Intraoperative pacemaker malfunction during total hip arthroplasty.
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Aged↗
Biomedical subjects
E D Miller
Publications and source records attributed to E D Miller.
Esmolol hydrochloride, sodium nitroprusside, and isoflurane differ in their ability to alter peripheral sympathetic responses.
To demonstrate that esmolol, sodium nitroprusside, and isoflurane differ in their abilities to alter adrenal medullary blood flow and other peripheral sympathetic responses to hypotension, 16 mongrel dogs anesthetized with pentobarbital were allocated randomly to one of four test groups and given two hypotensive stimuli, separated by 1 h, to a mean arterial blood pressure of 60 mm Hg for 10 min. The first stimulus, induced by blood loss into a pressurized bottle system, constituted the control for each animal. The second hypotensive stimulus was created by either repeat blood loss (Group 1), esmolol infusion (Group 2), sodium nitroprusside infusion (Group 3), or isoflurane administration (Group 4). Before and 10 min into hypotension, the variables of abdominal organ blood flow, adrenal medullary blood flow, arterial norepinephrine and epinephrine concentrations were measured. In the control animals (Group 1), comparable decreases in abdominal organ blood flow and similar increases in adrenal medullary blood flow, norepinephrine, and epinephrine were elicited by the first and second hypotensive stimulus. Esmolol-induced hypotension (Group 2) abolished the increase in adrenal medullary blood flow and attenuated the increase in epinephrine by 65% (P < 0.03). The decrease in abdominal organ blood flow and the increase in norepinephrine were similar to that observed during baseline hemorrhagic hypotension. In contrast, sodium nitroprusside-induced hypotension (Group 3) abolished abdominal organ vasoconstriction whereas the increases in adrenal medullary blood flow, norepinephrine, and epinephrine were comparable to baseline hemorrhagic hypotension. In fact, abdominal organ blood flow increased 2.5-fold (P < 0.001) during hypotension with SNP. Isoflurane 2%, 1.54 minimum alveolar anesthesia concentration (Group 4), abolished the increases in adrenal medullary blood flow, norepinephrine, and epinephrine observed during baseline hemorrhagic hypotension and attenuated the decrease in abdominal organ blood flow by 70% (P < 0.001). These data demonstrate that esmolol, sodium nitroprusside, and isoflurane differ radically in their ability to alter or blunt peripheral sympathetic responses to hypotension, and suggest that isoflurane is the drug most effective in blunting multiple responses of the peripheral sympathetic system.
Adrenergic beta-Antagonists↗
Isoflurane-induced splanchnic sympathectomy.
To ascertain whether isoflurane produces a peripheral splanchnic sympathectomy as compared to fentanyl or pentobarbital anesthesia, 12 mongrel dogs (30-45 kg) were allocated randomly to one of three anesthetic test groups, tracheally intubated, surgically prepared, and subjected to unilateral electrical stimulation of the greater splanchnic nerve. Anesthetically, Group 1 animals (n = 4) received pentobarbital, Group 2 animals (n = 4) were administered fentanyl, and Group 3 animals (n = 4) received isoflurane. Stimulation continued for 90 min. Each second of stimulation consisted of 20 stimuli of 0.5 minimum alveolar anesthetic concentration duration and 5 V intensity, delivered during a 0.2-s interval, followed by an 0.8-s pause. To assess splanchnic sympathetic responses, mean arterial blood pressure, heart rate, pulmonary artery diastolic, cardiac output, adrenal blood flow, adrenal and arterial norepinephrine (N) and epinephrine (E) were obtained before and at 5, 10, 15, 30, 45, 60, and 90 min during stimulation. In Group 1 animals (pentobarbital), electrical stimulation elicited marked increases in mean arterial blood pressure, pulmonary artery diastolic, and cardiac output (P < 0.001). Examination of the adrenal effluent, which was exteriorized from the animal during the protocol, revealed that adrenal blood flow, adrenal vein N and E concentrations dramatically increased (P < 0.0001). Arterial N and E concentrations remained unchanged. Results of Group 2 animals (fentanyl) were similar to those of Group 1; mean arterial blood pressure, pulmonary artery diastolic, and cardiac output increased (P < 0.005). Adrenal blood flow, adrenal vein N and E increased dramatically (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Pregnancy alters the hemodynamic responses to cocaine in the rat.
