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Biomedical subjects

J B Morris

Publications and source records attributed to J B Morris.

At least 73 records · Page 4Linked to original sources
PubMed1990

Role of surgery in antibiotic-induced pseudomembranous enterocolitis.

With the increased use of prophylactic and broad-spectrum antibiotics, pseudomembranous colitis has emerged as a significant clinical problem. Management with specific anti-Clostridium difficile therapy (vancomycin or metronidazole) has reduced mortality to less than 2%. Nevertheless, the disease may progress to a fulminant toxic colitis or colonic perforation. Additionally, another subset of patients will present with a dramatic clinical picture, suggesting acute peritonitis, eventuating in unnecessary laparotomy. This report reviews both the medical and surgical literature during the past 15 years of patients treated for pseudomembranous colitis. Analysis of this clinical data has provided us with the opportunity to both define the role of surgery in this disorder and illustrate the necessity for a combined medical and surgical cooperative approach in the early management of this iatrogenic disease.

Enterocolitis, Pseudomembranous↗
PubMed1990

The "right stuff": five Nobel Prize-winning surgeons.

Alfred Nobel's will specified that his estate be placed in a fund, the interest of which was to be distributed on an annual basis "to those who during the preceding year had conferred the greatest benefit on mankind." The first Nobel Prize in Physiology or Medicine was awarded in 1901, and its receipt is widely regarded as one of the highest accolades in science. This article reflects upon five surgeons who have been recognized as worthy of this honor. They are Emil Theodore Kocher, Alexis Carrel, Frederick Grant Banting, Werner Theodor Otto Forssman, and Charles Brenton Huggins. By winning this coveted prize these men have elevated the discipline of surgery to the summit of the scientific world. We review their legacy as an inspirational reminder of what we, the future of surgery, are capable.

Berlin↗
PubMed1989

Comparative pneumotoxicity of cyclopentadienyl manganese tricarbonyl and methylcyclopentadienyl manganese tricarbonyl.

The acute pneumotoxic effects of cyclopentadienyl manganese tricarbonyl (CMT) and methylcyclopentadienyl manganese tricarbonyl (MMT) were compared to delineate the role of the methyl side chain in the toxicity of these organomanganese compounds and to further our understanding of the mechanisms by which these compounds act. Specifically, lung manganese (Mn) burdens and the pneumotoxic response, as measured by bronchoalveolar lavage parameters, were determined in male Sprague-Dawley rats 24 hr after sc administration of 0.5, 1.0, or 2.5 mg Mn/kg as CMT or MMT. The pneumotoxic response to either compound was characterized by large increases in lavage albumin and protein content with smaller increases in lactate dehydrogenase levels. CMT was approximately twice as potent as MMT. This difference in potency may be due to methyl side chain oxidation, a metabolic detoxification pathway unavailable to CMT. Lung Mn content was significantly elevated after treatment with either CMT or MMT. Heptane extraction studies revealed that Mn was accumulated in a nonlipid soluble form, suggesting the accumulation of metabolites rather than heptane soluble parent MMT or CMT. A strong correlation between pulmonary Mn content and toxicity was observed, suggesting a causal relationship between the accumulation of CMT or MMT metabolites and toxicity. Piperonyl butoxide diminished both the pneumotoxicity and Mn accumulation resulting from CMT or MMT, suggesting both phenomena are due to monooxygenase metabolites. Pulmonary nonprotein sulfhydryl (NPSH) levels were increased twofold 24 hr after administration of either CMT or MMT. Depletion of NPSH was not observed 1.5 or 6 hr after administration. The mechanisms of this response are unclear but may be due to the metabolism of CMT or MMT to unstable compounds which release inorganic Mn within pulmonary cells.

Albumins↗
PubMed1988

Haemodynamic characterization of the isolated (denervated) parabiotically perfused rat jejunum.

The isolated (denervated) parabiotically perfused rat jejunum was characterized for base-line haemodynamics, autoregulation of blood flow and oxygen consumption and long-term (3 h) stability with respect to both haemodynamics and the absence of tissue injury. In short-term experiments, the parabiotically perfused preparation autoregulated oxygen consumption but not blood flow over a wide range of perfusion pressures (25-85 mmHg). When the intestinal segment was subjected to near total ischaemia for I h, followed by I h of reperfusion, mucosal injury was induced which could be prevented by i.v. administration of superoxide dismutase after ischaemia just prior to reperfusion, or allopurinol prior to ischaemia. These findings support the concept of post-ischaemic reperfusion injury in the denervated preparation without hepatic ischaemia. This preparation could thus serve as an improved model for the study of the pathophysiology of post-ischaemic reperfusion injury in the rat intestine.

