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Biomedical subjects

S Bloom

Publications and source records attributed to S Bloom.

At least 55 records · Page 3Linked to original sources
PubMed1989

Anti-inflammatory drugs in experimental atherosclerosis. 7. Spontaneous atherosclerosis in WHHL rabbits and inhibition by cortisone acetate.

The Watanabe heritable hyperlipidemic (WHHL) rabbit, an animal model for familial hypercholesterolemia, has a deficiency in low density lipoprotein (LDL) receptor binding and exhibits elevated plasma lipoprotein levels and spontaneous atherosclerosis. Since atherosclerotic plaque formation has a number of features in common with the inflammatory process, we have investigated the effect of dietary supplementation with an anti-inflammatory steroid (cortisone acetate, 5 mg daily for 3 months) on atherosclerosis using the WHHL rabbit as a model. Atherosclerotic plaque formation in cortisone-fed animals was reduced by about 60% compared to control WHHL rabbits. Steroid administration increased circulating cholesterol levels modestly and triglycerides were increased about 6-fold. While very low density lipoprotein (VLDL)-cholesterol was increased, LDL-cholesterol levels were decreased and the particle was more triglyceride-enriched as well as less dense. Steroid-fed animals also exhibited decreased platelet aggregation and increased aortic 15-lipoxygenase activity. The histological observations showed typical fibrous plaques in aortas of both control and cortisone-fed rabbits, with intima thickened by foamy macrophages and subcellular lipoproteinaceous debris covered by a fibrous cap. These findings thus indicate that steroids reduce the rate of plaque initiation or progression but do not significantly change the histological appearance of the lesion.

Animals↗
PubMed1989

Geographic variation in the incidence of myocardial calcification associated with acute myocardial infarction.

There is reason to believe that calcium influx into heart muscle during acute myocardial infarction (AMI) can aggravate myocyte injury. Furthermore, the degree of such influx might correlate with the occurrence of microscopic myocyte calcification observed at autopsy. We have searched for evidence of myocyte calcification in hearts of patients found to have AMI at autopsy at the Veterans Administration Medical Center in Salt Lake City (SLCVA), a region with a low myocardial infection death rate, and at the George Washington University Medical Center in Washington, DC (GWUMC), a region with a high myocardial infection death rate. Of 23 consecutive cases examined under "blind" conditions at the GWUMC in which AMI was found, there were 15 instances of cardiac myocyte calcification observed in von Kossa-stained sections. Not a single example of myocyte calcification was found in 23 comparable cases at the SLCVA. The basis of this difference in myocyte calcification is unknown, but may be related to the fact that the Salt Lake City drinking water contains a higher level of magnesium, which is known to protect against soft tissue calcification, than does that of Washington, DC. This may be the basis for the apparent protection that dietary magnesium exerts against myocardial infarction death.

Black People↗
PubMed1989

Sodium pump and calcium channel modulation of Mg-deficiency cardiomyopathy.

Hamsters fed a Mg-deficient diet (MD) develop a cardiomyopathy (CM) with foci of myocardial necrosis, calcification, and modest mononuclear and giant cell infiltration. We hypothesize that the lesions are secondary to Ca overload following an increase in myocardial Na due to inhibition of (Na.K)-ATPase and secondary Na-Ca exchange. Nifedipine and digoxin were selected as agents to test this hypothesis. Hamsters were given nifedipine, digoxin, or placebo as sustained release subcutaneous pellets the same day they were started on the MD diet. Animals were killed after 14 days, and MD lesions were quantified in H&E stained slides. Regression analysis showed that nifedipine produced a dose-dependent reduction in lesion abundance (p less than .005) and diameter (p less than .05), while digoxin produced a dose-dependent increase in lesion abundance (p less than .005) and diameter (p less than .005). These results support the hypothesis that MDCM is secondary to Ca overload coupled to inhibition of (Na.K)-ATPase of cardiac myocytes.

