Laser coronary angioplasty: experience with 9 cadaver hearts

Experience with laser angioplasty in 16 coronary arteries in 9 cadaver hearts is presented. Coronary obstructions were due to experimentally created thrombi as well as to naturally occurring calcified plaques. Successful laser angioplasty was achieved in 14 of 15 arteries. One artery was sacrificed to etermine factors necessary for deliberate perforation of the arterial wall. This procedure required more than 30 seconds of laser energy at 3.0 W with the catheter tip almost perpendicular to the wall. Penetration of the arterial wall occurred only in the second left anterior descending artery which was plaque-occluded because of operator inexperience.     

Renal response to mechanical ventilation in patients with chronic hypercapnia

Alkalosis in hypercapneic patients caused by abrupt respirator-induced reduction of the partial pressure of carbon dioxide leads to bicarbonate diuresis. Potassium is the predominant cation accompanying bicarbonate loss in the urine.The determining variable for induction of proportional changes in renal bicarbonate and potassium excretion is the partial pressure of carbon dioxide. The reduction of the partial pressure of carbon dioxide modifies bicarbonate regeneration directly by limiting the hydration reaction and facilitates potassium loss indirectly by reducing extracellular, and by inference intracellular, hydrogen ion activity.     

Nutrition and cancer

Nutrition and cancer interact at several levels. Both dietary deficiencies and dietary excesses have been linked with changes in prevalence of certain human cancers. With respect to one particular nutrient, riboflavin, a dietary deficiency may decrease the development of spontaneous tumors in experimental animals but increase carcinogenesis due to certain agents. Cancer itself has profound effects upon nutritional status, and neoplastic tissue appears in general to resist dietary deficiency more effectively than normal tissues. Nutrition has a major role in therapy of cancer, but as an adjunct to the treatment plan rather than as an alternative. Parenteral nutrition, either peripheral or total, can provide support that is critically needed when patients cannot eat or swallow, have obstruction or malabsorption, or are otherwise unable to utilize dietary nutrients in adequate amounts. The advent of home parenteral nutrition now provides a means for long-term rehabilitation of cancer patients.     

Augmented lipolysis in rat adipose tissue upon repeated exposure to epinephrine.

A perfusion system was used to investigate the lipolytic response to epinephrine of minced epididymal fat pads from fed and 24-hr fasted rats. Epinephrine was infused at a final concentration of 1 X 10(-6) M for 60-min periods. Basal glycerol release from tissue and cells of fed animals was 3 mumoles/min/ml of sample. Epinephrine stimulated lipolysis 20-fold in tissue pieces. There was an additional two-fold increase during a repeated epinephrine infusion after 30 min with buffer alone. In contrast, tissue from fasted rats showed no difference upon successive infusions of epinephrine. Isolated cells of fed and fasted animals also produced peaks of equal magnitude on both exposures to epinephrine. Preincubation of fed tissue with anti-insulin serum did not abolish the augmented response to the hormone. Preincubation of the fed tissue for 90 min with omission of the first epinephrine exposure did not produce an augmented response. It is concluded that exposure of adipose tissue to 1 X 10(-6)M epinephrine will produce augmented stimulation of lipolysis on a second exposure. Fasting and isolation of cells abolishes the augmented response by a mechanism which does not involve removal of insulin from the fat cell.     

Extreme hypocapnia in the critically ill patient

Respiratory alkalosis was the most common acid-base disturbance observed in a computer analysis of 8,607 consecutive arterial blood gas studies collected over an 18 month period in a large intensive care unit.Through a retrospective review of the randomly selected hospital records of 114 patients, we defined four groups based upon arterial carbon dioxide tension (PaCO₂) and mode of ventilation. Group 1, with a PaCO₂ of 15 mm Hg or less, consisted of 25 patients with an over-all mortality of 88 per cent. Group II, with a PaCO₂ of 20 to 25 mm Hg, consisted of 35 patients with a mortality of 77 per cent. Group III, with a PaCO₂ of 25 to 30 mm Hg, consisted of 33 patients with a mortality of 73 per cent, and Group IV, with a PaCO₂ of 35 to 45 mm Hg, consisted of 21 patients with a mortality of 29 per cent (p <0.001). Shock and sepsis were most common in group I patients.These findings suggest that extreme hypocapnia in the critically ill patient has serious prognostic implications and is indicative of the severity of the underlying disease.     