Animals↗
PubMed1987

Protection of the small intestine from nonocclusive mesenteric ischemic injury due to cardiogenic shock.

In a pericardial tamponade model of cardiogenic shock in pigs, we had previously shown that acute reductions in cardiac output produce severe mesenteric ischemia due to disproportionate splanchnic vasoconstriction. In this study, we extended the period of cardiogenic shock in order to investigate the pathogenesis of ischemic injury to the small intestinal wall. Four hours of tamponade produced sustained changes in splanchnic hemodynamics, similar to those observed in the prior short-term experiments. The resultant mesenteric ischemia caused necrotic lesions of the small intestine which were characteristic of those seen in nonocclusive mesenteric ischemia in human subjects. Prior alpha-adrenergic blockade failed to prevent either sustained mesenteric vasospasm or ischemic injury. In contrast, prior blockade of the renin-angiotensin axis, whether by nephrectomy or angiotensin-converting enzyme inhibition, blocked the splanchnic vasoconstriction, and thereby protected the small intestine from ischemic injury. The primary hemodynamic and pathologic features of this model of nonocclusive mesenteric ischemia appear to be mediated by the renin-angiotensin axis.

Animals↗
PubMed1987

Metabolism and deposition of propanol and acetone vapors in the upper respiratory tract of the hamster.

While it is thought that local metabolism may enhance nasal deposition of inspired vapors, there have been no studies designed to quantitate this effect. In the current study, deposition of 1-propanol (a metabolized vapor) and acetone (a nonmetabolized vapor) was studied in the surgically isolated upper respiratory tract (URT) of the anesthetized Syrian hamster. The effect of inspiratory flow rate on URT deposition of acetone could be described by a ventilation-perfusion (V-P) model with a nasal perfusion rate of 0.046 ml/min. Theoretical considerations predict that at enzyme saturation, deposition efficiency will be dependent upon the inspired concentration and the URT metabolism rates can be estimated from the concentration-dependence data. A concentration dependence on propanol deposition efficiency was observed at a flow rate of 200 ml/min, but not at 38 or 71 ml/min. At a flow rate of 200 ml/min, an apparent URT metabolism rate of 3.8 micrograms/min (95% confidence limits 0.5-7.1 micrograms/min) was estimated. In vitro studies on nasal tissue homogenates provided metabolism rates of approximately 2 micrograms/min, values which did not differ significantly from, and therefore, were in reasonable agreement with, the estimates from the deposition studies. After correction for the effect of metabolism, URT propanol deposition could be described by the V-P model with a nasal perfusion rate of 0.050 ml/min. This value did not differ significantly from that observed in the acetone studies. Thus, deposition of both propanol and acetone in the URT of the Syrian hamster could be described by the V-P model.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Propanol↗
PubMed1987

Disposition and toxicity of methylcyclopentadienyl manganese tricarbonyl in the rat.

The disposition and toxicity of methylcyclopentadienyl manganese tricarbonyl (MMT) was studied in Sprague-Dawley rats after subcutaneous administration at a dose of 4 mg/kg. Blood, lung, liver and kidney Mn levels were increased between 1.5 and 96 h after MMT injection, with peak organ levels occurring at 3-6 h. At this time the MMT-derived Mn concentration in lung, liver and kidney averaged 13-, 4- and 4-fold higher, respectively, than in the blood, indicating the accumulation and retention of MMT (or metabolite) in these tissues. Maximal pulmonary toxicity, as assessed by pulmonary lavage protein levels, occurred 24-48 h after injection. Plasma urea and sorbitol dehydrogenase levels were not increased at any time after MMT, suggesting minimal or no hepatic or renal injury. That maximal pulmonary toxicity occurred after peak Mn accumulation, and that the organ-specific toxicity of MMT correlated with its accumulation and retention, suggests a causal relationship between tissue Mn accumulation and MMT-induced toxicity.

Animals↗
PubMed1987

Mucus protection and airway peroxidation following nitrogen dioxide exposure in the rat.

