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Biomedical subjects

R D Rink

Publications and source records attributed to R D Rink.

At least 19 recordsLinked to original sources
PubMed2000

Analysis of pulmonary fat embolism in blunt force fatalities.

OBJECTIVE: To investigate the incidence, severity, and origin of pulmonary fat embolism (PFE) in persons dying from blunt force trauma within 24 hours of injury. METHODS: The study population consisted of blunt force fatalities. Controls were subjects dying from natural causes or nonblunt force injury. Tissue was removed from lung lobes and prepared for histologic examination using osmium tetroxide to stain for fat. Lung sections were graded for PFE on a scale of 0 (no emboli) to 4 (five or more emboli in a majority of fields). RESULTS: The blunt force group consisted of 56 decedents. Mortality was 93% within 4 hours. Fractures were present in 54 (96%) of decedents, and soft tissue injury was universal. Thirty eight (68%) of decedents were positive for PFE vs. 3 of 20 (15%) in controls. Mean score for PFE was 2.94 +/- 1.15 and 1.01 +/- 0.94, respectively (p < 0.005). Bone marrow emboli were not observed in any of the sections. Severity of PFE was positively associated with survival time. Analysis of PFE against sex, age, height, weight, number of injuries, and number of fractures showed no significant correlations. CONCLUSIONS: A significant degree of PFE develops rapidly in a majority of persons dying of blunt force trauma. Although the source of fat for embolization has been suggested to be bone marrow, no evidence of myeloid tissue was found in any of the lung sections. Nor was there a correlation of PFE and number of fractures. Soft tissue injury is considered the primary cause of PFE.

Adolescent↗
PubMed2000

Inframammary fold: a histologic reappraisal.

The inframammary fold is a defining element in the shape and structure of the female breast. It should be preserved whenever possible in ablative procedures and recreated accurately when the breast is reconstructed after mastectomy. To date, no accurate anatomic description of this essential structure exists. Previous studies have suggested that the fold is produced by a supporting ligament running from the dermis in the fold region to a variety of locations on the rib cage. This clinic's experience with mastectomy, augmentation mammaplasty, and breast reconstruction does not support the existence of a ligamentous structure. To define the structure of the inframammary fold, 10 female and 2 male cadavers were studied. The anterior chest wall was removed en bloc and frozen in orthostatic position. Parasagittal sections were made of the inframammary fold with the chest wall intact. After decalcification of the ribs and routine histologic preparation, thin sections were stained with Gomori's trichrome. On light microscopic examination, no demonstrable ligamentous structure of dense regular connective tissue could be identified in the fold region in any of the 12 specimens. Superficial and deep fascial layers were uniformly observed anterior to the pectoralis major and serratus anterior muscles. The superficial fascia was connected to the dermis in the fold region in a variety of configurations. In some cases, the deep fascia fused with the superficial fascia and dermis at the fold level. In other cases, bundles of collagen fibers arising from the superficial fascial layer were found to insert into the dermis at the inframammary fold, slightly inferior to it, or both. These bundles were observed consistently in sections from the sternum to the middle axillary line. They were distinct from Cooper's suspensory ligaments, which are seen more superiorly in the glandular tissue.

Aged↗
PubMed1986

Ultrastructure of bone marrow of rats after severe hemodilution with starch or modified hemoglobin.

The ultrastructure of bone marrow of rats was studied 24 h after exchange-transfusion with solutions of starch or modified hemoglobin to a hematocrit of 10-15. Blood smears of the transfused rats had 17-20% reticulocytes as compared to 5-6% for sham operated controls. In the transfused rats marrow macrophages had numerous heterolysosomes apparently containing the starch or hemoglobin from the transfused solutions. Endothelial cells and reticular cells also possessed a few heterolysosomes thought to contain starch or hemoglobin. Reticular cells of the transfused rats contained numerous glycogen particles scattered throughout the cytoplasm or arranged in large masses. Synthesis of glycogen may indicate a metabolic change in reticular cells in response to tissue hypoxia induced by the exchange-transfusion procedure.

Animals↗
PubMed1985

Effects of exchange transfusion with perfluorochemical emulsions on hepatic oxygen supply and blood flow in the rat.

Exchange-transfusion to hematocrit 20 with isotonic perfluorochemical (PFC) emulsions containing 3% hydroxyethylstarch (HES) in rats breathing 100% oxygen produced significant reductions of hepatic PO2 and blood flow in comparison to rats hemodiluted with isotonic 3% or 6% HES solution. The results indicate that PFC and/or emulsifiers were associated with adverse effects on liver blood supply.

Animals↗
PubMed1985

Effects of scald injury on hepatic PO2, blood flow, and ultrastructure in the rat.

