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Biomedical subjects

E D Miller

Publications and source records attributed to E D Miller.

At least 55 records · Page 3Linked to original sources
PubMed1984

Microvascular aspects of acquired immune deficiency syndrome retinopathy.

Twelve of 13 patients with the acquired immune deficiency syndrome exhibited ophthalmoscopically detectable retinal findings, including cotton-wool spots, hemorrhages, Roth spots, and microvascular changes. When we used fluorescein angiography, we detected focal nonperfusion and microvascular changes in all 13 of our patients. Most patients had no visual complaints unless they had cytomegalovirus involvement of the optic papilla or the central retina. One patient lost central visual acuity from loss of perfusion in a portion of his perifoveal capillary net. Histopathologic studies demonstrated the loss of retinal capillary cells and focal occlusions of small vessels. Retinal vessel walls were also thickened with PAS-positive material.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Captopril reduces the dose requirement for sodium nitroprusside induced hypotension.

The authors studied 12 patients who required deliberate hypotension for spinal fusion operations in order to investigate the efficacy of captopril for reducing dose requirement for sodium nitroprusside (SNP). Six patients, selected at random, were pretreated with captopril, 3 mg/kg po, and the remaining six patients served as controls. All patients received a similar anesthetic technique, consisting of thiopental 3 mg/kg, pancuronium 0.1 mg/kg, morphine 0.5 mg/kg, plus nitrous oxide 70% in oxygen. SNP was used to maintain mean arterial pressure (MAP) at 50-55 mmHg during deliberate hypotension lasting 140 +/- 13 minutes (mean +/- SE). Patients who received captopril required less SNP than untreated patients both early during hypotension (1.4 +/- 0.5 micrograms X kg-1 X min-1 vs. 4.8 +/- 0.8 micrograms X kg-1 X min-1, P less than 0.05), as well as late during hypotension (2.2 +/- 0.2 micrograms X kg-1 X min-1 vs. 5.6 +/- 0.6 micrograms X kg-1 X min-1, P less than 0.05). Whole blood cyanide was significantly lower in the patients pretreated with captopril than the untreated controls both early in the hypotensive period (2.7 +/- 0.6 mumol/l vs. 13 +/- 4 mumol/l, P less than 0.05) and also late in the hypotensive period (3.7 +/- 0.8 mumol/l vs. 30 +/- 10 mumol/l, P less than 0.05). MAP was reduced by captopril pretreatment both following induction of anesthesia (64 +/- 4 mmHg captopril vs. 80 +/- 4 mmHg control, P less than 0.05) and during surgery before deliberate hypotension (86 +/- 5 mmHg captopril vs. 100 +/- 4 control, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Central depletion of catecholamines--importance of hypertension and anesthesia.

The importance of the brain noradrenergic sympathetic nervous system in blood pressure control during anesthesia with halothane and enflurane was investigated in normotensive and hypertensive rats. Central noradrenergic neurons were destroyed by instillation of 6-hydroxydopamine (6-OHDA) into the cerebral ventricle of both normotensive Wistar rats and spontaneously hypertensive rats (SHR). One week later, arterial and venous lines were placed in the rats under anesthesia; the rats were allowed to recover; and blood pressure and plasma renin activity were measured while the rats were awake. Anesthesia then was induced with 1.3 vol% halothane (Wistar n = 8, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6) or 2.2 vol% enflurane (Wistar n = 6, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6). A control group (Wistar n = 10, Wistar 6-OHDA n = 6, SHR n = 8, SHR 6-OHDA n = 6) was treated identically, but remained unanesthetized throughout the experiment. The untreated normotensive and hypertensive rats received no intraventricular injections. After 1 hr of stable anesthesia, plasma renin activity was measured again, and saralasin, a competitive inhibitor of angiotensin II, was infused to determine the importance of the renin--angiotensin system in blood pressure control. Treatment with 6-OHDA resulted in a 60-90% depletion of norepinephrine in the medulla and hypothalamus. Normotensive Wistar rats treated with 6-OHDA responded to halothane and enflurane anesthesia in a manner similar to untreated normotensive rats. In contrast, hypertensive animals treated with 6-OHDA and then anesthetized with halothane had a significantly greater decrease in blood pressure than untreated hypertensive rats (100 +/- 4 mm Hg vs 125 +/- 4 mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Renovascular hypertension: effect of halothane and enflurane.

Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6-9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia. Principal responses were as follows: mean arterial pressure (MAP) was 193 +/- 4 mmHg awake and decreased to 114 +/- 3 mmHg and 135 +/- 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 +/- 3 mmHg and to 69 +/- 3 mmHg and 96 +/- 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 +/- 1.3 ng X ml-1 X h-1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1983

[Purification of an endogenous inhibitor of sodium-potassium-ATPase].

From human plasma of healthy subject, an inhibitor of Na+, K+-ATPase was prepared, using a gel filtration followed by anion exchange chromatography and by HPLC on reverse phase. This low molecular weight (less than 1,500 dalton) inhibitor is a substance which possesses anionic charges, and is absorbed on reverse phase. It inhibits Na+, K+-ATPase activity and the 3H-ouabain binding on human red blood cells.

Animals↗
PubMed1983

Femoral head blood flow in long-term steroid therapy: study of rabbit model.

Using a rabbit model, previous studies showed steroid-induced hyperlipidemia with subsequent fatty embolization of the subchondral arteries and hypertrophy of the marrow fat cells, followed by elevation of femoral head pressure from the normal level of 25 cm to nearly 60 cm H2O after eight weeks of treatment. This has led us to believe that pressure changes lead to decreased blood flow in the femoral head. In our study of 22 New Zealand white adult rabbits, weighing an average of 4.0 kg, 14 received a weekly dose of 12.45 mg of methylprednisolone (Depo-Medrol), and eight served as control. Femoral head blood flow was established using the radioactive microsphere technique. Control and cortisone-treated rabbits had femoral head blood flow measured 6, 8 and 10 weeks after treatment. The average blood flow in the control femoral heads averaged 0.2039 +/- 0.076 ml/min/gm, with no difference in the left side and the right side. In the treated group, the average blood flow at ten weeks was 0.162 +/- 0.039 ml/min/gm on the right and 0.164 +/- 0.037 ml/min/gm on the left, which was significantly different. This is parallel to unpredictable clinical findings in human beings.

Animals↗
PubMed1983

Acute hypoxemia and hypercapnia: increase in plasma catecholamines in conscious dogs.

To systemically evaluate the effects of acute hypoxemia and hypercapnic acidosis on the sympathetic nervous system, five unanesthetized mongrel dogs were studied during acute hypoxemia [arterial O2 tension (PaO2) 33 +/- 2 Torr], acute hypercapnic acidosis [arterial CO2 tension (PaCO2) 53 +/- 1 Torr; pH, 7.19 +/- 0.02], and combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 Torr; PaCO2, 52 +/- 1 Torr; pH, 7.18 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis resulted in increased mean arterial pressure, cardiac output, and heart rate. Moreover, combining acute hypoxemia and hypercapnic acidosis acted synergistically to increase circulating norepinephrine and epinephrine. Acute hypoxemia alone and acute hypercapnic acidosis alone resulted in reversible increases in mean arterial pressure, cardiac output, heart rate, and circulating norepinephrine. Although plasma epinephrine concentrations increased during acute hypoxemia, circulating epinephrine was unchanged during acute hypercapnic acidosis. These data indicate that acute hypoxemia and hypercapnic acidosis result in synergistic increase in circulating catecholamines.

Acidosis↗
PubMed1981

The role of the renin-angiotensin-aldosterone system in circulatory control and hypertension.