Animals↗
PubMed1988

Fate and effects of the alpha-glucosidase inhibitor acarbose in humans. An intestinal slow-marker perfusion study.

The alpha-glucosidase inhibitor acarbose has been successfully used in diabetic patients to decrease the postprandial rise in blood glucose. The aim of the present experiments was to investigate the fate and effects of acarbose along the small intestine using a slow-marker perfusion technique. In 8 healthy volunteers, jejunal and ileal loads of acarbose, glucose, and total carbohydrates were determined following a liquid, 400-kcal formula meal containing either 200 mg of acarbose or placebo. Preprandial and postprandial plasma concentrations of glucose and several polypeptide hormones were determined. Recovery of acarbose during 4 h was 65% +/- 9% (mean +/- SEM) of ingested dose in the ileum but 94% +/- 9% in the jejunum, indicating that the compound was neither degraded nor absorbed by the intestine to a major degree. After acarbose administration, ileal loads of glucose and total carbohydrates were considerably higher, whereas postprandial plasma concentrations of glucose, insulin, and gastric inhibitory polypeptide were lower when compared with placebo. The retardation of carbohydrate digestion to be inferred from these findings is confirmed by significantly elevated plasma concentrations of enteroglucagon after acarbose administration compared with placebo administration.

Acarbose↗
PubMed1987

Sinus of Valsalva aneurysm associated with multiple conotruncal congenital malformations.

A case of rupture of a sinus of Valsalva aneurysm in a middle-aged woman with an unusual assortment of associated conotruncal and other cardiac anomalies is reported. The anomalies included bicuspid aortic valve, aortic sinus aneurysm (ruptured), quadricuspid pulmonic valve, membranous coarctation of the aorta, subclavian and common carotid arteries arising directly from aorta, and atrial septal defect. Excluding the atrial septal defect, these anomalies may be explained by a single embryologic event affecting conobulbar septation and aortic arch development occurring at the level of neural crest development.

Aortic Rupture↗
PubMed1986

Characteristics of fibrolamellar hepatocellular carcinoma. A study of nine cases and a review of the literature.

Clinical and laboratory data for nine patients with hepatocellular fibrolamellar carcinoma treated at our institution have been summarized with emphasis on the relevance of plasma neurotensin levels as a tumor marker. The mean age of the patients was 22 years. Seven underwent hepatic resection, and two of these had later surgical removal of recurrent disease. Plasma neurotensin levels were initially elevated in five of the seven patients in whom it was measured. Neurotensin levels were within normal limits in three of four patients with recurrent disease, but were elevated in one patient who also had elevated plasma neurotensin levels preoperatively. In addition, a review of 80 patients reported since 1980 was performed. The mean age of these patients was 23 years, and only 6 percent were older than 50. The male to female ratio was 3:4. Eight percent were positive for hepatitis B antigen and 11 percent had elevated alpha-fetoprotein levels. Four percent had cirrhosis of the liver. The resectability rate was 58 percent. Five year survival for patients who underwent hepatic resection was 56 percent. Patients treated nonsurgically had a median survival of 13 months, and none of these patients lived for 5 years. Fibrolamellar hepatoma seems to be a distinct clinical entity that mainly occurs in young patients. The prognosis in patients treated with a curative resection is good. Plasma neurotensin levels may be of value as a tumor marker, but further studies are necessary to substantiate this theory.

Adolescent↗
PubMed1986

Atrial natriuretic peptide: an endogenous factor enhancing sodium excretion in man.

For many years experimental evidence has suggested the existence of a circulating factor able to enhance sodium excretion. Very recently peptides with natriuretic activity in experimental animals have been isolated from mammalian and human cardiac tissue. In order to determine whether this natriuretic activity has relevance to man we have studied the effects of an infusion of alpha-human atrial natriuretic peptide (alpha-h-ANP) in normal subjects. Sodium excretion trebled (P = less than 0.005) during the infusion of a calculated dose of 15 pmol of alpha-h-ANP min-1 kg-1 and there was an accompanying diuresis; radioimmunoassay of plasma alpha-h-ANP during the natriuresis indicated a mean peak incremental concentration of 203 +/- 78 (SEM) pmol/l. The infusion of a calculated dose of 1.5 pmol min-1 kg-1 did not affect sodium excretion. There were no haemodynamic changes and no side effects were noted.

