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J Serur

Publications and source records attributed to J Serur.

13 recordsLinked to original sources
PubMed1986

Mechanical and inotropic reserve in conscious dogs with left ventricular hypertrophy.

We studied the left ventricular (LV) responses to infusions of norepinephrine and prenalterol, a specific beta 1-adrenergic receptor agonist, in conscious, chronically instrumented adult dogs with severe LV hypertrophy. The goal of this study was to determine the extent of compensation induced by LV hypertrophy in an animal model in which the pressure overload was gradually increased, as occurs in human pathological states. One to 2 yr after banding the ascending aorta of puppies, six dogs with severe LV hypertrophy (LV free-wall weight-to-body weight ratio 7.0 +/- 0.4 g/kg), and nine sham-operated littermates (LV free-wall weight-to-body weight ratio 4.0 +/- 0.2 g/kg) were studied. The dogs were instrumented with ultrasonic dimension crystals (to measure LV short-axis diameter and wall thickness), miniature LV pressure transducers, and LV and aortic catheters. In the control dogs norepinephrine (0.4 micrograms X kg-1 X min-1) increased LV systolic/diastolic pressure from 121 +/- 2/9 +/- 1 to 177 +/- 9/20 +/- 2 mmHg, mean arterial pressure from 97 +/- 2 to 143 +/- 9 mmHg, LV dP/dt from 3,363 +/- 123 to 5,174 +/- 343 mmHg/s, and mean systolic wall stress from 194 +/- 14 to 299 +/- 22 g/cm2, while mean velocity of circumferential fiber shortening (Vcf), (dD/dt/D)max, and heart rate did not change from base line. In dogs with LV hypertrophy norepinephrine increased LV pressure from 224 +/- 16/11 +/- 1 to 305 +/- 22/19 +/- 1 mmHg, mean arterial pressure from 90 +/- 2 to 132 +/- 4 mmHg, LV dP/dt from 3,246 +/- 156 to 5,619 +/- 345 mmHg/s, and mean systolic wall stress from 224 +/- 11 to 307 +/- 24 g/cm2.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1983

A catheterization technique for reproduction of a human atherosclerotic lumen within the dog coronary artery in vivo.

Reproduction of a human atherosclerotic lumen within the arterial lumen of an intact animal would facilitate angiographic and hemodynamic studies of stenoses. Accordingly, a male silicone rubber cast of a human atherosclerotic lumen was obtained from a cadaver artery, and a thin-walled replicate arterial phantom was constructed from the cast by use of a rapidly polymerizing liquid plastic. The casting properties of both materials were such that the topography of the arterial lumen was duplicated precisely in the phantom with 20 x microscopic detail preserved. The phantom was coated with a banzalkonium-heparin solution and introduced over a guidewire into an epicardial segment of a coronary lumen of the dog. Similarly, a larger phantom was placed within the dog femoral artery either directly via an arteriotomy or indirectly via a catheterization technique. Since the plastic material used to make a phantom had the same radiographic density of tissue, the angiographic appearance of an intra-arterial phantom was that of a human stenosis.

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PubMed1983

In vivo coronary angioscopy.

The feasibility of in vivo coronary angioscopy was tested utilizing a 1.8 mm angioscope in vessels where blood had been replaced by optically clear liquids, including a new perfluorocarbon emulsion. After trials in postmortem canine and human coronary arteries, in vivo intraluminal visualization was accomplished in the dog with a catheterization technique and in patients during open heart surgery. The results demonstrate the feasibility and potential clinical usefulness of direct visualization of intravascular anatomy and disease, analogous to endoscopy of other organ systems.

Animals↗
PubMed1983

Fluorescence of experimental atheromatous plaques with hematoporphyrin derivative.

Fluorescence of hematoporphyrin derivative (HPD) has been used clinically to localize malignant neoplasms because of its selective accumulation in these tissues. We tested the hypothesis that HPD may also be selectively concentrated within atheromatous plaques. 48 h after HPD injection in a variety of species, selective fluorescence of atheromatous plaques of the aorta was seen in each animal (rabbits and Patas monkey) exhibiting such lesions. No fluorescence could be demonstrated in aortic segments free of atheromatous involvement. Since the efficacy of photodynamic destruction of malignant tumors with HPD has been demonstrated in clinical studies, the observations of the present study may have therapeutic implications in atheromatosis.

Animals↗
PubMedDate not supplied

[Progressive decrease of the causes that maintain ventricular fibrillation after experimental coronary occlusion].

Progressive diminution of the causes that maintain ventricular fibrillation after coronary occlusion. Extracorporeal circulation was performed on a group of normal dogs in which a ligature was placed on the left anterior descending coronary artery, immediately beneath the bifurcation of the left coronary artery. The incidence of ventricular fibrillation was of 15 dogs out of 20 (table 1). In a control group without extracorporeal circulation ventricular fibrillation appeared in 24 dogs out of 30 (table 2). These results demonstrate that extracorporeal circulation performed with the idea of improving coronary circulation does not prevent ventricular fibrillation in coronary occlusion. In those dogs with the cross circulation, attempts to defibrillate the ventricles with an electric a.c. defibrillator (three electrical shocks applied directly on the myocardium every 4 or 5 minutes) were uniformly unsuccessful until a period ranging from 12 to 80 minutes elapsed after the onset of ventricular fibrillation. After these periods all fibrillating dogs were defibrillated and recovered either normal or idioventricular rhythm. It is assumed that a "fibrillator substance" liberated by the injury in the initial state of infarction is washed out of the myocardium, or a zone of increased excitability and conduction disturbance is progressively eliminated so that the chances of originating circus movements are diminished.

Animals↗
PubMedDate not supplied

Studies of the pathogenesis of arteriosclerosis induced in rats by intrarenal injection of a carcinogen, nickel subsulfide.

Widespread arteriosclerotic lesions were detected by histological examinations of rats killed at seven or nine weeks after an intrarenal (ir) injection of nickel subsulfide (Ni3S2, 5 mg per rat). Arteriosclerotic plaques were readily visualized by administering hematoporphyrin derivative (HPD) iv to rats at 24 hours before sacrifice. At necropsy, the major arteries were inspected under ultraviolet light, revealing patches of intense HPD-fluorescence in the arterial endothelium of Ni3S2-treated rats, but not in control rats. Consistent with previous reports, the Ni3S2-treated rats developed pronounced erythrocytosis; blood hematocrit values averaged 70 +/- 4 percent at seven weeks after ir injection of Ni3S2 (P less than 0.001 vs corresponding value of 49 +/- 2 percent in vehicle controls). At seven weeks, blood platelet counts averaged 17 percent lower and serum glucose concentrations averaged 23 percent lower in Ni3S2-treated rats than in controls; serum lipids, lipoproteins, non-protein nitrogen constituents, electrolytes, proteins, and enzymes were not significantly affected. Body weights and systolic blood pressures of rats at two, four, and six weeks after ir injection of Ni3S2 did not differ from corresponding values in controls. Addition of egg yolk to the diet caused mild hypercholesterolemia, but it did not enhance the incidence or severity of arterial lesions in Ni3S2-treated rats. These findings exclude hypertension and hyperlipidemia as pathogenic factors in Ni3S2-induced arteriosclerosis.

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