The control of arterial pressure in normal and pathological states is governed by many mechanisms. The renin-angiotensin-aldosterone system is one mechanism which may be activated. The formation of the potent vasoconstrictor angiotensin II and the synthesis of aldosterone provide a means of arterial pressure regulation. With the recent introduction of specific agents which block the renin-angiotensin system, new appreciation of the role of this system is being formed. It is premature to predict whether we, as anaesthetists, will use such agents in our anaesthetic practice. However, we will see some patients who present for surgery taking such medication. How this will influence the patient's response to surgery is unknown. Inhibition of the renin-angiotensin system may allow better perfusion of vital organs. It may, however, be detrimental to the patient who needs this defense mechanism for support of his arterial pressure. At the present time these are all unsettled questions. Through the use of specific inhibitors of the renin-angiotensin system its importance will be defined, much as alpha- and beta-adrenoceptor antagonists have clarified our understanding of the sympathetic nervous system.

Aldosterone↗
PubMed1981

Blood flow alteration induced by saralasin or sodium nitroprusside in rats.

The radioactive microsphere technique was used to investigate the distribution of blood flow during halothane anesthesia when either sodium nitroprusside (SNP) or saralasin, a competitive inhibitor of angiotensin II, was infused. Seventeen fasted male Wistar rats were anesthetized with halothane and received either saralasin (n = 6) or SNP (n = 11) to decrease mean arterial pressure 20 torr. Cardiac output was unchanged with SNP, but blood flow decreased 23 per cent to the brain, and 25 per cent to the kidney, while splanchnic flow increased 19 per cent (P less than .05). There were 37 per cent less microspheres present in the lung after drug treatment. Saralasin did not alter cardiac output or flow to other organs but did cause a 49 per cent decrease in the number of microspheres found in the lung after drug treatment. An additional group of rats first received SNP, and then saralasin. This combination was not well tolerated, resulting in lethal hypotension and a mortality of 60 per cent. In the thirteen animals which were able to complete the protocol, increases in blood flow to the heart, kidney and splanchnic circulation were seen while brain flow decreased (P less than .05). The number of microspheres in the lung also decreased after combined therapy. These studies demonstrate the differential effects of SNP and saralasin in lowering blood pressure. The use of combined drug treatment, when tolerated, may improve organ perfusion.

Anesthesia↗
PubMed1981

The effects of lidocaine on the whole body distribution of radioactively labeled microspheres in the conscious rat.

Radioactively labeled 15-micrometer microspheres were used to evaluate the effects of intravenous lidocaine on cardiac output and distribution of tissue blood flow in awake rats. After a one-hour control period, all animals (n = 22) received 85Sr-labeled microspheres for a control measurement. The animals were then divided into three groups. The control group (n = 6) received a bolus of saline and then an infusion of saline. After 40 minutes, a second microsphere (141Ce) was injected, the animals killed, and tissue blood flow determined. A second group of rats (n = 8) were similarly treated except that they received a bolus and infusion of lidocaine resulting in a plasma concentration of 1.98 +/- 0.3 microgram of lidocaine/ml. A third group of rats (n = 8) received a higher dose of lidocaine which resulted in a plasma concentration of 6.37 +/- 0.3 microgram of lidocaine/ml. In the control and low-dose lidocaine group, there were no changes in blood pressure, heart rate, cardiac output or tissue blood flow. At the higher lidocaine concentration, blood pressure remained the same but cardiac output and heart rate were decreased. Tissue blood flow to brain, heart and muscle was responsible for the increased peripheral resistance. These results suggest that high blood concentrations of lidocaine alter flow to vital organs in the rat.

Animals↗
PubMed1981

Effects of propranolol on the cardiovascular and renin-angiotensin systems during hypotension produced by sodium nitroprusside in humans.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.

Adolescent↗
PubMed1981

Influence of surgically induced varicocele on testicular blood flow, temperature, and histology in adult rats and dogs.

