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Biomedical subjects

S Bloom

Publications and source records attributed to S Bloom.

At least 73 records · Page 4Linked to original sources
PubMed1985

Treatment with danazol and plasma glucagon concentration.

The association between treatment with danazol and hyperglucagonaemia was studied. Plasma glucagon concentrations were measured during an oral glucose tolerance test in seven women taking danazol and six healthy controls not taking danazol. Results showed that treatment with danazol is associated with severe hyperglucagonaemia, and in three patients glucagon concentrations reached the range suggestive of glucagonoma. It is important to recognise that this increasingly used drug may cause severe hyperglucagonaemia to prevent patients treated with danazol undergoing unnecessary investigations to localise glucagonoma.

Adult↗
PubMed1985

Lung cancer in women. Lahey Clinic experience, 1957-1980.

The incidence of lung cancer is increasing dramatically worldwide. Cancer of the lung, the number one cause of death from cancer in men in the United States, will soon surpass breast cancer to become the most frequent cause of cancer death in women. To detail the changing pattern of lung cancer, we reviewed the clinical features of all 1752 patients whose lung cancer was diagnosed at the Lahey Clinic from 1957 through 1980. Women comprised a constant proportion of the total number of clinic patients during this 24-year period. Lung cancer in women increased markedly from 13% of all patients (1 to 6.8 ratio of women to men) in 1957 through 1960 to 35% (1 to 1.8 ratio) in 1977 through 1980. The authors reviewed pathologic specimens of 394 women with lung cancer. No significant change occurred in cell type distribution over the years: adenocarcinoma, 38%; epidermoid carcinoma, 20%; large cell carcinoma, 15%; small cell undifferentiated tumor, 13%; and other cell types, 14%. The incidence of all lung cancer cell types (Kreyberg Group 1 and Group 2) increased in women who smoked. Our study suggests that smoking is a major causal factor in the rising occurrence of all lung cancer cell types in women as contrasted to the preponderance of Kreyberg Group 1 tumors in men who smoke.

Adenocarcinoma↗
PubMed1985

Magnesium deficiency and myocardial infarct size in the dog.

Although epidemiologic data suggest a relation between myocardial infarction death rates and dietary intake of magnesium, there are no experimental studies reflecting such a phenomenon. It is now reported that beagle dogs kept on a severely magnesium-deficient diet for 100 days develop a larger infarct than do control animals. Control animals were either kept on the same diet as experimental animals with supplementary magnesium, or were fed standard dog chow. The control groups were indistinguishable and were therefore pooled. Infarction was produced by occlusion of the left anterior descending coronary artery for 1 hour followed by 4 hours of reperfusion. Slices of ventricular myocardium, 5 mm thick, were made from the apex to the base. Ischemic muscle, considered to be the muscle at risk, was delineated by a microsphere-autoradiographic method, and necrotic muscle was delineated by tetrazolium stain. Involved areas were measured by planimetry, and these integrated to produce the volume. The volumes of muscle made ischemic were similar in the experimental and control groups. The volumes of necrotic muscle, however, were less in the control than in the experimental animals. The ratio of necrotic muscle volume to the volume of muscle at risk was greater in the experimental animals than in the control animals by a factor of almost two (p less than 0.004). These experiments indicate that, under the conditions used here, animals fed a magnesium-deficient diet develop a larger infarct than do control animals. This could occur either through decreased postocclusion collateral flow or increased vulnerability of the ischemic muscle in magnesium-deficient animals. Although these experiments cannot rule out an effect on postocclusion collateral flow, they do suggest that electrolyte abnormalities related to magnesium deficiency are of such a character as to increase myocardial vulnerability to injury.

Animals↗
PubMed1985

Interrelationship of dietary Mg intake and electrolyte homeostasis in hamsters: I. Severe Mg deficiency, electrolyte homeostasis, and myocardial necrosis.

