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Biomedical subjects

E M Wagner

Publications and source records attributed to E M Wagner.

At least 73 records · Page 4Linked to original sources
PubMed1988

Effect of hypoxia on bronchial circulation.

We studied the effect of systemic hypoxia on the bronchial vascular pressure-flow relationship in anesthetized ventilated sheep. The bronchial artery, a branch of the bronchoesophageal artery, was cannulated and perfused with a pump with blood from a femoral artery. Bronchial blood flow was set so bronchial arterial pressure approximated systemic arterial pressure. For the group of 25 sheep, control bronchial blood flow was 22 ml/min or 0.7 ml.min-1.kg-1. During the hypoxic exposure, animals were ventilated with a mixture of N2 and air to achieve an arterial PO2 (PaO2) of 30 or 45 Torr. For the more severe hypoxic challenge, bronchial vascular resistance (BVR), as determined by the slope of the linearized pressure-flow curve, decreased acutely from 3.8 +/- 0.4 mmHg.ml-1.min to 2.9 +/- 0.3 mmHg.ml-1.min after 5 min of hypoxia. However, this vasodilation was not sustained, and BVR measured at 30 min of hypoxia was 4.2 +/- 0.8 mmHg.ml-1.min. The zero flow intercept, an index of downstream pressure, remained unaltered during the hypoxic exposure. Under conditions of moderate hypoxia (PaO2 = 45 Torr), BVR decreased from 4.6 +/- 0.3 to 3.8 +/- 0.4 mmHg.ml-1.min at 5 min and remained dilated at 30 min (3.6 +/- 0.5 mmHg.ml-1.min). To determine whether dilator prostaglandins were responsible for the initial bronchial vascular dilation under conditions of severe hypoxia (PaO2 approximately equal to 30 Torr), we studied an additional group of animals with pretreatment with the cyclooxygenase inhibitors indomethacin (2 mg/kg) and ibuprofen (12.5 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Is serum fructosamine assay specific for determination of glycated serum protein?

We compared the fructosamine activity in sera from healthy and diabetic subjects with the degree of protein glycation detected by a liquid-chromatographic method. The latter technique measures furosine as a specific product after hydrolysis of epsilon-amino-fructose-lysine. Our results indicate that the fructosamine assay measures the extent of glycation of purified human serum albumin correctly. On the other hand, we found no correlation between the two methods for sera from healthy subjects, although for diabetics' sera the values obtained with both methods were related. However, only about half of the reducing activity (fructosamine) was due to specific nonenzymatic glycation of proteins in healthy subjects and well-controlled diabetics. The remaining unspecific activity varied from serum to serum. It was not reducible with NaBH4 and was independent of the glycation of albumin, which normally accounts for about 80% of glycated serum proteins. The fructosamine assay is therefore of limited specificity for the exact measurement of glycated proteins in serum.

Blood Proteins↗
PubMed1987

Haemodilution therapy in ischaemic stroke: plasma concentrations and plasma viscosity during long-term infusion of dextran 40 or hydroxyethyl starch 200/0.5.

In 21 patients with ischaemic strokes we have monitored plasma viscosity, total plasma concentration, numeric average molecular weight (Mn), and weight average molecular weight (Mw) of Dextran 40 (dextran) and hydroxyethylstarch 200/0.5 (HES) during 10 days of treatment (days 1-4, 2 X 500 ml; days 5-10, 1 X 500 ml). Plasma concentrations of dextran increased during the first 4 days (8.3 mg X ml-1 on the first day to 18.0 mg X ml-1 on the fifth day), reached an apparent steady state of 17.2 mg X ml-1 during the next 6 days, and declined subsequently with a half-time (t1/2) of 4.03 days. After ten days treatment Mn and Mw were shifted towards higher values. Plasma viscosity increased from 1.26 mPas to 1.69 mPas on Day 10 (p less than 0.01) and was linearly correlated with the total plasma concentration of dextran (p less than 0.001; r = 0.88). Total plasma concentrations of HES averaged 11.7 mg X ml-1 on Day 1 and 12.4 mg X ml-1 on Day 5. The molecular weight distribution did not change during the infusions but decreased in comparison with the administered solution. Plasma viscosity fell from 1.40 mPas to 1.30 mPas at Day 10 (p less than 0.05) and was not related to the concentration of HES. The haemodiluting effect, as indicated by a decrease of the haematocrit, was 22% and 16.8% for dextran and HES respectively. These data suggest several advantages of HES compared with dextran in haemodilution therapy of ischaemic stroke.

