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Biomedical subjects

R A Mason

Publications and source records attributed to R A Mason.

At least 55 records · Page 3Linked to original sources
PubMed1989

Clinical and chemical characterization of an adventitial popliteal cyst.

We present further evidence that adventitial cysts of the popliteal artery are ganglions, based on studies of a lesion found in a 51-year-old man. The cyst was located entirely within the adventitia, lacked a cellular lining, and did not communicate with either the arterial lumen or the synovial space. The contents were gel-like and composed of 1.64 gm of hyaluronic acid and 0.20 gm of protein per dl. This material did not possess boundary-lubricating ability in a test system that slides natural latex rubber against glass. The histologic appearance, chemical composition, and absence of lubricating ability more closely resemble the characteristics of ganglions. These findings suggest that the cyst was not synovial but rather ganglionic in origin.

Exudates and Transudates↗
PubMed1989

An animal model for small-diameter arterial grafts.

A rabbit model was developed to study small-diameter arterial grafts. A total of 158 2-mm-diameter polytetrafluoroethylene (PTFE) grafts and 35 autogenous carotid artery (AA) grafts were interposed in the carotid arteries of New Zealand white rabbits. A pilot study of 16 PTFE grafts used to develop operative and anesthetic techniques had a 20% mortality and 38% early (less than 2 day) thrombosis rate. Subsequent to the pilot study 177 grafts were placed and a 92% postoperative survival with 100% AA graft patency and 93% PTFE graft patency at 2 weeks was observed. AA grafts followed beyond 16 weeks continued to have 100% patency, while PTFE grafts began to show increased failure. Closure was found to be due to the development of anastomotic myointimal hyperplasia.

Animals↗
PubMed1988

Identification of autonomic dysfunction with a pulse oximeter.

Chart recordings of the pulse oximeter waveform were taken during the performance of a standard Valsalva manoeuvre, in one subject with and another without autonomic dysfunction. They demonstrate that certain types of pulse oximeter may be used for the rapid pre-operative identification of patients who have an autonomic neuropathy in which the cardiovascular responses to stress are impaired.

Autonomic Nervous System Diseases↗
PubMed1988

Complete heart block during anaesthesia in a patient with sarcoidosis.

An apparently fit young man with sarcoidosis developed complete heart block during an emergency mastoidectomy. A temporary transvenous pacemaker was inserted, but permanent pacing was required in the postoperative period. The clinical and pathological features of cardiac sarcoidosis are described; complete heart block is the commonest presentation of cardiac involvement. The role of anaesthesia as the precipitating factor in this case is discussed.

Adult↗
PubMed1987

The effects of endothelial injury on smooth muscle cell proliferation.

The endothelial injury induced by the placement of a synthetic graft has been implicated as a stimulus for the development of MIH. In this study we compared the degree of EC coverage and the early SMC-PR in the arterial segments proximal and distal to 2 mm diameter PTFE grafts that had been placed in rabbit carotid arteries (n = 49). In vivo labeling with 3H-thymidine and Evans blue was carried out at intervals of 2 to 33 days after grafting. The SMC-PR was measured as the degree of 3H-labeled DNA divided by the total DNA for each segment, and the EC coverage was determined by planimetry of the area of Evans blue exclusion. There was an early rise in the SMC-PR in both arterial segments, but it was more marked in the distal segment (p less than 0.001). There was no correlation between the SMC-PR and the degree of EC coverage in either the proximal (r = 0.25) or the distal segments (r = 0.10). The data suggest that there is a greater SMC-PR at the distal end of an implanted PTFE graft. The degree of endothelial loss and its regrowth does not appear to be an important factor.

Animals↗
PubMed1987

How often does maternal preeclampsia-eclampsia incite thrombocytopenia in the fetus?