Stagnant hypoxia has been suggested as a significant factor underlying acute liver disease following thermal injury. To examine this possibility in circumstances of moderate scald injury, rats were dipped (15% body surface area) in 90-95 degrees C water for 25 sec, fluid resuscitated, and studied at 1, 6, and 24 h. Hepatic PO2, obtained by multicathode surface measurement, was reduced significantly at 1 h (10.8 vs. 20.8 mm Hg in controls), although clearance times for low dose indocyanine green (ICG) suggested normal liver blood flow. The reduction of PO2 was transient; at 6 h levels were only slightly lower than in controls. At 24 h, however, liver PO2 was again reduced significantly, albeit less deeply (14.9 mm Hg). Increased clearance times for low and high dose ICG at 24 h suggested impairment of both blood flow and hepatocyte function. Hepatic ultrastructure showed foci of cells with anomalous and degenerate mitochondria, atypical of those associated with hypoxia. Sinusoids were often occluded by aggregates of vesicles of hepatocyte origin. It is not clear that acute restriction of oxygen availability during the first hour postburn was of sufficient intensity to cause the liver pathology evident at 24 h.

Animals↗
PubMed1983

Hepatic oxygen supply during early and late sepsis in the rat.

Hepatic oxygen supply and related parameters were evaluated during early (8-10 h) and late (18-26 h) stages of lethal septic peritonitis induced in rats by cecal ligation and puncture. In the early phase, hepatic pO2 was reduced significantly (mean 9.3 versus 22.2 mmHg in sham-operated controls). This was accompanied by elevations of serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase (p less than 0.02 and p less than 0.10, respectively), and increased hematocrit (p less than 0.001). Total body oxygen consumption was decreased by 19% (p less than 0.001). By the late stage of sepsis, hepatic oxygen supply was depressed profoundly (mean 2.0 versus 24.5 mmHg in controls) concomitant with further elevations of serum transaminases. Lactacidemia, respiratory alkalosis, and tachycardia were also present. Hypoxemia and hypotension were not observed during either early or late stages. Our results may be interpreted as representing early and progressive impairment of hepatic oxygen delivery in rats subjected to cecal ligation and puncture.

Alanine Transaminase↗
PubMed1982

An experimental model of intraabdominal abscess in the rat.

Suitable small animal models of intraabdominal abscess are not available. We have developed a reliable model of intraabdominal abscess in the rat by fasting the animal overnight, devascularizing and ligating the cecum, and injecting 2.5 X 10(8) Escherichia coli and 2.5 X 10(9) Bacteroides fragilis into the ligated cecum. This model results in 39% coli acute mortalities within 48 hours from acute peritonitis, and abscess in 76% of survivals. Subsequent abscesses are 1.0--1.5 ml in volume and contain 4 X 10(8) E coli/ml of pus and 1.4 X 10(9) B fragilis/ml. This model allows chronic evaluation of sepsis in small animals and provides a convenient means to study the abscess microenvironment.

Abdomen↗
PubMed1982

Effects of pure or combined inocula of Escherichia coli and Bacteroides fragilis on the liver and related metabolism.

To test for synergy between a facultative and anaerobic bacterium and the role hepatic hypoxia may have in its development, rats were subjected to intravascular infusion of 10(8) Escherichia coli, 10(9) Bacteroides fragilis, or a combination of both. Acute effects were evaluated by selected 6-hour measurements, including hepatic pO2, and longer range effects by liver cultures and histology in rats surviving 7 days. During the acute period, systemic arterial pressure and pO2 in bacteremic groups did not differ from saline-infused controls. However, hepatic oxygen supply was significantly reduced in E. coli rats and those given the combined bacteria (mean hepatic pO2 less than 10 mm. Hg versus 20.8 mm. Hg in controls). Significant increases of plasma lactate and pulse rate were also recorded. By comparison, hepatic pO2 was not reduced significantly in the B. fragilis rats, and pulse rate was similar to controls. Plasma lactate, however, increases more rapidly than in other groups. Survival rates were 100 per cent in the B. fragilis group, 88 per cent in the E. coli group, and 65 per cent in the combined group. The difference between the latter groups was not significant. Hepatic histology was normal in rats of the B. fragilis group at 7 days postchallenge. In survivors of the E. coli and combined inoculum groups, there was evidence of anoxic damage and occasional foci of neutrophilic infiltration. Liver cultures were more often positive in rats of the combined inoculum group (p less than 0.05), most often for E. coli, than in the other groups. In summary, although the acute effects of E. coli were not changed appreciably by combination with B. fragilis, the higher rate of E. coli liver infection in survivors suggests that its viability was enhanced. The role of hepatic hypoxia in this remains unclear. It is feasible that hypoxic foci provided temporary protection for B. fragilis, enabling the organisms to affect favorably the survival of E. coli.