Aged↗
PubMed1987

Effects of airway pressure on bronchial blood flow.

We studied the effects of increased airway pressure caused by increasing levels of positive end-expiratory pressure (PEEP) on bronchial arterial pressure-flow relationships. In eight alpha-chloralose-anesthetized mechanically ventilated sheep (23-27 kg), the common bronchial artery, the bronchial branch of the bronchoesophageal artery, was cannulated and perfused with a pump. The control bronchial blood flow (avg 12 +/- 1 ml/min or 0.48 ml X min-1 X kg-1) was set to maintain mean bronchial arterial pressure equal to systemic blood pressure. Pressure-flow curves of the bronchial circulation were measured by making step changes in bronchial blood flow, and changes in these curves were analyzed with measurements of the pressure at zero flow and the slope of the linearized curve. The zero-flow pressure represents the effective downstream pressure, and the slope represents the resistance through the bronchial vasculature. At a constant bronchial arterial pressure of 100 mmHg, an 8 mmHg increase in mean airway pressure caused a 40% reduction in bronchial blood flow. Under constant flow conditions, increases in mean airway pressure with the application of PEEP caused substantial increases in bronchial arterial pressure, averaging 4.6 mmHg for every millimeters of mercury increase in mean airway pressure. However, bronchial arterial pressure at zero flow increased approximately one-for-one with increases in mean airway pressure. Thus the acute sensitivity of the bronchial artery to changes in mean airway pressure results primarily from changes in bronchovascular resistance and not downstream pressure.

Animals↗
PubMed1987

Effect of sodium intake on blood pressure, serum levels and renal excretion of sodium and potassium in normotensives with and without familial predisposition to hypertension.

1. Seventeen normal volunteers aged 19 to 22 were randomly subjected, in a trial of crossover design, to three distinct regimens of sodium chloride intake: high (16 to 20 g), normal (8 to 12 g) and low (0.5 to 1 g). Each regimen lasted nine days, with determination of blood pressure and heart rate (in the supine position and after sudden rising), body weight, and urinary output of creatinine, sodium and potassium on the third, sixth and ninth days. In addition, plasma levels of creatinine, sodium and potassium were determined on the ninth day so that sodium and potassium clearance and fractional excretion could be calculated. 2. Eleven of the volunteers had a family history of hypertension. Compared to the six without such a history, these subjects showed: 1) higher supine systolic blood pressure on the third day of sodium overload (124.7 +/- 3.0 vs 112.3 +/- 2.9 mmHg, P less than 0.02); 2) higher supine diastolic blood pressure on the third day of sodium overload (76.5 +/- 2.8 vs 64.5 +/- 4.3 mmHg; P less than 0.05); 3) higher supine diastolic blood pressure on the sixth day of sodium overload (73.7 +/- 2.3 vs 63.8 +/- 3.2 mmHg, P less than 0.05); 4) lower supine heart rate on the ninth day of sodium overload (61.0 +/- 3.1 vs 72.7 +/- 4.6, P less than 0.05), and 5) lower plasma potassium on the ninth day of sodium overload (4.10 +/- 0.05 vs 4.28 +/- 0.06 mEq/l, P less than 0.05). 3. These results suggest that normal individuals whose familial history places them at risk for the development of hypertension differ from those not at risk during their adaptation to sodium load by suffering a transient elevation of blood pressure within a few days of the increase in load. The low levels of plasma potassium observed in these volunteers after a period of sodium load may be due to the operation of different renal mechanisms of sodium excretion in this group, leading to increased kaliuresis, and may explain the high vascular reactivity of such individuals.

Adult↗
PubMed1986

[Dextran 40 or HES 200/0.5? Hemorheology of the long-term treatment of ischemic cerebral attacks].

Haemorheological parameters on long-term treatment of ischaemic stroke were measured in two groups of 12 patients receiving dextran 40 or hydroxyethyl starch (HES 200). Both substances similarly lowered haematocrit and whole-blood viscosity. Dextran produced a clear-cut increase in plasma viscosity and red-cell aggregation. The effects were due to a marked increase in the plasma concentration of dextran caused by an accumulation of large molecules. HES 200 improved plasma viscosity and red-cell aggregation. Since these haemorheological parameters are of special importance for improving a disordered microcirculation as would occur at the margins of the ischaemic lesion, HES 200 would seem to be the appropriate plasma expander in long-term treatment with haemodilution. The differences between dextran 40 and HES 200 become the more marked the higher the volume infused.