Overt thrombocytopenia (defined as a platelet count of less than 100,000/microL) was not identified at or soon after delivery in any of 262 infants of mothers with hypertension induced or exacerbated by pregnancy. The platelet counts were 100,000 to 149,000/microL in 11 (4.2%) of the offspring and 150,000/microL or higher in the rest, even though the platelet counts of the 258 mothers were less than 150,000/microL in 77 (30%), less than 100,000/microL in 51 (20%), and less than 50,000/microL in 17 (7%). Some infants of hypertensive mothers did develop overt thrombocytopenia later; however, the frequency and intensity appeared to be no greater than it was in infants with similar complications (prematurity, growth retardation, infection, and meconium aspiration) whose mothers were normotensive. We conclude that the fetus whose mother has preeclampsia-eclampsia is very unlikely to be thrombocytopenic during labor and delivery, even when the mother is thrombocytopenic. Therefore, neither cesarean delivery to avoid labor nor scalp blood platelet counts during labor need be performed.

Eclampsia↗
PubMed1986

Methylprednisolone and gentamicin effects on hepatosplanchnic blood flow and carbohydrate metabolism in endotoxemic Yucatan miniature pigs.

Conjoint therapy of a glucocorticoid and aminoglycoside antibiotic have been recommended for septic shock. These studies examined the hemodynamic and metabolic effects of methylprednisolone sodium succinate (MPSS) with and without gentamicin sulfate in a nonanesthetized model of nonseptic endotoxemia in Yucatan miniature pigs. Methylprednisolone sodium succinate alone had no effect on endotoxin-induced systemic hypotension. Endotoxemic pigs treated with MPSS in combination with gentamicin sulfate had lower mean arterial pressures than did MPSS-treated and nontreated endotoxemic pigs. Methylprednisolone sodium succinate alone and with gentamicin sulfate improved portal and hepatic venous blood flows moderately. Net hepatic lactate extraction, glucose production, and whole body [6-3H]glucose-derived rates of glucose appearance were also improved, but [6-3H]glucose-derived rates of glucose disappearance and blood lactate concentrations were increased, leading to no improvement in plasma glucose concentration. Pancreatic insulin secretion was higher in treated groups, which may have contributed to greater glucose utilization rates. Hepatic oxygen extraction efficiency was not affected by treatment, but increased in all groups to maintain hepatic oxygenation at base-line values. Although a calcium-antagonistic activity of gentamicin has been reported to synergize with endotoxin, thereby adversely affecting cardiovascular function, such effects did not complicate the metabolic response to steroid in the present studies.

Animals↗
PubMed1985

Renal dysfunction after arteriography.

Acute renal failure has been observed in patients undergoing angiography in which a hypertonic triiodinated contrast medium is used. To ascertain the incidence of renal dysfunction and the clinical risk factors, we did a prospective study in which creatinine clearance was measured before and immediately after 120 arteriographic procedures. Thirty-seven patients (31%) sustained a significant reduction in creatine clearance after arteriography. No specific risk factor could be determined. Our findings, however, indicate that patients with preexisting renal insufficiency or diabetes mellitus are not at a higher risk for sustaining a fall in creatinine clearance after angiography.

Acute Kidney Injury↗
PubMed1985

Variational anatomy of the deep femoral artery.

The deep femoral artery is frequently incorporated in vascular reconstructive procedures in the proximal leg. To study the branching variations of this artery, we dissected 100 legs and then classified the anatomical patterns. The deep femoral artery originates a median distance of 4.4 cm from the inguinal ligament. The origin of the lateral circumflex artery varied greatly. When it branched from the deep femoral, the origin of the lateral circumflex was 1.5 cm (median) from the origin of the deep femoral. The medial circumflex artery originated from the deep femoral in 63% of the specimens. It arose separately from the common femoral and more proximally in 26% of the specimens, branching an average of 2.15 cm (median) above the deep femoral origin. Familiarity with these variations is essential to the vascular surgeon and,therefore, we have included diagrams based on our study as a ready reference.

Female↗
PubMed1984

Naloxone therapy in awake endotoxemic Yucatan minipigs.

