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Biomedical subjects

M Nugent

Publications and source records attributed to M Nugent.

At least 37 records · Page 2Linked to original sources
PubMed1987

Effects of isoflurane on coronary arteries and coronary arterioles in the intact dog.

To determine the site of isoflurane-associated coronary vasodilatation, the authors measured epicardial coronary artery diameter and examined the effects of isoflurane on coronary arteriolar tone. Angiograms of the left coronary system were obtained in seven fentanyl-pentobarbital anesthetized dogs and quantitated with a computerized analysis system. Cross-sectional areas of the proximal, mid, and distal left anterior descending and proximal circumflex coronary arteries were obtained at three arterial pressures, and then the measurement repeated following administration of 0.75%, 1.5%, and 2.25% end-tidal isoflurane. At the same time coronary blood flow was measured using a 123Xe washout technique. Isoflurane was found to have no effect on epicardial coronary artery dimensions. No dilatation was observed throughout the range of isoflurane concentrations and coronary perfusion pressures investigated. However, despite the absence of epicardial coronary effects, coronary arterioles were dilated by both 1.5% and 2.25% isoflurane. Coronary blood flow corresponding to a myocardial oxygen consumption of 7.5 ml oxygen X 100 gm-1 X min-1 was calculated as 99 +/- 17 ml X 100 gm-1 X min-1 (mean +/- SD) during control conditions, and it increased to 150 +/- 26 ml X 100 gm-1 X min-1 at 1.5% isoflurane (P less than .004) and to 197 +/- 35 ml X 100 gm-1 X min-1 at 2.25% isoflurane (P less than .001). Although higher concentrations of isoflurane dilated intramyocardial arterioles, isoflurane had no effect on epicardial coronary arteries.

Animals↗
PubMed1987

Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries.

The authors sought to determine if isoflurane would attenuate effects of three different types of vasoconstrictors on isolated segments of canine epicardial coronary arteries removed from healthy dogs. As the endothelium has a major role in regulating epicardial coronary artery tone, and as it modulates the effect of many vasoactive substances, experiments were conducted both on normal rings and on rings whose endothelium had been mechanically removed. In addition, the endothelium is thought to be damaged in human atherosclerosis. Rings were suspected in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% oxygen and 5% carbon dioxide, and connected to strain gauges for the measurement of isometric tension. Isoflurane 2.3% (1.5 MAC in the dog) was added to the aerating gas mixture in half the preparations, while the other rings served as control. The vasoconstrictors serotonin, phenylephrine, or prostaglandin F2 alpha were added in increasing concentrations to the bath solution. In the presence of endothelium, vasoconstrictor evoked contractions were attenuated by isoflurane. Maximal tension generated by prostaglandin F2 alpha in untreated rings was 114 +/- 18% (mean +/- SEM) of a reference contraction, while, following isoflurane, it was 46 +/- 8% (P less than 0.005). In the absence of endothelium, isoflurane attenuated neither prostaglandin F2 alpha nor serotonin evoked contraction, and had decreased effectiveness against phenylephrine mediated contraction (P less than 0.001). It is concluded that isoflurane attenuates vasoconstrictor-evoked contraction of isolated canine epicardial coronary arteries, and that this effect is mediated by the endothelium.

Animals↗
PubMed1985

Verapamil does not alter succinylcholine-induced increases in serum potassium during halothane anesthesia in normal dogs.