Sex difference in the influence of obesity on the 24 hr mean plasma concentration of cortisol

The 24 hr mean plasma cortisol concentration was measured in 65 healthy women ranging from 21% below to 218% above desirable weight and in 47 healthy men ranging from 5% below to 330% above desirable weight. In the women, there was a clear-cut inverse linear correlation between the plasma cortisol concentration and the percent deviation from desirable weight (y = 7.5 ? 0.3 x; r = ?0.49; p < 0.001); the relation of free to total cortisol concentration was weight-invariant; the MCR of cortisol in the most obese women was much higher than that of nonobese women (340 ± 76 versus 211 ± 31 liters/gm urinary creatinine; p < 0.01). In the men, the plasma cortisol level and MCR were weight-invariant. To account for the finding in women of a linear correlation of the decrement in plasma cortisol level with the percent deviation from desirable weight (which in turn is nearly perfectly correlated with the total body fat content), we postulate that a given weight of adipose tissue in women takes up a constant amount of cortisol; this in turn suggests that their adipose tissue contains a saturable binding system such as corticosteroid receptor. By the same logic, the weight-invariance of plasma cortisol and MCR in men suggests the absence of significant amounts of corticosteroid receptor in their adipose tissue. The finding that the increased cortisol MCR of obese women results in decreased plasma cortisol levels rather than an increase in cortisol production (the latter, corrected for muscle mass, is normal in obesity: Strain et al, Metabolism 29:980, 1980) suggests a defect in their cortisol ACTH feedback system. Such a defect, presumably hypothalamic, is not unexpected in the light of reports of defective hypothalamic control of prolactin and growth hormone secretion in obesity.     

Acute cortical necrosis. Case report and review of the literature

Confluent acute cortical necrosis is a rare but catastrophic disease. Described here is one case which was heralded by abruptio placenta and occurred in concert with a disseminated intravascular coagulopathy (DIC). All causes of acute cortical necrosis share one common denominator: a procoagulant factor capable of activating the coagulation mechanism. This aspect of the pathogenesis, the pathophysiology and clinical aspects of acute cortical necrosis are reviewed and contrasted to acute tubular necrosis and irreversible postpartum renal failure. Preparation for an extended period of treatment is emphasized as recovery from acute cortical necrosis is protracted.     

Hereditary nephritis with a characteristic renal lesion

Light and electron microscopic studies were performed on renal tissue from four involved members of a family with hereditary nephritis.The two females studied had no apparent deafness or renal insufficiency, but a nonspecific mild increase in mesangial matrix was noted on light microscopic examination of the renal biopsy specimen. The two males had neurosensory deafness. One had advanced renal insufficiency with glomerular sclerosis, whereas the other had no azotemia and less histopathologic change.However, all four had a characteristic ultrastructural lesion consisting of glomerular basement membrane splitting separated by clear spaces with the accumulation of small dense particles between the thin layers. This change may be specific for certain forms of hereditary nephritis.     

Linking the kallikrein and renin systems via activation of inactive renin: New data and a hypothesis

An inactive form of renin occurs in normal plasma and in various diseases in amounts capable of generating much more renin than is generally present in active form. The inactive renin-like material in plasma seems largely, but not completely, of renal origin and can be converted to an active renin-like substance in vitro by either acid or cold treatment. These observations are of considerable practical relevance for improving routine renin measurements since certain methods which acidify plasma have inadvertently measured both inactive and active renin. Avoidance of chilling during collection of blood will also improve the precision of renin measurements.A series of observations has demonstrated that both acid- and cryoactivation of inactive plasma renin are enzymatic processes involving a neutral serine protease. Characterization of these in vitro activation processes has led to the demonstration that an intrarenal enzyme with similar biochemical characteristics, urinary kallikrein, is an extremely powerful activator of inactive renin. In view of the location of this enzyme, adjacent to renin in the kidneys, it seems possible that it may function physiologically to trigger the renin system.In the light of these findings a hypothesis has been proposed to explain the coordinated control of systemic pressure and local tissue flow in which renal kallikrein may activate the renin system which, in turn, releases angiotensin II to maintain or defend systemic arterial pressure. Concurrently, the kallikrein-kinin system would function within the kidney to maintain local tissue flow in the face of angiotensin-induced systemic vasoconstriction. In this construction kinins are not viewed as circulating hormones. More research is needed to test this hypothesis and to work out the steps involved in its organization.     

Hyperbilirubinemia and cholestasis.

Although the morphologist continues to describe cholestasis on the basis of precipitated bile seen on light microscopic sections of the liver or dilated canaliculi with loss of microvilli seen by electron microscopy, the physiologist can distinguish clearly between hyperbilirubinemia and cholestasis. Both bilirubin and bile acids are specifically removed from sinusoidal plasma by the normal hepatocyte and appear in bile in high concentration. Bilirubin conjugation and excretion appear to be governed by hepatocellular mechanisms that are, for the most part, separate from the conjugation and excretion of bile acids. Disturbances in bilirubin transport are recognized by hyperbilirubinemia which represents a number of clinical syndromes that can be classified by the nature of the block in the transport system. Serum bile acids appear to remain normal in hyperbilirubinemic syndromes. By contrast, cholestatic syndromes are characterized by marked bile acidemia with normal to slightly elevated bilirubin levels. Severe cholestasis, because of the marked reduction in bile flow, can however, engender jaundice. Further exploration of these excretory pathways will provide interesting new insights on the numerous cholestatic and hyperbilirubinemic syndromes that occur in nature.     

Bacteroides fragilis resistant to the administration of clindamycin.