Epidemiological studies indicate a strong relationship between dietary Mg intake and the incidence of sudden cardiac death. The mechanism by which dietary Mg leads to an increased incidence of cardiovascular disease is unknown but may involve alteration of electrolyte balance. In the present study, tissue electrolyte levels and myocardial pathology were investigated in adult hamsters fed a diet containing no added Mg. Control animals were fed the same diet supplemented with Mg or standard laboratory chow. Hamsters were killed after 4, 8, 12, or 18 days on the test diet, and levels of Na, K, Ca, and Mg were measured in the serum, myocardium, bone, and kidney. The earliest change induced by the test diet was a decrease of the serum Mg and an increase in the Na concentration of the myocardium and other tissues. Following the rise in myocardial Na, the myocardial Ca rose, attaining a fourfold increase by 18 days. K fell in heart and kidney, but not significantly. Although there was no significant change in myocardial Mg, foci of myocardial necrosis, considered to be typical of acute severe Mg deficiency, were found. Myocardial necrosis and the increase in myocardial Ca occurred in parallel. Because of the pattern of observed changes in electrolyte levels, and the potential role of Ca in myocardial injury, the occurrence of myocardial necrosis in these Mg-deficient hamsters is attributable to the increased level of myocardial Ca, rather than to any change in intracellular Mg levels. It is postulated that reduced extracellular Mg levels increase [Na]i through reduction of sarcolemmal (Na+ + K+)-ATPase activity. This would lead to an increase in [Ca]i through Na-Ca exchange.

Acid-Base Equilibrium↗
PubMed1985

Coronary arterial lesions in Mg-deficient hamsters.

Dietary Mg deficiency is thought to promote coronary artery spasm, probably through Ca overloading of vascular smooth muscle (VSM) cells. We now report the demonstration of a coronary arteriopathy in hamsters fed a Mg-deficient diet for 10 days or more. Affected arteries showed endothelial and VSM cell hyperplasia and pleomorphism, chronic inflammation of the media and adventitia, and fibrinoid necrosis. Lesions of myocardial ischemia, distinct from the well-known lesions of myocardial necrosis and calcification common in Mg deficient animals, were also present. Von Kossa positive granules were found in the VSM of Mg-deficient, but not control, hamsters. This vasculopathy is a new factor to be considered in the pathophysiology of Mg deficiency. It is consistent with the view that Ca loading of VSM plays an important role in this condition and could be related to the occurrence of coronary artery spasm.

Animals↗
PubMed1984

Use of a biothesiometer to measure individual vibration thresholds and their variation in 519 non-diabetic subjects.

A series of 519 non-diabetic subjects had vibration thresholds at three points measured using a biothesiometer. Thresholds appeared to be log normally distributed and increased with age. Centile charts of this relation were derived from the data giving a range for normal thresholds. The biothesiometer provides a quick and reliable assessment of vibration thresholds, which when related to the centile charts gives an objective measure of the progress of diabetic peripheral neuropathy.

Adolescent↗
PubMed1984

A double-blind randomized, controlled study to investigate the efficacy of cimetidine given in addition to conventional therapy in the prevention of stress ulceration and haemorrhage in patients with acute spinal injury.

The efficacy of cimetidine, 1.2 and 2.4 g/day, compared to placebo treatment given in addition to conventional therapy, which included antacids, in the prevention of gastroduodenal lesions associated with stress in 105 patients with acute spinal injury was investigated. Haematemesis was only observed in 1 placebo-treated patient. Of the 84 patients who completed the 10-day treatment and underwent endoscopy, 12 out of 43 cimetidine-treated patients and 11 out of 41 patients who received placebo were found to have gastroduodenal ulceration and/or erosions. Mean circulating concentrations of gastrin, pancreatic polypeptide and secretin were similar in all groups of patients. Whilst cimetidine has been shown to reduce the incidence of ulceration in patients suffering cranial and thermal injuries, the present study failed to demonstrate a prophylactic effect of cimetidine in the primary prevention of ulcers or erosions in patients with acute spinal injury exceeding that of conventional antacid therapy.

Adolescent↗
PubMed1984

Passive stiffness of isolated cardiac and skeletal myocytes in the hamster.