Blood Viscosity↗
PubMed1986

Hydrostatic determinants of cerebral perfusion.

We examined the cerebral blood flow response to alterations in perfusion pressure mediated through decreases in mean arterial pressure, increases in cerebrospinal fluid (CSF) pressure, and increases in jugular venous (JV) pressure in 42 pentobarbital anesthetized dogs. Each of these three pressures was independently controlled. Cerebral perfusion pressure was defined as mean arterial pressure minus JV or CSF pressure, depending on which was greater. Mean hemispheric blood flow was measured with the radiolabeled microsphere technique. Despite 30-mm Hg reductions in mean arterial pressure or increases in CSF or JV pressure, CBF did not change as long as the perfusion pressure remained greater than approximately 60 mm Hg. However, whenever perfusion pressure was reduced to an average of 48 mm Hg, cerebral blood flow decreased 27% to 33%. These results demonstrate the capacity of the cerebral vascular bed to respond similarly to changes in the perfusion pressure gradient obtained by decreasing mean arterial pressure, increasing JV pressure or increasing CSF pressure, and thereby support the above definition of cerebral perfusion pressure.

Animals↗
PubMed1986

Peripheral circulatory alterations in canine anaphylactic shock.

We have examined peripheral circulatory variables that might contribute to the decrease in cardiac output and arterial pressure characteristic of anaphylactic shock. In six dogs instrumented with a right heart bypass, the intravenous administration of Ascaris suum antigen caused a 53% decrease in cardiac output and a 58% decrease in arterial pressure. Resistance to venous return increased from 0.0038 +/- 0.0004 to 0.0056 +/- 0.0006 mmHg X ml-1 X min (P less than 0.05), mean systemic pressure decreased from 7.0 +/- 0.6 to 4.4 +/- mmHg (P less than 0.005), and vascular compliance did not change. Assuming a constant vascular volume, the decrease in mean systemic pressure could be explained by a rightward shift of the systemic pressure volume curve. This constant-volume assumption was tested in intact (n = 6) and splenectomized dogs (n = 7). Serial measurements of protein oncotic pressure and hematocrit were used to estimate plasma volume changes during anaphylaxis. Both methods for estimating volume showed small increases in plasma volume at the time of the largest decrease in arterial pressure in both groups of animals. These results suggest that the primary circulatory mechanisms responsible for anaphylactic shock are an increase in resistance to venous return and a shift of the systemic pressure volume curve and not an acute loss of plasma volume.

Anaphylaxis↗
PubMed1985

Cerebrovascular transmural pressure and autoregulation.

The cerebral blood flow (CBF) response to changes in perfusion pressure mediated through decreases in arterial pressure, increases in cerebrospinal fluid (CSF) pressure and increases in jugular venous pressure was studied in anesthetized dogs. A preparation was developed in which each of the three relevant pressures could be controlled and manipulated independently of each other. In this preparation, the superior vena cava and femoral vein were cannulated and drained into a reservoir. Blood was pumped from the reservoir into the right atrium. With this system, mean arterial pressure and jugular venous pressure could be independently controlled. CSF pressure (measured in the lateral ventricle) could be manipulated via a cisternal puncture. Total and regional CBF responses to alterations in perfusion pressure were studied with the radiolabelled microsphere technique. Each hemisphere was sectioned into 13 regions: spinal cord, cerebellum, medulla, pons, midbrain, diencephalon, caudate, hippocampus, parahippocampal gyrus, and occipital, temporal, parietal and frontal lobes. Despite 30 mm Hg reductions in arterial pressure or increases in jugular venous pressure or CSF pressure, little change in CBF was observed provided the perfusion pressure (arterial pressure minus jugular venous pressure or CSF pressure depending on which pressure was of greater magnitude) was greater than the lower limit for cerebral autoregulation (approximately 60 mm Hg). However, when the perfusion pressure was reduced by any of the three different methods to levels less than 60 mm Hg (average of 48 mm Hg), a comparable reduction (25-35%) in both total and regional CBF was obtained. Thus comparable changes in the perfusion pressure gradient established by decreasing arterial pressure, increasing jugular venous pressure and increasing CSF pressure resulted in similar total and regional blood flow responses. Independent alterations of arterial and CSF pressures, and jugular venous pressure produce opposite changes in vascular transmural pressure yet result in similar CBF responses. These results show that cerebral autoregulation is a function of the perfusion pressure gradient and cannot be accounted for predominantly by myogenic mechanisms.