Adult↗
PubMed1986

The influence of residual coronary stenosis on size of infarction after reperfusion in a canine preparation.

The effect of a residual coronary artery stenosis on size of myocardial infarction was studied in an open-chest canine preparation of coronary occlusion and reperfusion. Eighteen male mongrel dogs (16 to 26 kg) underwent left thoracotomy under general anesthesia; the circumflex artery was instrumented with a hydraulic cuff occluder, a screw clamp, and an electromagnetic flow probe. Animals were randomized to one of three groups: group I (n = 6) had a 6 hr circumflex occlusion, group II (n = 6) had a 2 hr occlusion followed by 4 hr of partial reperfusion through a residual stenosis adjusted to approximately 30% of baseline flow, and group III (n = 6) had full reperfusion for 4 hr after a 2 hr occlusion. Zones of risk, infarction, and no reflow were defined by staining with Evans blue, triphenyl tetrazolium chloride, and fluorescein, respectively. At 6 hr the hearts were excised and areas of risk, infarction, no reflow, and hemorrhage were determined by planimetry of serial transverse heart slices (5 mm thick). Infarction as a percent of the risk area was 96 +/- 1% in group I, 90 +/- 2% in group II, and 79 +/- 4% in group III (p less than .001), and the differences between each of the groups were significant. Gross hemorrhage was seen in none of the six dogs in group I, two of the six in group II, and five of the six in group III, but did not affect infarct size. We conclude that residual stenoses may exert a deleterious effect on the outcome of coronary reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Hyperthyroidism due to non-tumoural inappropriate TSH secretion. Effect of a long-acting somatostatin analogue (SMS 201-995).

Inappropriate hypersecretion of TSH was investigated in a 25 year old man whose hyperthyroidism had relapsed 4 years after subtotal thyroidectomy. Serum TSH levels were further increased by both TRH and metoclopramide and were partially suppressed by triiodothyronine (120 micrograms/day). The serum alpha-subunit: TSH molar ratio was less than 1.0, and computerised axial tomography showed no evidence of a pituitary tumour. These features are characteristic of inappropriate TSH secretion due to thyrotroph resistance to thyroid hormones. A long-acting somatostatin analogue (SMS 201-995), 50 micrograms injected sc twice-daily for three days, suppressed TSH levels and nearly normalised thyroid hormone levels. Somatostatin analogues may be therapeutically useful in thyrotoxicosis due to non-tumoural inappropriate TSH hypersecretion.

Adult↗
PubMed1986

Effects of magnesium deficiency on the pathogenesis of myocardial infarction.

The death rate due to myocardial infarction appears to vary with dietary consumption of Mg. This could be due to effects on atherosclerosis, coronary artery spasm, altered pathogenesis of myocardial infarction, increased vulnerability to arrhythmia, or some combination of these. Mg deficiency (MD) has been found to increase the severity of a coronary occlusive event in terms of the amount of necrosis produced by a given occlusion. MD is also associated with increased likelihood of arrhythmia development. In addition, reduced extracellular magnesium concentration (Mgo) is associated with contraction of vascular smooth muscle that may be the equivalent of arterial spasm. In hamsters, MD leads to fibrinoid necrosis thought to be secondary to Ca overload. These 3 effects: coronary artery spasm, cardiac arrhythmia, and increased vulnerability to myocardial necrosis following coronary occlusion, may all be dependent on changes in myocardial and vascular smooth muscle electrolyte metabolism that follow from the reduced Mgo that is associated with MD.

Action Potentials↗