Single cardiac myocytes and skeletal myocyte fragments, devoid of interstitial collagen but with intact glycocalyx, were prepared by mechanical disaggregation of hamster ventricular myocardium and caudal gracilis muscle, respectively. Passive stiffness was studied by examining the sarcomere length-tension relationship over the approximate Eulerian stress range of 0-20 mN/mm2 for cardiac myocytes and 0-120 mN/mm2 for skeletal myocytes. Creep and stress-relaxation became apparent only when cells were stretched to sarcomere lengths close to, or exceeding, 2.2 micron for the cardiac myocytes, and 2.7 micron for the skeletal myocytes. Stress-relaxation and creep occurred simultaneously, suggesting that the sarcomere is at least one of the structural components responsible for viscoelasticity. The differential strain stiffness constant was calculated from the regression of natural stress [Ln(mN/mm2)] against differential strain [(L-Lo)/Lo] and found to be 7.48 +/- 1.73 for the ventricular myocytes and 5.77 +/- 0.87 for the skeletal myocyte fragments. The natural strain stiffness constant was obtained from the regression of natural stress against natural strain [Ln(L/Lo)]. The natural strain stiffness constant was 30-50% higher than the differential strain constant. The high correlation coefficients obtained for both regressions indicate that the length-tension relationships for these isolated cardiac and skeletal myocytes can be very closely fitted to the single exponential function, sigma = C X exp[K(epsilon)]. The length-tension curves obtained for the skeletal myocyte fragments are qualitatively and quantitatively similar to those obtained by others with intact skeletal muscle. The cardiac myocyte length-tension curves are qualitatively, but not quantitatively, similar to those obtained with cardiac muscle. Isolated ventricular myocytes are stiffer than similarly isolated skeletal myocytes. These findings suggest that cellular structures contribute to myocardial stiffness in the hamster.

Animals↗
PubMed1984

Human pancreatic tumor growth hormone-releasing factor: dose-response relationships in normal man.

Human pancreatic GRF (hpGRF-40; 1 microgram/kg, iv) selectively stimulates GH release in normal men (9). We now report the effects of graded doses of hpGRF-40 on GH release in 12 normal men. Mean peak increments in serum GH after vehicle and the various doses of hpGRF-40 were 1.13, 11.40, 14.60, 17.01, 14.45, and 15.60 ng/ml after vehicle and 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40 (iv bolus), respectively. Peak values were observed 30-60 min after hpGRF-40 treatment. There was considerable variability of responsiveness among individual subjects, and no dose-response relationship between the doses and maximal GH values was found. However, the higher doses of 3.3 and 10.0 micrograms/kg resulted in a more prolonged and biphasic pattern of GH release. A side effect of facial flushing of less than 5-min duration occurred in 4 or 6 subjects who received 3.3 micrograms/kg and in all 5 who received 10 micrograms/kg of hpGRF-40. No changes in serum glucose, LH, TSH, PRL, plasma cortisol, or 8 enteropancreatic hormones occurred after hpGRF-40 treatment. There were small increases in serum somatomedin C levels 24 h after the administration of various doses of hpGRF-40 in 11 of 13 studies. Plasma immunoreactive GRF levels measured 5 min after injection were 0.09, 2.0, 4.9, 23.9, and 66.6 ng/ml after 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40, respectively. Serum GH responses after insulin-induced hypoglycemia were compared to GH responses after hpGRF-40. Comparable peak GH stimulation occurred with both provocative tests. Mean +/- SEM peak GH was 20.2 +/- 1.0 ng/ml after insulin and 20.9 +/- 3.2 after hpGRF-40 treatment. hpGRF-40 selectively stimulates GH release in normal men over a dose range of 0.1-10 micrograms/kg and is an effective probe to investigate the dynamics of GH release.

Adult↗
PubMed1984

Bile diversion from the duodenum: its effect on gastric and pancreatic function.

The effect of diverting bile from the duodenum in four dogs by cholecysto-jejunostomy was studied using a double-marker perfusion technique. During digestion of a liquid meal, acid secretion increased from 0.8 mmol H+/min to 1.48 mmol H+/min (p less than 0.05, paired t test); there was an associated rise in serum levels of gastrin 120 minutes after feeding (p less than 0.001, paired t test). Pancreatic secretion of trypsin decreased from 3.91 IU/min to 2.66 IU/min after bile diversion (p less than 0.01, paired t test) and the level of CCK was significantly lower 60 mins after feeding (p less than 0.05, paired t test). There was no significant change in the rate at which the liquid meal emptied from the stomach after bile diversion but the pH of duodenal contents was lower during the later stages of digestion. These changes may explain the reported increase of peptic ulcer after diverting bile from the duodenum and the procedure should not be considered unless the consequences of acid hypersecretion and pancreatic inhibition have been anticipated.