Animals↗
PubMed1981

Alterations of oxygen metabolism in experimental bacteremia.

To examine the mechanisms underlying organ failure and disordered cellular metabolism in sepsis, systemic oxygenation, hepatic tissue oxygenation, and hepatic mitochondrial metabolism were studied in rats subjected to an LD100 dose of E. coli bacteria administered intravascularly. The animals maintained normal systemic oxygenation and remained normotensive during the six-hour study period. Hepatic tissue pO2 declined nearly 90% in comparison to controls. Isolated hepatic mitochondria demonstrated statistically increased respiratory control indices that are characteristic of cellular hypoxia. Histologic examination of liver tissue showed obliteration of the sinusoids with debris and cellular aggregates. The data suggest that altered cellular oxygen delivery secondary to sinusoidal obliteration may have significance in hepatic failure and subsequent death in septic patients.

Animals↗
PubMed1981

Effects of live Escherichia coli and Bacteroides fragilis on metabolism and hepatic pO2.

Rats were infused intraaterially with 10(9) live E coli, or 10(10) live B fragilis, or 0.9% NaCl solution. Within 6 hr or sooner E coli-treated rats extensive hepatic hypoxia (mean hepatic pO2 less than 5 mm Hg), hypoglycemia, lactacidemia, and microscopic evidence of sinusoidal damage and hepatocyte hypoxia. Mortality was 100% within 24 hr. Rats which received B fragilis showed significantly less hepatic hypoxia (mean hepatic pO2 13.8 mm Hg) and lactacidemia and were euglycemic at 6 hr. Hepatic tissue showed congested sinusoids and depletion of glycogen. Mortality was 0% in 24 hr. NaCl-treated rats were stable over 6 hr of observation; mean hepatic pO2 was 20.6 mm Hg. We suggest that the events associated with acute lethal E coli bacteremia are related in part to strutural interference of the hepatic microcirculation. Although the effects of B fragilis bacteremia were appreciably less pronounced, the ability to establish hypoxic foci may have important implications.

Animals↗
PubMed1980

Effects of phentolamine on hepatic PO2 in endotoxemia.

The effect of phentolamine, an alpha-adrenergic blocker, on hepatic oxygen supply, plasma glucose, and lactate, and survival in fasted male rats administered Echerichia coli endotoxin (25 mg/kg, ip) has been studied. Survival at 24 h was 8% in untreated endotoxic rats, 83% in rats receiving phentolamine (5 mg/kg, ip) and endotoxin, and 100% in phentolamine controls. Measurements during the initial 8 h postendotoxin recorded transiently lower systemic arterial pressure in the phentolamine-endotoxic rats. Arterial PO2 and increases of pH and heart rate were similar in both endotoxic groups. Lactacidemia, present by 4 h in untreated endotoxic rats, did not develop in the phentolamine group and plasma glucose was significantly higher at 8 h (98 +/- 2.5 vs. 77 +/- 5.6 mg%, mean +/- SE). Mean hepatic PO2 at 6 h in phentolamine-endotoxic rats was 9.6 mmHg with 28% of the values below 5 mmHg. By contrast, the mean in untreated endotoxic rats was 1.9 mmHg with 88% of values below 5 mmHg. Phentolamine controls were stable over 8 h; mean hepatic PO2 was 17.7 mmHg. The differences in plasma glucose and lactate suggest protection of hepatic metabolism in phentolamine-treated endotoxic rats by prevention of excessive hepatic hypoxia.

Animals↗
PubMed1979

The effect of methylprednisolone on hepatic oxygen supply and plasma lactate and glucose in endotoxemia.

This study was designed to determine the effect of methylprednisolone on the profile of hepatic oxygen supply and selected blood parameters in fasted, male rats administered an LD85 dosage of E coli endotoxin intraperitoneally. Mortality rates within 24 hours were 85% in rats receiving endotoxin only, 9% in rats receiving a 30 mg/kg dosage of methylprednisolone intraarterially one hour subsequent to endotoxin insult, and 0% in methylprednisolone controls. Beginning with the fourth hour, untreated endotoxin rats had significantly higher heart rates and lower plasma glucose; by the sixth or eighth hour there was significantly greater hypocapnia, lower blood pH, and higher plasma lactate levels in comparison to endotoxic rats receiving methylprednisolone. In addition, mean hepatic pO2 between the sixth and seventh hours was 2.6 mm Hg in endotoxic rats, 10.6 mm Hg in endotoxic methylprednisolone rats, and 17.7 mm Hg in methylprednisolone controls. Methylprednisolone controls showed a steady increase of plasma glucose levels through eight hours but were otherwise stable. Maintenance of hepatic circulation is cited as the probable basis for differences of morbidity and mortality between treated and glucocorticoid-treated endotoxic rats.