In the current study, biochemical measures of lipid peroxidation following 4-h inhalation exposure to 76 mg/m3 (40 ppm) nitrogen dioxide were correlated with measures of deposition and tissue antioxidant levels in the nasal cavity and the trachea of the Fischer rat. In addition, respiratory-tract mucus samples were collected via esophageal cannulation and nasopharyngeal lavage over known time periods, and were analyzed for phospholipid (PL) content to provide an index of the unsaturated lipids (UL) that they may contain. UL are thought to be important in the scavenging of oxidants by the mucous lining layer. Nasal deposition efficiency, as measured in the surgically isolated upper respiratory tract under unidirectional flow conditions, averaged 25%, corresponding to an absolute deposition rate of 41 nmol/min. Vitamin E levels averaged 1.7, 5.9, and 0.7 nmol/mumol PL in nasal, tracheal, and pulmonary tissues, respectively. The level in the trachea was significantly (p less than 0.005) higher than in the other tissues. As estimated from the increase in lavage PL content over 1 h, the overall mucous PL transport rate was less than 0.013 nmol/min, suggesting the PL of the mucous lining layer could not offer significant protection against the inhaled NO2. Conjugated dienes were detected in two of four pooled nasal tissue samples. Thiobarbituric acid-reactive material levels in tracheal tissues were significantly elevated over control levels by NO2 (p less than 0.05). Thus, despite the relatively high vitamin E levels, 4-h NO2 exposure appeared to result in lipid peroxidation in the trachea and, perhaps, in the nasal airways of the rat, a result that correlated with the apparent lack of oxidant-scavenging species in the mucus lining these airways.

Animals↗
PubMed1987

The fundamental hemodynamic mechanism underlying gastric "stress ulceration" in cardiogenic shock.

Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such that cardiac output was reduced to 38 +/- 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. "Blinded" gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric "stress ulceration" syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal "stress ulceration" is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the "shock liver" syndrome, gastric "stress ulceration" is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis.

Animals↗
PubMed1987

Group psychotherapy for prolonged postnatal depression.

Twelve women who had been depressed for more than one year after the birth of a child were offered group psychotherapy. Seven accepted. Our therapy aimed at providing the opportunity for supportive and confiding relationships to develop between the women in the group and the therapists. The Kelly repertory grid and Beck Depression Inventory administered before and after group therapy showed that group psychotherapy helped the women considerably.

Adult↗
PubMed1986

Species differences in upper respiratory tract deposition of acetone and ethanol vapors.

Regional deposition patterns determine the dose of inhaled gaseous toxicant received by various areas of the respiratory tract. To study potential species differences in upper respiratory tract (URT) deposition of acetone and ethanol vapors, and to determine if deposition of these vapors could be described by a ventilation-perfusion (V-P) model, URT deposition efficiencies of these vapors were measured over a 12- to 18-min period at selected flow rates in the surgically isolated URT of urethane-anesthetized Fischer rats and Hartley guinea pigs. For both gases in both species, deposition efficiencies were significantly dependent upon inspiratory flow rate (p less than 0.0005). The V-P model predicts a linear relationship will exist between the ratio of the deposited to the nondeposited fraction and the inverse of the inspiratory flow rate. Such relationships were observed for deposition of acetone (r = 0.93, p less than 0.0005) and ethanol vapors (r = 0.95, p less than 0.0005) in the guinea pig and for deposition of acetone vapor (r = 0.95, p less than 0.0005) in the rat. In contrast, a linear relationship was not observed for ethanol in the rat suggesting that deposition mechanism(s) differ for this vapor in this species. Despite the fact that the surface area of the URT of the guinea pig is greater than that of the rat, URT deposition of these vapors was as much as twice as efficient in the rat as in the guinea pig (p less than 0.0005). This effect was not due to different blood:air partition coefficients as they were identical in both species. In toto, these results suggest there may be important anatomic and/or physiologic differences in the URT of the Hartley guinea pig and Fischer rat. Such differences may have to be considered when comparing the response(s) of these species to toxic gases or when extrapolating data obtained from these species to the human.

Acetone↗
PubMed1986

Quantitation of mucous glycoprotein removed from the respiratory tract of the rat by pulmonary lavage.

Mucous glycoprotein (MGP) hypersecretion is a cause of chronic pulmonary obstructive disease and is also a common response of the pulmonary airways to toxicant-induced injury. To examine the feasibility of employing pulmonary lavage to assess the airway MGP content of the rat, the MGP removed from the lungs of male Sprague-Dawley rats by three successive lavages with cold isotonic saline were solubilized with urea and mercaptoethanol, and were purified by ultrafiltration and Sepharose CL-6B gel chromatography. MGP, which elute with the void volume of this gel, were quantitated by their carbohydrate content. Initial studies revealed that succeeding lavages removed succeedingly less MGP, suggesting that some pool of MGP was being washed out by this procedure. In a second study, isoproterenol was administered by a regimen known to produce MGP hypersecretion in the rat as assessed by histologic criteria (100 mg/kg/day, sc, for 6 days). Lavage MGP content of isoproterenol-treated rats averaged 450 micrograms compared to 210 micrograms in vehicle-treated controls (p = 0.01). In summary, it is possible to purify and quantitate the MGP removed from the airways of the rat by pulmonary lavage and the amount of lavagable MGP is approximately doubled by isoproterenol, an agent known to induce the morphologic signs of mucous hypersecretion.