Varicocele had been repeatedly implicated as a cause of infertility in selected men, although neither a causal relationship nor a mechanism has been documented. The purpose of this investigation was to create a varicocele model in animals and to study the subsequent alterations in testicular physiology. Secondary dilatation of the left internal spermatic vein was achieved either by partial ligation of the left renal vein in rats and dogs or by surgical destruction of the valve of the left testicular vein in a second group of dogs. 1 mo after partial ligation in the rats and 3 mo after partial ligation or valve destruction in the dogs, testicular blood flow was measured using Strontium 85 (SR-85)-labeled microspheres (15 +/- 1.1 micrometer). Intratesticular temperature was measured with a Bailey needle probe thermometer and biopsies were obtained for histologic sections. Mean testicular blood flow in milliliters per minute per 100 g was significantly greater in the partially ligated rats; right testis control 26 +/- 2, left testis control 24 +/- 2 compared to right testis experimental 35 +/- 3, left testis experimental 35 +/- 4 (p less than 0.02). Dogs undergoing either partial vein ligation or valve destruction showed similar increases in mean testicular blood flow; right testis control 8 +/- 1, left testis control 8 +/- 1 vs. right testis experimental 16 +/- 3, left testis experimental 18 +/- 4 (p less than 0.01). The mean difference between intratesticular and intraperitoneal temperature in control rats was significantly higher (4.02 +/- 0.25 degrees C right testis, 3.77 +/- 0.14 degrees C left testis), than rats who underwent partial vein ligation (right testis 2.14 +/- 0.09 degrees C, left testis 2.34 +/- 0.12 degrees C) (p less than 0.001). Control dogs also had a significantly higher mean difference between intratesticular and rectal temperatures; (right testis control 3.61 +/- 0.42 degrees C, left testis control 3.60 +/- 0.40 degrees C) than the partially ligated or valve destruction dogs (right testis 2.31 +/- 0.17 degrees C, left testis 2.67 +/- 0.32 degrees C) (p less than 0.05). In addition, histologic evaluation revealed abnormalities in spermatogenesis in some of the animals. Thus, venous dilatation secondary to partial vein ligation or testicular vein valve obliteration is followed by large bilateral increases in testicular blood flow in these two species. A consequence of this increased flow is an elevation in bilateral testicular temperature, which it is postulated, leads to impaired spermatogenesis in some of the animals. In selected men varicocele may impair spermatogenesis by a similar physiologic mechanism.

Animals↗
PubMed1980

Whole-body distribution of radioactively labelled microspheres in the rat during anesthesia with halothane, enflurane, or ketamine.

Cardiac output and distribution of blood flow using 15-micron radioactively labelled microspheres were determined in 25 Wistar rats. In seven awake control animals, first and second injections of microspheres did not change cardiac output (137 +/- 8 ml/min) or result in alteration in apparent blood flow to the various organs studied. Halothane anesthesia (n = 6) (1.3 per cent inspired) resulted in a decrease in cardiac output, with increases in the percentages of cardiac output going to the brain, kidney, liver and large intestine. Enflurane anesthesia (n = 6) (2.2 per cent inspired) did not decrease cardiac output. The percentages of cardiac output going to the liver, lung, spleen, and large intestine increased. Both halothane and enflurane caused decreases in the percentages of cardiac output going to the heart and skeletal muscle. Ketamine anesthesia (n = 6) (125 mg/kg, im) differed from the other two agents in that few changes occurred from the awake state except in brain, lung and muscle, Microspheres that were trapped after the first injection were released from muscle and skin with ketamine anesthesia, resulting in an apparent decrease in the distribution of cardiac output to muscle in the controls and an apparent increase in "flow" to the lung. The microsphere method gives reliable information about cardiac output and distribution of flow in rats anesthetized with halothane or enflurane. Further studies are necessary to determine whether microsphere studies are valid indicators of organ flow during ketamine anesthesia in the rat.

Anesthesia↗