Animals↗
PubMed1985

Effect of repeated antigen exposure on antigen-and mediator-induced bronchospasm in sheep.

We studied the effects of repeated exposures of antigen on airway reactivity to mediators of anaphylaxis and immediate response to the antigen. Seven antigen-sensitive sheep were exposed to aerosols of Ascaris suum antigen 5 times biweekly; a control group of seven sheep underwent the same exposure regimen with saline vehicle. Sheep were assigned to experimental (Ascaris) or control groups so the distribution of animals with regard to bronchial reactivity to mediators was about the same. Airway reactivity was assessed by determining the effects of aerosolized histamine (10-1,000 micrograms), prostaglandin F2 alpha (PGF2 alpha, 10-300 micrograms), and a stable analogue of thromboxane A2 (U-46619, 1-100 micrograms) on lung resistance (RL) and dynamic lung compliance (Cdyn). Before treatment, experimental and control groups showed similar changes in RL and Cdyn, with analogue greater than histamine greater than PGF2 alpha. At the highest dose of each agonist, mean increases in RL were 50, 123, and 29%, respectively, and mean decreases in Cdyn were 21, 45, and 12%. During the first 15-min exposures to antigen aerosol, mean RL had increased by 125% and Cdyn decreased by 38% of base-line values; hyperinflation following the exposures reduced the changes to 56 and 31%, respectively. Changes in RL and Cdyn during the final antigen exposures and following postexposure hyperinflation were reduced significantly (P less than 0.05) compared with the initial exposures. Baseline RL and Cdyn before and after the exposures to antigen or saline were not significantly different. Airway reactivity to histamine, PGF2 alpha, or analogue was not significantly altered in these atropinized animals over the range of doses studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1985

Increased in vitro airway responsiveness in sheep following repeated exposure to antigen in vivo.

We have studied the effect of repeated in vivo antigen exposure on in vitro airway responsiveness in sensitized sheep. Fourteen sheep underwent five biweekly exposures to aerosolized Ascaris suum antigen or saline. Following this exposure regimen, the animals were killed and tracheal smooth muscle and lung parenchymal strips were prepared for in vitro studies of isometric contraction in response to histamine, methacholine, prostaglandin F2 alpha, and a thromboxane A2 analogue. No alteration in tracheal smooth muscle responsiveness was observed between saline- and antigen-exposed tissue. In contrast, by use of lung parenchymal strips as an index of peripheral airway responsiveness, significant increases in responsiveness to histamine and a thromboxane A2 analogue (10(-6) and 10(-5) M) were observed in antigen-exposed tissue compared with saline controls. These results demonstrate that repeated antigen exposure in vivo selectively increase the responsiveness of peripheral lung smooth muscle to certain chemical mediators of anaphylaxis.

Animals↗
PubMed1983

Cerebral venous outflow and arterial microsphere flow with elevated venous pressure.

The cerebral blood flow response to cerebral venous pressure elevation was studied in pentobarbital-anesthetized dogs using the cerebral venous outflow and radiolabeled microsphere techniques. Cerebral venous pressure elevation resulted in a significant reduction in cerebral venous outflow at a pressure of approximately 2.0 mmHg (referenced at the level of the external auditory meatus). At higher pressures, cerebral venous outflow decreased at a rate of 0.5 ml x min-1 x mmHg-1. Mean arterial pressure was 102.0 mmHg, and thus cerebral perfusion pressure (mean arterial pressure minus cerebral venous pressure) was well within the range for cerebral autoregulation. These results were obtained regardless of whether cerebrospinal fluid pressure was allowed to rise concomitantly with cerebral venous pressure (11 dogs) or was maintained at atmospheric pressure (7 dogs). However, simultaneous measurement of cerebral venous outflow and total and regional cerebral blood flow with the radiolabeled microsphere technique with venous pressure elevation (6 dogs) produced discrepant results. As cerebral venous pressure was elevated to approximately 16.0 mmHg, cerebral venous outflow decreased to 40% of control while total and regional cerebral blood flow values remained unchanged, so that regional and cerebral vascular resistances decreased. These results suggest that cerebral venous pressure elevation opens intracranial venous anastomotic channels and diverts blood flow from the measured venous drainage through other drainage sites. In addition, our results suggest that the dominant mechanism of cerebral autoregulation is metabolic, not myogenic.

Animals↗