Twelve Yucatan miniature pigs were fitted with jugular, portal, hepatic vein, and carotid artery catheters, and hepatic artery and portal vein flow cuffs to quantitate portosystemic and transhepatic kinetics. Seventy-two hours later they were placed in slings, and following a 3-hr control period were infused with Escherichia coli endotoxin at 15 micrograms/kg/hr for 6 hr. Eight were controls and 4 received a primed (2 mg/kg) continuous infusion (2 mg/kg/hr) of naloxone 1 hr after initiation of endotoxin. In the naloxone group, arterial hypotension developed by 60 min. Arterial pressure increased to 125 mm Hg by 80 min (20 min post naloxone) and maintained this level for 3 hr. [6-3H]Glucose-derived rate of disappearance (Rd) values were increased above their own control period at 60 and 80 min, but were approximately 55% lower than untreated controls. Rate of appearance (Ra) values remained unchanged in the naloxone group resulting in a net glucose deficit. After 1 hr of endotoxin, blood pyruvate increased from 1.0 to 1.8 mg%, reached 3.3 mg% at 80 min, and remained elevated. Blood lactate similarly increased from 11 to 35 mg% by 60 min, increasing further to 82 mg% 20 min after naloxone infusion, in concert with signs of severe distress. Portal and hepatic total O2 decreased by 60 min and 100 min, respectively, reflecting depressed hepatic O2, input. Lethality was 75% in naloxone-treated pigs by the end of the experiment, vs 0% in untreated animals. Naloxone improves some hemodynamic parameters. However, in these conscious postsurgical patients, naloxone blocked some beneficial effects of endogenous opiates resulting in severe metabolic derangements and increased mortality.

Animals↗
PubMed1984

Ankylosing spondylitis. The case for awake intubation.

The major problems of long-standing ankylosing spondylitis are described and the surgical and anaesthetic literature reviewed. The upper airway problems are discussed with reference to four cases and the advantages of an awake intubation technique are stressed.

Adult↗
PubMed1984

Effects of captopril on hemodynamic and metabolic parameters in awake endotoxemic Yucatan minipigs.

Angiotensin II (AII), a potent vasoconstrictor, contributes to ischemic and decompensatory phases of shock. Captopril may benefit vital organ and tissue perfusion by inhibiting AII formation. We fitted 13 approximately 50-kg pigs with jugular, portal, hepatic vein, and carotid artery catheters, and hepatic artery and portal vein flow cuffs to quantitate portosystemic and transhepatic kinetics. We placed them in slings 72 hr later and following a 3-hr control period, they were infused with E. coli endotoxin at 15 micrograms/kg/hr for 6 hr. We kept eight as controls and five received a primed (2 mg/kg) continuous infusion (2 mg/kg/hr) of captopril 1 hr after initiation of endotoxin. Arterial hypotension developed by 60 min and hypoglycemia by 100 min in both groups; captopril had no effect on these parameters. Blood lactate increased from 7.8-32.1 mg/dl 80 min postendotoxin, and for the third to fifth hours of endotoxin infusion was significantly higher than those of the control group. 6-3H-glucose-derived appearance (Ra) values remained at 1.88-2.35 mg/kg/min throughout the experiment. Glucose disappearance (Rd) values were elevated from 60-120 min of endotoxin, increasing to 2.68-3.13 mg/kg/min versus 1.86 mg/kg/min preendotoxin. These changes corresponded to those in lactate, and incurred only a brief significant net glucose deficit (%Rd-%Ra) that peaked at 61.1% at 100 min. For 140-360 min postendotoxin, glucose balance was at most 8.3% in deficit (200 min) and 13.6% in positive balance (280 min) versus a net deficit of up to 25.4% (220 min) for the untreated group for much of the experiment. Portal and hepatic venous blood flow in captopril-treated pigs was lower than that in untreated pigs before endotoxin (8.2 and 10.0 ml/kg/min versus 12.9 and 17.9 ml/kg/min, respectively), but was not depressed following endotoxin infusion, versus 50% reductions in the untreated pigs, postendotoxin. Captopril maintained hepatosplanchnic blood flow and effected modest improvements in glucose kinetics.

Animals↗
PubMed1984

Lidocaine therapy in awake endotoxemic Yucatan minipigs. I. Metabolic parameters and glucose biokinetics.