Animals↗
PubMed1986

Deposition of ethanol and acetone vapors in the upper respiratory tract of the rat.

The deposition of nonreactive gases in the lungs is well studied and is dependent on the ventilation-perfusion relationships of that organ. The current investigation was undertaken to determine if pulmonary ventilation-perfusion models could be successfully applied to quantitatively describe upper respiratory tract (URT) deposition of acetone and ethanol vapors. Toward this end, the deposition of these vapors was measured in the surgically isolated URT of the anesthetized rat at selected inspiratory flow rates (ranging from 70 to 500 ml/min) and exposure times (ranging from 3.3 to 13.3 min). The deposition of acetone in the URT followed apparent quasi-steady-state conditions, suggestive of a ventilation-perfusion relationship. Pulmonary ventilation-perfusion models predict the ratio of the amount deposited to the amount not deposited should be linearly related to the inverse of the inspiratory flow rate. Such a relationship was observed for URT acetone (r = 0.988, N = 16,p less than 0.0001) and ethanol (r = 0.963, N = 20, p less than 0.0001) deposition. From the deposition-flow relationships estimates of 0.31 and 0.33 ml/min were obtained for nasal blood flow in the ethanol and acetone studies, respectively. The 95% confidence limits for these estimates overlapped. The successful application of a ventilation-perfusion model to describe URT deposition suggests that acetone and ethanol vapors equilibrate between the inspired airstream and the capillary blood of the URT and that their deposition is dependent on both the URT ventilation and perfusion rates.

Acetone↗
PubMed1986

Pathogenesis of nonocclusive ischemic colitis.

The nonocclusive component of ischemic colitis in anesthetized pigs was mimicked using cardiogenic shock produced by pericardial tamponade. Increases in pericardial pressure produced decreases in arterial pressure (PA) and cardiac output (CO), with corresponding rises in total peripheral resistance (i.e., cardiogenic shock). This was associated with marked reductions in blood flow through the inferior mesenteric artery (IMA), due primarily to disproportionate increases in IMA vascular resistance. Levels of plasma renin activity correlated closely with these changes in mesenteric hemodynamics. Confirmed, total alpha adrenergic blockade with phenoxybenzamine failed to block this selective mesenteric vasoconstriction, while ablation of the renin-angiotensin axis with captopril completely abolished it, thereby ameliorating the colonic ischemia. Central intravenous infusions of pathophysiologic levels of angiotensin II, without tamponade, mimicked the response to shock seen with tamponade alone. In an additional group of pigs, 4 hours of sustained shock (tamponade) followed by 2 hours of normotension (release of tamponade and resuscitation) produced lesions characteristic of ischemic colitis, including full-thickness mucosal ulceration. Such lesions were ameliorated significantly in pigs in which the renin-angiotensin system had been ablated by bilateral nephrectomy. Nonocclusive ischemic colitis appears to be mediated primarily by a remarkable sensitivity of the colonic vasculature to the renin-angiotensin axis.

Animals↗
PubMed1983

Identification of two forms of fluorine in tissues of rats inhaling hydrogen fluoride.

Nonionizable fluorine has been detected in the plasma of several species including the human, however, the exact nature and source of this fluorocompound(s) remain unknown. In the current investigation, the fluoride ion sensitive electrode was employed to determine the fluoride content of ashed (total F) and unashed (ionic F-) tissues of rats exposed to hydrogen fluoride (HF). Total fluorine concentration consistently exceeded ionic fluoride concentration in tissues of HF-exposed rats, suggesting the presence of fluorine in unashed tissue which did not respond to the F- ion sensitive electrode. The concentration of this nonresponding fluorine fraction, termed the delta F fraction, was estimated by subtracting the ionic F- from the total F concentration of each sample. Pulmonary and plasma delta F concentrations increased with time following whole body inhalation exposure to HF. It was possible to separate delta F from ionic F- by calcium phosphate adsorption, indicating that the delta F fraction consists of nonionizable fluorine. Upon Sephadex G-25 gel chromatography, plasma delta F migrated near the bed volume, providing evidence that it is of low molecular weight. Finally, a strong correlation (r = 0.99, p less than 0.01) between plasma delta F concentration and airborne HF concentration was observed, indicating that inorganic fluoride (as HF) is the ultimate source of the low-molecular-weight, nonionizable fluorine species present in tissues of HF-exposed rats.

Animals↗