Animals↗
PubMed1979

Hepatic cellular hypoxia in murine peritonitis.

Reduced oxygen consumption and lactic acidosis were observed frequently in patients with peritonitis. This study was designed to evaluate whether reduced oxygen consumption is secondary to deficient oxygen delivery or is a function of primary injury to mitochondria. Peritonitis was produced in rats by cecal ligation and perforation. Animals were killed at 2, 4, and 6 hours and agonally. Oxygen utilization was studied polarographically in isolated hepatic mitochondria with glutamate, pyruvate, and succinate substrates. State 3, state 4, respiratory control index (RCI), and ADP:O ratios were determined. Whole tissue and isolated mitochondrial ultrastructure were examined by electron microscopy. Systemic blood pressure and oxygenation were monitored. Hepatic tissue oxygenation was examined using a surface oxygen electrode. Peritonitis resulted in acceleration of state 3 respiratory rates and increased respiratory control indices at all time intervals. Maximal respiratory control was observed at 4 hours with all substrates. Whole tissue mitochondria demonstrated mild swelling and thinning of membranes and matrix. Experimental and control isolates showed similar orthodox-to-condensed conformational changes. Hepatic tissue oxygenation declined to less than 10% of control by 6 hours, while arterial Po2 was unchanged. The conclusions of this study are that lethal peritonitis results in (1) no primary injury to the hepatic mitochondria, (2) increased efficiency of hepatic mitochondrial oxygen utilization, and (3) reduced hepatic tissue oxygenation. The exact mechanisms of defective oxygen delivery require further study.

Animals↗
PubMed1978

The acute effects of nicotine, tobacco smoke and carbon monoxide on myocardial oxygen tension in the anaesthetized cat.

1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo(2)) were estimated amperometrically in 33 anaesthetized open-chest cats with a glass-insulated 25 mum platinum cathode within a 22-gauge needle implanted in the left ventricular wall.2 MPo(2) was 1.6-60 mmHg (mean 23.5 mmHg) when arterial Po(2) was >80 mmHg. Sequential intravenous infusions of nicotine (2-3 mug/kg every 45 s) or intracheal puffs (3-5 ml) of tobacco smoke commonly produced transitory increases (25-35 mmHg) of arterial pressure and 4-6 mmHg increments of MPo(2). Intratracheal puffs (5 ml) of 5% carbon monoxide sufficient to increase carboxyhaemoglobin from 0.8 to 1.5% to 4-7% had no effect on arterial Po(2) or blood pressure but typically decreased MPo(2) by approximately 1-4 mmHg. Augmentation of MPo(2) often succeeded carbon monoxide administration.3 Arterial hypoxia (arterial Po(2) < 60 mmHg) reduced mean MPo(2) to 14.4 mmHg but anoxic levels were not observed. Pressor responses to nicotine and tobacco smoke were accompanied by small increases (usually 1-3 mmHg) of MPo(2). Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo(2) (<10 mmHg) were unaffected as carboxyhaemoglobin was raised to 7-11% during hypoxaemia.4 It is concluded that nicotine and tobacco smoke cause augmentation of myocardial oxygen supply, even during moderate hypoxaemia. By contrast, smoking dosages of carbon monoxide have the potential of producing a small reduction of MPo(2) during normoxia, but the effect is negligible during moderate hypoxaemia.

Animals↗
PubMed1978

Hepatic oxygen supply and plasma lactate and glucose in endotoxic shock.

Hepatic oxygen supply and selected blood parameters were recorded in fasted male rates given 20--30 mg/kg Escherichia coli endotoxin intraperitoneally. Mortality was 70% within 24 hours. Measurements during the initial eight hours postendotoxin recorded no differences of hematocrit, systemic arterial pressure, or arterial pO2 between survivors and eventual nonsurvivors. However, by the sixth or eighth hour nonsurvivors showed significantly higher plasma lactate, lower plasma glucose and blood pH, and a greater degree of hypocapnea. In addition, a mean hepatic pO2 had decreased from 25.2 mm Hg during the control to 3.8 mm Hg after six hours. A decline of hepatic oxygen supply also occurred in surviving rats but was significantly less severe. Control rats showed a mild degree of respiratory alkalosis but were otherwise stable over eight hours. The relationship of hepatic oxygen supply to differences of plasma lactate and glucose is discussed. Failure of hepatic circulation is cited as the probable cause of extensive liver anoxia and related developments in nonsurviving endotoxic rats.

Acid-Base Equilibrium↗