The susceptibility of Bacteroides fragilis to the administration of clindamycin, and the efficacy of this agent in Bacteroides infections are well documented. Clindamycin-resistant strains of B. fragilis were isolated from two patients with bacteremia at two institutions. Clinically significant resistance to clindamycin therapy has not been noted previously in B. fragilis infections.     

Accidental hypothermia in an alcoholic population

Thirty-nine cases of accidental hypothermia are reviewed. Data indicate that mortality varies with the presence of underlying disease rather than with the degree of hypothermia or the methods of rewarming. In 31 patients with hypothermia alone (average temperature 85 °F) mortality was 6.25 per cent. In eight patients with hypothermia and another primary condition (average temperature 84 °F) mortality was 75 per cent.Intractable cardiac arrhythmia has been reported as the primary cause of death in hypothermia. In these patients, death during hypothermia resulted from pulmonary complications. Ventricular arrhythmias, when they occurred, were responsive to routine measures such as electrical cardioversion and myocardial suppressant drugs. Methods of treatment are discussed.     

Adipose cell morphology and control of lipolysis in a patient with partial lipodystrophy.

A previously unreported patient with partial (cephalothoracic) lipodystrophy is described. Glucose tolerance and plasma lipids were normal, but plasma insulin increased to 340 muU/ml during an oral glucose tolerance test. Plasma free fatty acids were appropriately suppressed by oral glucose, insulin, and nicotinic acid, and were increased by infusion of norepinephrine. The lipolytic responses was also normal in response to two stimuli for endogenous catecholamine release: upright posture and 2-deoxyglucose infusion. There was a gradual development of postural hypotension in response to upright posture despite appropriate reflex tachycardia. Anhidrosis was present over the lower half of the body during this test, in a distribution corresponding to the area of adipose tissue hypertrophy. Anhidrosis was also seen in this region in response to warm ambient temperature. Adipose cells from the atrophic area were smaller than those from the hypertropic area, but the atrophic cells were only 65% of the volume of the hypertrophic cells by two different methods. Thus, loss of cells occurred. Glucose-1(-14)C utilization and in vitro lipolysis were similar in the two cell preparations; the difference were explicable by cell size and did not suggest a metabolic abnormality. Counts of unmyelinated nerves were similar in the two areas. These findings indicate that in this patient the lipodystrophy was associated with normal fat cells and an autonomic dysfunction. However, the findings cannot completely explain the pathogenesis of her disorder. Loss of fat cells, rather than symmetrical shrinkage, occurred in the upper half of the body.     

Mechanisms of pulmonary injury

Considered here are recent concepts concerning pathogenetic mechanisms underlying alterations in lung tissue structure and function. Mechanisms of pulmonary injury are described and include (1) the capacity of proteolytic enzymes to induce experimental pulmonary emphysema with particular emphasis on the effects of elastases and collagenases on connective tissue components, (2) the effects on distal lung units of specific chemical toxins, and (3) the capacity of the circulating polymorphonuclear leukocyte to induce pulmonary injury by the action of lysosomal enzymes. Evidence is reviewed which indicates a predominant role for alterations in alveolar elastin as the basis for alveolar tissue destruction along with the delayed effects on lung function and morphology of proteolytic injury. Newer developments in the understanding of the functions of the alpha₁-globulin and other proteolytic enzyme inhibitors in the respiratory tract are considered. The special characteristics of cell damage induced by noxious agents such as cadmium, nitrogen dioxide, ozone, high oxygen concentrations as well as alpha-napthyl-thiourea, alloxan and paraquat are discussed. Finally, the proteolytic capacity of the polymorphonuclear leukocyte and the links between the leukocyte proteases and the activation of leukokinin and bradykinin generating systems are summarized, and their role in the tissue injury induced by antibody-antigen reactions, shock lung and nonspecific tissue damage is indicated.     

Clinical effects of bilateral nephrectomy

The effects of removal of all renal tissue on hematopoiesis, osteodystrophy, blood pressure regulation and metabolic functions are reviewed; and, the indications for, and results of, bilateral nephrectomy are discussed. Nephrectomy results in a more severe anemia in dialysis patients which is poorly responsive to androgen therapy. No differences were detected in the severity of osteodystrophy between nephric and anephric patients. However, bilateral nephrectomy can occasionally result in the acute onset of hypocalcemia. Blood pressure regulation must be accomplishedin the absence of a functioning renin-angiotens in system. This is largely on the basis of volume, but changes in vascular tone may also be significant. Little is known about the metabolic consequences of nephrectomies. The effect on substances metabolized by the kidney is an area for further investigation. Kidney tissue should be preserved, if at all possible, and nephrectomy performed only for specific indications.     

Effect of glycerol on weight loss and hunger in obese patients

The effectiveness of oral glycerol as a dietary component or as a supplement to a 1000-kcal/day diet was examined in two studies involving obese patients. Glycerol did not differ from an equicaloric dose of glucose in its effect on hunger ratings, diet compliance or overall weight loss. We conclude that oral glycerol is not a useful adjunct to weight reduction programs.