To test our hypotheses that the hemodynamic response to cocaine may be altered during pregnancy, cocaine (0.33 mg/kg/min) was infused intravenously to chronically catheterized pregnant and nonpregnant female rats. Cardiac output and regional blood flow were measured, and cocaine concentrations in plasma and tissues, as well as plasma cholinesterase activity were determined. Results were compared between pregnant and nonpregnant groups. Cocaine produced a significant decrease in heart rate, accompanied by a fall in cardiac output, and decreased cerebral, myocardial, and placental blood flow in pregnant rats. The plasma cocaine concentration in pregnant animals was lower than that of nonpregnant ones, but tissue concentrations were similar in both groups. These results indicate that pregnancy enhances cardiovascular responses to subtoxic doses of cocaine. There was little placental transfer of cocaine with a fetal to maternal plasma concentration ratio of 0.28.
Animals↗
Subarachnoid blockade alters homeostasis by modifying compensatory splanchnic responses to hemorrhagic hypotension.
To demonstrate that sympathetic responses transmitted by the splanchnic nerve help maintain intravascular stability, 12 mongrel dogs (35-45 kg each), anesthetized with pentobarbital, were given two separate but identical hypotensive stimuli (mean arterial blood pressure of 60 mm Hg for 15 min) by the withdrawal of appropriate amounts of blood. The first stimulus was performed in the absence of drug or surgical manipulation. The second stimulus was performed after animals were subjected to no intervention (n = 4), bilateral splanchnic nerve section (n = 4), or spinal anesthesia (n = 4). Before and 10 min after the onset of hypotension, arterial epinephrine concentration and adrenal medullary and abdominal organ blood flow were measured. In the group without intervention, the second hypotensive stimulus (like the first) elicited 3-fold increases in adrenal medullary blood flow, 40-fold increases in arterial epinephrine concentration, and a 61% reduction in abdominal organ blood flow (P greater than 0.002). The volume of blood withdrawn to produce hypotension was similar (approximately 21 ml.kg-1). Bilateral splanchnic nerve section attenuated the adrenal medullary blood flow, arterial epinephrine concentration, and abdominal organ blood flow responses to hypotension by 86, 64, and 66%, respectively (P less than 0.008), and the blood volume withdrawn was reduced by 42% (P less than 0.02). Spinal anesthesia eliminated the adrenal medullary blood flow response to hypotension, attenuated the arterial epinephrine concentration and abdominal organ blood flow responses by 78 and 57%, respectively (P less than 0.01), and decreased the blood volume extracted by 55% (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Medulla↗
Waking up to desflurane: the anesthetic for the '90s?
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Anesthetics↗
Hemodynamic effects of dobutamine in patients following mitral valve replacement.
Mitral valve replacement is frequently complicated by a low cardiac output syndrome and elevated pulmonary arterial pressures. In the present study, we used dobutamine to increase cardiac index and measured the pulmonary hemodynamic effects in 10 patients with increased pulmonary vascular tone following mitral valve replacement. Using increasing doses of dobutamine up to 10 micrograms.kg-1.min-1, we observed a statistically significant increase in mean cardiac index (from 2.39 +/- .14 liters.min-1.m-2 to 3.52 +/- .33, P less than 0.01) and mean heart rate (from 71.6 +/- 5.2 beats.min-1 to 84.3 +/- 8.1, P less than 0.01). This was associated with stable mean systemic arterial pressures and mean pulmonary arterial pressures. Both mean systemic and pulmonary vascular resistances decreased significantly (from 1210 +/- 99 dynes.sec.cm-5 to 809 +/- 90 [P less than 0.01], and from 195.9 +/- 30.6 dynes.sec.cm-5 to 129.4 +/- 41.2 [P less than 0.01] respectively) with dobutamine. Intrapulmonary shunt flow increased significantly in the five patients studied. Though increases in heart rate and pulmonary shunt flow may limit it use, dobutamine increases cardiac output and decreases pulmonary vascular resistance in patients with increased pulmonary arterial pressure following mitral valve replacement.
Adult↗
The role of atrial natriuretic peptide in cardiac surgery.
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Atrial Natriuretic Factor↗
Hypoxemia and hypercapnia in conscious dogs: opioid modulation of catecholamines.