Cellular membrane destabilization induced by endotoxin and endogenous inflammatory mediators contributes significantly to the progression of metabolic and hemodynamic dysfunction in endotoxemia. Owing to its membrane-stabilizing properties, lidocaine may prove beneficial in the treatment of endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular venous and carotid arterial catheters. Seventy-two hours later they were placed in restraint slings, and following a 3-h control period, were infused with Escherichia coli endotoxin (Difco 055:B5) at 15 micrograms/kg for 6 h. Eight were controls and four received a primed (2 mg/kg) continuous infusion (2 mg/kg/h) of lidocaine 1 h following the initiation of endotoxin infusion. In the lidocaine-treated group, arterial hypotension (113 mmHg) developed by 60 min, continued to fall to 104 mmHg by 200 min and rose terminally to 118 mmHg. These values were higher than the control group, but were below those of the control period of the lidocaine group. Six -3H-glucose-derived Rd values were increased above their own control period at 60 min, but were approximately 55% lower than in the untreated group. Ra values were not significantly changed in the lidocaine-treated group resulting in a net glucose deficit which was more profound than in untreated pigs, whose Ra values did increase. The degree of hypoglycemia was more profound in lidocaine-treated pigs from 100-260 min, stabilizing at 29-37 mg/dl. Blood lactate (70 mg/dl) was above those of the control pigs (44 mg/dl) from 160 to 220 min. U-14C-glucose-derived glucose recycling was increased above the lidocaine group's preendotoxin control period and reached values twice those of the untreated pigs' endotoxin infusion period. Compared to their own control period and the untreated group's endotoxin infusion period, percentage lactate/glucose was decreased from 40 min on. Lidocaine treatment elicited modest improvements in systemic arterial blood pressure and reduced relative glucose utilization and gluconeogenesis, but in itself, was not a sufficient therapy for endotoxic shock in this model.

Acid-Base Equilibrium↗
PubMed1984

Lidocaine therapy in awake endotoxemic Yucatan minipigs. II. Hepatosplanchnic metabolism.

Reductions in hepatosplanchnic blood flow and oxygen delivery contribute to the hepatic metabolic dysfunction observed in endotoxemia. Through its membrane-stabilizing activity, systemic lidocaine therapy may modify visceral hemodynamics and preserve hepatocellular metabolic function in endotoxic shock. Twelve 50-kg pigs were surgically fitted with jugular, portal, hepatic venous and carotid arterial catheters, and hepatic arterial and portal venous flow cuffs to quantitate portosystemic and transhepatic kinetics. Seventy-two hours later they were placed in slings, and following a 3-h control period were infused with Escherichia coli endotoxin (Difco 055:B5) at 15 micrograms/kg/h for 6 h. Eight were controls and four received a primed (2 mg/kg) continuous infusion (2 mg/kg/h) of lidocaine 1 h following the initiation of endotoxin infusion. Hepatosplanchnic blood flow was relatively unaffected by lidocaine infusion. In both untreated and treated pigs, hepatic arterial flow decreased by 25-30%, portal venous flow fell by approximately 60%, and hepatic venous flow was reduced by 50%. Following 2 h of endotoxin infusion, net splanchnic glucose uptake was increased significantly in lidocaine-treated pigs, but not in untreated endotoxemic animals. Transhepatic lactate kinetics were unaffected by treatment, but net hepatic pyruvate uptake in the lidocaine-treated group increased as compared to the untreated group by 140 min postendotoxin, being significantly greater at 220, 280, and 320 min. Hepatic oxygen input was significantly reduced by 25-30% in both groups within 1 h of the onset of endotoxemia, but hepatic oxygen extraction efficiency increased two-to-three-fold, thereby maintaining net hepatic oxygen uptake. Despite the maintenance of hepatic oxygen uptake and improved hepatic pyruvate extraction in lidocaine treated endotoxemic pigs, no significant improvements in glucose homeostasis were incurred, leading to the conclusion that lidocaine therapy offered few significant advantages in the treatment of overall metabolic derangements during acute endotoxemia.

Animals↗
PubMed1984

Persistent hyperinsulinemia due to induced euglycemia in awake endotoxic minipigs.