Animals↗
PubMed1983

Determinants of resistance to the cardiotoxicity of isoproterenol in rats.

Induction of myocardial necrosis by isoproterenol produces resistance to the necrogenic effects of subsequent doses of the drug. A series of experiments were performed to further define the determinants of resistance. Myocardial necrosis was induced in male Sprague-Dawley rats by sc injection of isoproterenol at 50 micrograms/kg daily for 10 consecutive days or as a single dose at 50, 5, or 0.5 micrograms/kg. These preconditioning doses were followed, at various times, by a challenge dose of 50 micrograms/kg. The rats were killed 48 hr after the challenge dose, and their hearts were analyzed morphometrically to determine the amount of acute necrosis and scarring. The amount of scar tissue was a reflection of necrosis caused by the preconditioning dose whereas acute necrosis reflected response to the challenge dose. Resistance occurred and lasted longer than 19 to 20 weeks after both single or multiple isoproterenol injections of 50 micrograms/kg, but it was not observed 5 days after administration of a single preconditioning dose. Isoproterenol at 0.5 micrograms/kg produced only very minimal or no myocardial necrosis and did not produce resistance. The resistance was not dependent on the size of the area of necrosis produced during the preconditioning period, showing that it was not due to destruction of all vulnerable muscle by the preconditioning dose(s). The preexistence of lesions, however, was necessary for the development of resistance. It is concluded that development of resistance to the necrogenic effects of isoproterenol reflects an adaptive alteration in the myocardium which survives after a necrogenic dose.

Animals↗
PubMed1983

A simple ashing method for determination of Mg and Ca in laboratory animal feed and tissues.

A simple procedure has been developed for preparation of animal tissues and diet mixtures for Mg and Ca analysis by atomic absorption spectroscopy. This procedure involves wet ashing in warm 30% hydrogen peroxide and extraction of metals, from the dried ash, into cold, dilute nitric acid. Less than 200 mg of tissue or feed are required. Measurements obtained by this method for hamster and rat myocardium give values similar to those found previously by more cumbersome methods. Concentrations of Mg and Ca in hamster serum, bone, kidney, and liver are also reported. Recovery of magnesium from bone and heart tissue was 101% and 102%, respectively. For calcium the respective values were 99% and 98%. This procedure is simple to carry out, does not generate corrosive fumes or require expensive equipment. It can be conveniently used to prepare large numbers of samples for atomic absorption spectrophotometry.

Animal Feed↗
PubMed1982

Microemboli observed in deaths following cardiopulmonary bypass surgery: silicone antifoam agents and polyvinyl chloride tubing as sources of emboli.

Refractile foreign particles within clear vacuoles were observed in capillaries of 17 patients who underwent cardiopulmonary bypass surgery, died, and were autopsied at the George Washington University Hospital from December 1978 through April 1981. The postoperative survival time ranged from less than one day to more than eight months. The approximate maximal diameter of the individual particles was 10 micrometer and that of the vacuoles 60 micrometer. The particle-droplet complexes showed affinity for hydrophobic stains. In all 17 cases, the kidneys were involved in combination with several other organs. In two patients, the emboli were associated with microinfarcts in one or more organs. Scanning electron microscopy (SEM) of the polyvinyl chloride tubing used during four cardiopulmonary bypasses showed spallation and shredding of the luminal surface in the areas exposed to the roller pump heads. This suggested that fragments of polyvinyl chloride might be the particles in the emboli. Another possible source was the antifoam agent used in the bubble oxygenator. Scanning electron microscopy x-ray microprobe analysis of the foreign material within capillaries of several organs showed it to be strongly positive for silicon but not for chlorine. Therefore, it was concluded that the microemboli were droplets of antifoam agent, the refractile particles corresponding to the particulate silica component and the vacuoles corresponding to the dimethylpolysiloxane liquid component. Since x-ray microprobe analysis of the microemboli did not reveal a strong chloride peak, there is as yet no evidence that polyvinyl chloride fragments were involved in the microembolism. The morphologic findings reported here indicate that antifoam microembolization continues to complicate cardiopulmonary bypass surgery and must, therefore, be considered a potential cause of postoperative morbidity. The consequence of the fragments of polyvinyl chloride tubing released into the circulation remains to be established.

Antifoaming Agents↗