The role of endogenous opioids in systemic and renal circulatory changes during combined acute hypoxemia and hypercapnic acidosis was evaluated in seven conscious female mongrel dogs in rigid sodium balance. Animals were studied 2 wk apart in separate protocols of combined acute hypoxemia (arterial O2 tension = 33 +/- 1 mmHg) and hypercapnic acidosis (arterial CO2 tension = 56 +/- 1 mmHg, pH = 7.19 +/- 0.01) of 40 min duration during 1) naloxone, 5 mg/kg iv bolus followed by an intravenous infusion of 5 mg.kg-1.h-1, and 2) vehicle (5% dextrose in water) alone. Systemic circulatory changes during the combined acute blood-gas derangement including increased mean arterial pressure, heart rate, and cardiac output and decreased total peripheral resistance were comparable between naloxone and vehicle treatments. However, in striking contrast to the brief fall in renal hemodynamic function during combined acute hypoxemia and hypercapnic acidosis with vehicle, naloxone administration during the combined acute blood-gas derangement resulted in a sustained decrease in effective renal plasma flow, glomerular filtration rate, and filtered sodium load and enhanced rise in circulating norepinephrine and epinephrine. Changes in plasma renin activity were comparable between vehicle and naloxone protocols except that plasma renin activity increased from the first to the second 20-min periods of combined hypoxemia and hypercapnic acidosis with naloxone. These observations suggest that endogenous opioids may contribute to preservation of renal hemodynamic function during acute blood-gas derangements, possibly through attenuation of sympathetic nervous system and renin-angiotension activation.
Animals↗
A 2000 gm tubal pregnancy.
A multigravid patient in Papua New Guinea had a fetal death at 33 weeks' gestation. After nine attempts at induction of labor failed, a laparotomy revealed that the 2000 gm fetus was enclosed in the midsegment of the left Fallopian tube.
Adult↗
Presence of angiotensinogen messenger RNA in various cultured cell lines.
The presence of angiotensinogen messenger RNA (mRNA) was assessed in total RNA extracted from hepatoma, glioma, neuroblastoma, and glioma-neuroblastoma hybrid cell lines. Total RNA from 1 X 10(7) cells was extracted, transferred to a membrane, and hybridized with a 32P-labeled, full-length (1650-base pair) rat angiotensinogen complementary DNA (cDNA). Angiotensinogen RNA sequences could be definitively detected only in hepatoma cells. Steroids were used in an attempt to increase the angiotensinogen mRNA level. Dexamethasone (2 X 10(-6) M) or 17 beta-estradiol (1 X 10(-7) M) was added to the cultures 18 to 24 hours prior to harvest. Dexamethasone treatment of the hepatoma cells resulted in a large increase in angiotensinogen mRNA, whereas estradiol had no effect. Steroids failed to induce detectable levels of angiotensinogen mRNA in total RNA from the other cell lines. That the RNA was intact was ensured by hybridizing duplicate Northern blots to a 32P-labeled actin cDNA. Actin mRNA sequences were detected in all cell lines. Blot hybridization of poly(A)+RNA resulted in the visualization of a weak angiotensinogen mRNA signal for a glioma cell line and a glioma-neuroblastoma hybrid line. However, the ability to detect angiotensinogen mRNA in a cell may depend on the phenotype expressed, which can be governed by culture conditions.
Angiotensinogen↗
Effects of U-50488H, a selective kappa-analgesic, on the minimum anesthetic concentration (MAC) of halothane in the rat.
The effects of U-50488H, a selective kappa-analgesic, on the minimum anesthetic concentration (MAC) of an inhalational agent (halothane) were studied in the rat. U-50488H was given subcutaneously in doses of 3, 10, and 30 mg/kg body weight. The maximal MAC reduction was about 60%. The potency ratio of U-50488H to morphine in this model was comparable with potency ratios in other analgesic assays. In separate experiments, the percent reduction in halothane MAC with U-50488H at 30 mg/kg was determined during the infusion of naloxone (5 micrograms X kg-1 X min-1 and 1 mg X kg-1 X min-1) at doses shown to have reversed a 70% reduction in MAC by 10 mg/kg of morphine. Only when naloxone was infused at 1 mg X kg-1 X min-1 was there a significant reversal of the U-50488H-induced reduction in halothane MAC. This observation suggests that the reduction in MAC of halothane with U-50488H was not mediated by a mu-receptor. In conclusion, through the use of a selective pharmacologic tool that stimulates kappa-receptors we have demonstrated potential utility of kappa-analgesics as supplements to general anesthesia.