Transient hyperinsulinemia has been incriminated as a contributing factor to endotoxin-induced hypoglycemia. However, a recent study using endotoxic minipigs noted an increase in the rate of glucose utilization prior to when hyperinsulinemia was seen. Based on this, the "misinformed beta-cell" hypothesis was proposed. If endotoxic pancreatic beta-cells experience an early increase in glucose uptake, they could over-estimate the true glycemic state and release insulin, further contributing to the hypoglycemia. Hypoglycemia would offset increased glucose uptake by the beta-cell and insulin secretion would return to basal rates, explaining the transient nature of the insulin response. According to this hypothesis, maintenance of euglycemia should elicit a sustained rather than transient insulin release. The hypothesis was tested with a euglycemic clamp technique in a group of five endotoxic (Difco 055:B5; 15 micrograms/kg/hr) minipigs (EC) compared to three nonclamped endotoxic minipigs (E). Persistent, profound hyperinsulinemia (15 ng/ml) occurred in the EC group, further supporting the hypothesis. The clamp appeared to be beneficial, since arterial pressure and pH were significantly (P less than or equal to 0.05) higher and arterial lactate levels were lower in EC pigs compared to E pigs. A significant discrepancy was noted between the radioisotope ( [6-3H] glucose)-derived rate of glucose appearance and the rate of exogenous glucose infusion (clamp), which may have been due to unaccounted for changes in glucose pool size and/or futile cycling of glucogenic substrates or glucose through glycogen and lipid.

Acid-Base Equilibrium↗
PubMed1984

Hepatosplanchnic insulin kinetics in awake endotoxemic Yucatan minipigs: the "misinformed B-cell" hypothesis revisited.

Increased pancreatic insulin secretion may be one of the factors associated with the insulinlike activity (ILA) of endotoxemia. While there is little doubt that the prominent hypoglycemia of endotoxicosis is often preceded by systemic hyperinsulinemia, the cause of this increased secretion and its cause-and-effect relationship to the glucose deficit is less obvious. Recently, a "misinformed B-cell" hypothesis was proposed in which it was suggested that increased glucose flux across the pancreatic B-cell early in endotoxemia might lead to a misinterpretation of the existing glycemic state, resulting in increased insulin release. This possibility was based in part on the observation that increased 6-3H-glucose-derived rates of glucose disappearance (Rd) in endotoxic Yucatan minipigs preceded the onset of systemic hyperinsulinemia. Examination herein of the chronological order of events in this group of pigs and three other groups treated with lidocaine, naloxone, or captopril reveals an increase in pancreatic insulin secretory rate most often before increases in systemic Rd. Each of the three therapies were administered as a primed continuous intravenous infusion, 1 hour after the initiation of a continuous intravenous infusion of Difco 055:B5 E. coli lipopolysaccharide at an LD67 dose of 15 micrograms/kg/hr. In those pigs receiving no therapy, lidocaine, or naloxone, significant increases in pancreatic insulin secretion recurred at 40, 40, and 60 min following the onset of endotoxemia respectively. This was followed in 20 min by the first significant increase in relative glucose disappearance rates (%Rd). Captopril-treated pigs experienced a significant increase in %Rd at 60 min, which was followed in 20 min by a significant increase in pancreatic insulin secretion. In all groups, a significant hyperinsulinemia occurred transiently at 80 min postendotoxin, followed in 20 min by the onset of significant hypoglycemia. These observations suggest that increases in %Rd and transient increases in insulin secretion may be simultaneous events at best, and that along with significant increases in absolute levels of hepatic insulin extraction (observed in all groups at 60 or 80 min postendotoxin) may indicate some local effect of insulin release on hepatic glucose.

Animals↗
PubMed1983

Increased glucose uptake precedes hyperinsulinemia in awake endotoxemic minipigs.

The role of hyperinsulinemia in the development of hypoglycemia was evaluated in awake Yucatan minipigs. Eight adult minipigs were fitted with jugular, portal, and hepatic vein and carotid artery catheters, and hepatic artery and portal vein flow cuffs for determination of transhepatic kinetics and insulin secretion. Three days later they were infused with E. coli endotoxin at 15 micrograms/kg/hr. Transient hyperinsulinemia was preceded by an elevation of the rate of glucose uptake (Rd) determined from [6-3H] glucose-specific activity. This finding suggested that hyperinsulinemia might be caused by, and then be contributory to, increased Rd. If an increase in glucose uptake was also experienced by pancreatic beta-cells, the existing glycemic state could be overestimated and an inappropriate insulin release elicited.

Animals↗