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Biomedical subjects

E D Robin

Publications and source records attributed to E D Robin.

At least 55 records · Page 3Linked to original sources

Cardiopulmonary function at maximum tolerable constant work rate exercise following human heart-lung transplantation.

Studies were performed measuring parameters of respiratory and circulatory function at rest and during maximum tolerable constant work rate treadmill exercise in 16 clinically well patients who had undergone heart-lung transplantation for end stage pulmonary hypertension. Ten patients were studied before and within eight weeks following transplantation. Long-term function with exercise was further evaluated with follow up studies at one year (n = 10) and two years (n = 6), posttransplantation. Posttransplant gas exchange and ventilation during exercise are essentially normal with neither being limiting to maximal exercise. Exercise capacity is significantly improved posttransplant, primarily as a result of improvement in the circulation over that found pretransplant in uncorrected pulmonary hypertension. Although improved, circulatory limitations of maximal exercise may still persist. Cardiorespiratory function at maximum tolerable exercise is well maintained following heart-lung transplantation for at least two years, providing no complications occur. This suggests that denervation of the heart and lungs, disruption of the bronchial circulation and pulmonary lymphatics, and the graft ischemia encountered at the time of transplantation impose no serious limitations on long-term cardiopulmonary function. The overall functional capacities of the transplanted heart and lungs are more than adequate for meeting the activities of normal life.

Adult↗

Lung immunogenicity, rejection, and obliterative bronchiolitis.

Evidence suggests that obliterative bronchiolitis (OB) following human heart-lung transplantation is a form of allograft rejection related to augmented expression of class II major histocompatibility complex antigens (MHCII) on airway epithelium and mediated by activated T cells. Other forms of OB, including those related to viral infection and autoimmune disease, may reflect a similar mechanism.

Bronchitis↗

Hyperbaric oxygen. A therapy in search of diseases.

The application of HBO to the therapy of various human diseases developed over a 300 year period. Like most of medicine, the basis of these applications was and continues to be pragmatic in nature, and involves uncritical and untested judgments. The possibility of risks has been understated and possible benefits have been overstated. Individual physicians offering HBO and organized groups, such as the Undersea Medical Society, advocating its use may well be highly motivated, well meaning, and sincerely convinced that HBO is an important therapeutic approach. It may be that, buried among the host of indications, will be some disorders for which HBO is uniquely and highly effective. If so, the present nonsystem for evaluating responses to HBO will require modification, so that these potentially valuable additions to therapeutics are not lost. Because of its almost global application to a wide variety of diseases, HBO therapy lends itself easily to medical adventurism (therapy in search of a disease) and economic exploitation. If there is some patient benefit to come from the experience of the last 300 years, changes in approach, initiated by baromedical devotees or by medicine generally, or resulting from pressures outside of medicine, will be required.

Decompression Sickness↗

Obliterative bronchiolitis after heart-lung transplantation: apparent arrest by augmented immunosuppression.

Obliterative bronchiolitis has been the major complication in long-term survivors of human heart-lung transplantation at our institution. We have assessed the effect of the introduction of a third immunosuppressive agent, azathioprine, on the rate of decline in airflow variables in eight heart-lung transplant recipients with obliterative bronchiolitis, and have compared this rate with that in five patients who did not receive augmented immunosuppressive therapy. Specifically, the rate of decline in forced expiratory flow rate between 25% and 75% of vital capacity improved considerably after institution of this therapy (-5.25 +/- 2.85 compared with -0.27 +/- 0.66 [mean +/- SD]; p less than 0.005), whereas the effect on the ratio of forced expiratory volume in one second to forced vital capacity was more modest (-3.61 +/- 1.52 compared with -0.54 +/- 0.93; p less than 0.005). The rate of decline in airflow variables was similar in both groups before the institution of therapy with azathioprine. These results show that augmented immunosuppressive therapy is capable of slowing the rate of progression of obliterative bronchiolitis in this population; they also suggest that the obliterative bronchiolitis may represent a form of chronic pulmonary allograft rejection.

Adult↗

Twenty-eight cases of human heart-lung transplantation.

Between March, 1981, and August, 1985, twenty-eight heart-lung transplant operations were done in 27 patients at a single institution. 8 patients died in the perioperative period and adhesions related to previous thoracic surgery proved to be a major risk factor for postoperative haemorrhage. Obliterative bronchiolitis developed in half of the 20 long-term survivors, a mean of 11.2 months (range 2-35 months) after surgery: 4 of these patients died, 3 are functionally limited, 2 were successfully treated with corticosteroids, and the remaining patient was successfully retransplanted. The other 10 long-term survivors returned to a normal life with essentially normal pulmonary function measured at a mean of 22.6 months (range 4-42 months) after transplantation. All the surviving patients have evidence of renal impairment related to cyclosporin nephrotoxicity. The results indicate that, although heart-lung transplantation is compatible with essentially normal long-term pulmonary function, the procedure should not yet be regarded as a routine clinical intervention.