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
Macular degeneration and elevated serum ceruloplasmin.
Macular degeneration associated with age and drusen, an important cause of visual loss, is associated clinically with alterations in the retinal pigmented epithelium. Because the pigmented epithelium is a copper-rich tissue with antioxidant properties, the copper economy in patients and controls were studied by measuring ceruloplasmin. Ceruloplasmin, a multifunctional, copper-binding alpha-globulin, was significantly elevated in non-related patients as compared with controls (691 +/- 153 mg/L vs 312 +/- 64; P less than .001), both by the p-phenylenediamine oxidation technique and radial immunodiffusion assay. When 53 members of a large family were divided clinically into persons with and without macular degeneration, the ceruloplasmin concentrations were not significantly different from each other, but were elevated as compared with non-related controls (P less than .001). These differences were not due to an intragroup age mismatch. A group of patients with retinitis pigmentosa had normal serum ceruloplasmin concentrations. This study suggests a relationship between serum ceruloplasmin, trace metals, and the tissue alterations associated with macular degeneration that deserves further investigation.
Ceruloplasmin↗
Perioperative hypertension.
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Anesthesia, General↗
Central serotonin depletion: effect on blood pressure during anesthesia.
Serotonin (5-HT) in the central nervous system has been implicated in blood pressure control in both normotensive and hypertensive states. Parachlorophenylalanine (PCPA) depletes 5-HT in the central nervous system. Normotensive Wistar rats, Wistar rats made hypertensive by renal artery clipping (RHR), and spontaneously hypertensive rats (SHR) were depleted of central serotonin by the administration of PCPA. Mean arterial blood pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) levels were measured in rats both before and after they were administered anesthesia with enflurane. Blood pressure was further decreased by the administration of saralasin, a competitive inhibitor of angiotensin II. Principal results are as follows. Central 5-HT was depleted by 70% or more with PCPA. In general, brain catecholamines were not altered by this treatment. No consistent pattern of change in MAP, HR, or plasma NE was observed for Wistar rats, RHR, or SHR during an awake control period in rats treated with PCPA compared with rats treated with vehicle. However, during enflurane anesthesia or enflurane anesthesia with saralasin, MAP, HR, and plasma NE were significantly greater in Wistar rats and RHR treated with PCPA compared to similar groups treated with vehicle. This was not observed in SHR: MAP, HR, and plasma NE were similar to vehicle-treated SHR. Nonsignificant changes in plasma epinephrine, plasma renin activity, or arterial blood gas tensions could not explain the differences seen in Wistar rats, RHR, or SHR. Central serotonin plays an important role in cardiovascular control during anesthesia with enflurane in Wistar rats but does not appear to play a dominant role in SHR.
Analysis of Variance↗
Analgetic contribution of sufentanil during halothane anesthesia: a mechanism involving serotonin.
Catecholamine and serotonin concentrations in the cord, medulla, and hypothalamus were measured in rats after saline, after sufentanil sufficient to reduce the minimum alveolar concentration (MAC) of halothane by 30% or less, or after sufentanil sufficient to reduce the MAC of halothane by 80% or more. In the cord, high doses of sufentanil resulted in a 13.4% reduction (P less than 0.05) in serotonin concentration compared to saline control and a 17.4% reduction (P less than 0.05) in serotonin concentration compared to low dosages of sufentanil. A 12.8% reduction (P less than 0.05) in medullary serotonin also was observed with high sufentanil compared to low sufentanil. Epinephrine decreased significantly in the hypothalamus at the high sufentanil dose. No other significant differences were found in catecholamine content. The experimental results support the hypothesis that sufentanil may contribute to an analgetic component of general anesthesia by modulating nociception via the release of 5-HT.
Analgesics↗
Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats.
Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.
Anesthesia, Inhalation↗
Subclavian vein catheterization for central line placement in children under 2 years of age.
Using subclavian vein catheterization after unsuccessful internal jugular venous puncture, the authors have been successful in 23 of 32 children younger than 2 years of age. There was no mortality, and minimal morbidity, with this procedure. Cannulation should be performed in most cases on the first insertion of the needle, and the Seldinger technique using a J-wire aids in catheter placement. Though we did not cause pneumothorax, the inability to obtain a chest x ray prior to the operative procedure in most patients causes us to suggest that this technique be used only on those patients requiring an open chest operative procedure.
Cardiac Surgical Procedures↗