO2 was in part the result of a significant alteration in coronary oxygen extraction. These results suggest that coronary flow, but not coronary pressure is an important determinant of MVO2 both in the presence or absence of vasomotor tone.

Angiotensin II↗
PubMed1977

The effect of propranolol on canine myocardial CPK distribution space and rate of disappearance.

Canine myocardial CPK was partially purified and injected into 11 conscious mongreal dogs. From serial serum CPK measurements in each dog, mean Kd was calculated as 0.0047 +/- 0.0009 (+/- SD) min-1. Correlation coefficients indicated that CPK disappearance rate was well described by a single exponential expression. Kd measured on consecutive days in four dogs varied minimally. CPK distribution space ranged from 74 to 134% of plasma volume. Propranolol loading with 0.3 mg/kg or 2 mg/kg, followed by hourly maintenance doses, resulted in increased Kd in eight of ten dogs, mean Kd rising from .0048 min-1 to .0059 min-1 (P less than 0.02). Propranolol appeared to increase plasma volume but had no significant effect on the relationship of CPK distribution space to plasma volume. If the serial CPK technique were used to measure infarct size, using an average Kd, propranolol might produce artifactual reduction of infarct size measuremnt by increasing Kd and possibly by increasing plasma volume. The obligation to assess the effect upon CPK Kd and distribution space of an agent designed to limit infarct size is apparent.

Animals↗
PubMed1976

Demonstration of a new mammalian isoleucine catabolic pathway yielding an Rseries of metabolites.

1. Normal human urine contains small amounts (less than 4 mg/g of creatinine) of 2-ethylhydracrylic acid, formed, we believe, by a previously undisclosed endogenous catabolic pathway for the oxidation of a newly described series of R metabolites of isoleucine. 2. Urinary excretion of 2-ethylhydracrylic acid is variably increased in defects of isoleucine oxidation at distal steps in the catabolic pathway (3-oxoacyl-CoA thiolase deficiency and methylmalonyl-CoA mutase deficiency) and is diminished when proximal steps of the oxidative pathway are blocked as in branched-chain oxo acid decarboxylase deficiency ('maple-syrup-urine' disease). 3. Precursors of R-pathway metabolites [R(-)-2-methylbutyrate and 2-ethylacrylate ] lead to increased 2-ethylhydracrylate excretion in the mammal(rat, rabbit and dog); the corresponding S metabolites [S(+)-2-methylbutyric acid and tiglic acid ], when given in equimolar amounts, have little effect on its excretion, suggesting that little or no interconversion between S and R metabolites occurs in vivo. 4. Studies with 2H-labelled precursors indicate that conversion of R 2-methylbutyrate into 2-ethylhydracrylic acid occurs by a direct pathway (apparently via 2-ethylacrylic acid). 5. The further oxidation of 2-ethylhydracrylic acid to ethylmalonic acid was demonstrated, and may be analogous to S-metabolite oxidation via methyl malonate. 6. Valine metabolites do not interact with the R=isoleucine pathway under the conditions of these experiments in vivo.

Acrylates↗
PubMed1976

Effect of physical training on hemodynamic performance following myocardial infarction: a controlled study.

The effect of physical training on hemodynamic performance was evaluated in a group of patients who had had a myocardial infarction and a group of healthy, age-matched controls. Before training, the patients' mean ventilatory equivalent was significantly less than that of the controls at the lowest workload (300 kpm/min), the mean stroke volume was significantly increased at the highest workload then achieved (600 kpm/min), and the mean arteriovenous oxygen content difference was significantly smaller at the highest workload. The patients had a relative bradycardia before training and there was no significant reduction in mean resting or submaximal heart rate after training. Their mean oxygen uptake was significantly reduced at the lowest exercise workload after training and this response was significantly different from that of the controls after 8 weeks of training. Mean cardiac output during exercise was significantly reduced in the patients after training, but only at the 600-kpm/min workload, the response being blunted at 900 kpm/min; mean stroke volume was also significantly reduced at this workload after training; both these responses were significantly different from those of the controls Mean arteriovenous oxygen content difference at 6oo kpm/min was significantly increased in the patients after training, though the response was not significantly different from that of the controls. Mean ventilatory equivalent was also significantly increased in patients after training, becoming similar to that of the controls.

Adult↗
PubMed1976

Unstable angina pectoris.

Unstable angina is a syndrome which comprises a spectrum of symptomatic manifestations of coronary artery disease which lies between stable angina pectoris and acute myocardial infarction. Patients fall into three groups: angina of recent onset (4 weeks), angina of changing pattern, and angina occurring at rest (longer than 15 minutes). The syndrome may presage acute myocardial infarction or sudden death, or may itself be the manifestation of a myocardial infarction. The pathophysiology may involve primary cardiac events or extracardiac precipitating factors, and does not appear to be the consequence of a particular anatomic pattern of coronary artery disease. Pain may occur as a result of regional reduction of coronary flow to pressure-dependent areas of myocardium during states of increased myocardial oxygen demand. Persisting ischemia leads to infarction via a series of events which may include myocardial edema formation, increased beta-sympathetic tone, and others which have been experimentally modified by interventions designed to limit infarct size. Although the incidence of acute myocardial infarction and death was high in early studies, in recent reports acute infarction occurs in under 15.5 per cent and death in under 2 per cent. Patients at high risk are those pain persists with bed rest, and those with preceding stable angina pectoris or myocardial infarction. Prognostic differences among Groups 1, 2, and 3 may exist but cannot be assessed from available studies. Studies of the management of unstable angina have generally been uncontrolled. Hospitalization, bed rest, and short- and long-acting nitrates are generally employed in Groups 2 and 3 patients and the marked reduction in myocardial infarction rates from early to recent studies tends to support these approaches. Anticoagulants are less used now than formerly. Propranolol can produce a significant reduction of myocardial oxygen consumption and may redirect coronary flow to ischemic areas. The drug has effectively controlled pain in several studies and is now widely used to manage unstable angina. Aortocoronary bypass surgery has been extensively employed but there is only one preliminary report of a controlled study available. The role of surgery is not yet defined. The optimal approach to therapy may eventually involve the use of medical therapy, including beta-blockade to stabilize patients, with delayed semielective coronary angiography and surgery in those who respond. Emergency angiography and surgery might then be reserved for the high-risk group of patients whose pain persists during optimal medical therapy.

Angina Pectoris↗
PubMed1976

Myocardial tissue recruitment in the dog as determined by double tracer dilution method.

The amount of tissue perfused, as determined from the difference in volume of distribution between a diffusible indicator (125I-antipyrine) and an intravascular indicator (131 I-albumin) was measured at different values of coronary flow, perfusion pressure, and vasomotor tone in the working left ventricle of an open-chest dog. Coronary pressure and flow were regulated independently from the systemic circulation and coronary vasomotor tone was reduced by dipyridamole. At each flow vasomotor tone was assessed by using as a reference the maximal vasodilation induced by arrest of flow. Measured tissue space was considered to be related to the capillary surface area available for tracer diffusion and therefore to the number of perfused capillaries per volume of muscle. A relationship between coronary blood flow and tissue volume was observed. It was found to be independent of vasomotor tone. Vasodilation was found to increase available exchanging capillary surface at a constant perfusion pressure.

Animals↗