Airway Obstruction↗

Indiscretion enteritis. A Rabelaisian syndrome.

A 76-year-old man had small bowel obstruction and organic small bowel disease following a series of bizarre massive gustatory insults that involved food, medications, and mega-mineral-vitamin supplements. Intestinal obstruction required partial small bowel resection. The dietary indiscretions resulted in severe enteritis (indiscretion enteritis). The sequence has been termed a Rabelaisian syndrome after the great French writer and physician, Francois Rabelais, who vividly described bizarre gustatory habits. Gut injury may result from unwise oral intake of various foods and mineral supplements.

Aged↗

Neurogenic hyperacute ascites in mice.

Four groups of mice were subjected to controlled fatal head trauma and then evaluated for the presence of ascites (neurogenic hyperacute ascites, NHA). The animals died virtually instantaneously and without evidence of maintained pain or suffering. The volume of ascites was determined in one group of animals. Two of the traumatized groups were pretreated, one with the beta-blocker propranolol and the other with the alpha-blocker phentolamine. A fifth, non-traumatized, group which was killed with either inhalation served as a control group. Two more groups of non-traumatized mice were administered either the alpha-adrenergic agonist methoxamine hydrochloride or the beta-agonist isoethrane mesylate before killing by ether inhalation, and then evaluated for ascites. Transudative ascitic fluid was found in 87-100% of untreated traumatized mice and in no control animals. Pretreatment with phentolamine had no effect on the prevalence of ascites. Pretreatment with propranolol produced a significant decrease in the prevalence of ascites compared with trauma alone (P less than 0.001). Isoethrane (beta-agonist) administration caused ascites in 100% of the treated animals. Methoxamine (alpha-agonist) administration did not cause ascites. A previously undescribed consequence of acute brain trauma is described (NHA) which appears to be mediated by beta-sympathetic activity of central origin. NHA is inhibited by beta-blockade and can be simulated with beta-agonist administration.

Acute Disease↗

Augmented ventilatory response to exercise in pulmonary hypertension.

The ventilatory response to submaximal exercise, defined as the slope of minute ventilation over carbon dioxide production (VE/VCO2), was determined in 12 normal subjects, ten patients with pulmonary hypertension before and after heart-lung transplantation, and eight patients following heart transplantation. Patients with pulmonary hypertension show an augmented ventilatory response compared to normal subjects (pulmonary hypertension [mean, 57.7 +/- 6.8 (SE) ml/ml VCO2; normal subjects, 22.3 +/- 1.4 ml/ml VCO2; p less than 0.001]). Following heart-lung transplantation, VE/VCO2 slope fell to 24.7 +/- 1.6 ml/ml VCO2, a value which is not significantly different than the value in normal subjects. Patients after heart transplantation show a mean slope value of 25.3 +/- 1.3 ml/ml VCO2, which is not significantly different than the normal value or the value found after heart-lung transplantation. The augmented ventilatory response to exercise did not correlate with the usual chemical modulators of ventilation (arterial pH, arterial carbon dioxide tension, or arterial oxygen tension). These results suggest the following: the existence of a neural system in patients with pulmonary hypertension which results in an augmentation of ventilatory drive in response to exercise; the augmented ventilatory response reflects excessive neural activity of pulmonary afferents during exercise; narrow regulation of the ventilatory response to exercise in normal subjects which is preserved in the denervated lung, indicating that pulmonary afferents are not critical to ventilatory control during exercise in the normal subject; and the possible use of measurements of the ventilatory response to exercise as a noninvasive screening test for pulmonary hypertension.

Adult↗

The recrudescent epidemic of retrolental fibroplasia.

We are probably observing a recrudescent epidemic of RLF which has elicited surprisingly little attention from the medical community. Given present data, it is not unreasonable to conclude that there is a true epidemic and that its etiologic basis involves a population of infants with high susceptibility to oxygen toxicity whose oxygen status is being monitored by methods which are not sufficiently accurate to provide the necessary narrow limits of permissible O2 administration. A clinical trial which looked at the outcome of premature infants with and without transcutaneous O2 monitoring would be useful not only to determine the impact on the prevalence of RLF, but also to determine the role of this technology in the management of premature infants generally.

Disease Outbreaks↗