Six dogs were studied to determine whether verapamil pretreatment exacerbates the increase in serum potassium levels associated with succinylcholine. Dogs were anesthetized with halothane, 1.26 +/- 0% (mean +/- SEM; end tidal). Arterial blood-gas tensions, blood pressure, heart rate, temperature, and serum potassium levels were measured. Each dog underwent control and experimental studies separated by seven days. In the experimental study, a 0.15 mg/kg bolus of verapamil was followed by a 4.0 micrograms X kg-1 X min-1 continuous infusion of verapamil. Normal saline was used in the control study. Succinylcholine, 1 mg/kg bolus, was given 10 min after the initial saline or verapamil bolus. Vital signs again were measured 1, 3, 5, 10, and 15 min after succinylcholine, and plasma verapamil levels were measured 8 and 15 min after verapamil administration. Serum potassium concentrations increased from 3.9 +/- 0.2 to 5.0 +/- 0.2 mEq/L in control studies and from 3.7 +/- 0.2 to 4.8 +/- 0.3 mEq/L in animals pretreated with verapamil. Verapamil pretreatment does not alter the increase in serum potassium induced by succinylcholine in normal dogs.

Anesthesia↗
PubMed1984

Verapamil worsens rate of development and hemodynamic effects of acute hyperkalemia in halothane-anesthetized dogs: effects of calcium therapy.

The hemodynamic effects of verapamil pretreatment versus no pretreatment were evaluated in five acutely hyperkalemic dogs. Using ECG evidence for severe hyperkalemia, the halothane-anesthetized dogs were rendered acutely hyperkalemic to similar plasma levels of K+ (K+ = 8.2 +/- 0.8 mEq/l verapamil plus hyperkalemia, K+ = 9.4 +/- 0.2 mEq/l hyperkalemic controls). The verapamil-hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 +/- 0.5 1 X min-1 X m-2 verapamil plus hyperkalemia vs. CI = 3.0 +/- 0.2 1 X min-1 X m-2 hyperkalemic controls) and lower mean arterial pressures (MAP = 60 +/- 13 mmHg verapamil plus hyperkalemia vs. MAP = 96 +/- 7 mmHg hyperkalemic controls). Calcium therapy for hyperkalemia that returned CI to control levels in hyperkalemic controls only partially reversed the severe hemodynamic depression and did not improve the AV block seen during hyperkalemia in the presence of the calcium entry blocker verapamil. Surprisingly, the total mEq of KCl infused at the same rate into verapamil-pretreated dogs to result in similar high serum potassium levels was only one-third that required in dogs not pretreated with verapamil (1.6 +/- 0.3 mEq/kg KCl in verapamil-hyperkalemia group vs. 5.0 +/- 0.7 mEq/kg KCl in hyperkalemic controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1984

Influence of propranolol plasma levels on hemodynamics during coronary artery bypass surgery.

Hemodynamic effects of propranolol during coronary artery surgery were investigated in 26 patients who chronically took propranolol and who received a standardized morphine/diazepam/pancuronium/halothane anesthetic. Effects were shown by correlating logarithm of the plasma propranolol concentrations versus percentage change in hemodynamics following stressful events (induction, intubation, skin incision, sternotomy, and sternal retraction). Log propranolol and hemodynamics following cardiopulmonary bypass also were correlated. A broad range of propranolol levels were observed. Levels (range and mean +/- SD) were preinduction 0-96 (25.6 +/- 21.6) ng/ml; preincision 0-86 (27.2 +/- 24.4) ng/ml; and sternal retraction 0-92 (28.2 +/- 25.4) ng/ml. The range of hemodynamic responses to stressful events also was broad. Representative changes between preincision control and sternotomy were (range and mean +/- SD): HR-8-30 (7 +/- 10) beats/min; PCWP 1-21 (8.5 +/- 4.6) mmHg; CI -0.2-1.1 (-0.2 +/- 0.7) 1 X min-1 X m-2, and SVR -244-1,288 (310 +/- 388) dyn X s X cm-3. By the time of sternal retraction, CI had declined from preincision values in 14 patients. Linear regression analysis demonstrated an inverse correlation between log propranolol and magnitude of HR, MAP, PCWP, and CI response to stressful stimulation. A direct but statistically weaker correlation with SVR also was seen. Significant correlations between log propranolol versus hemodynamic response to anesthetic induction and versus postcardiopulmonary bypass hemodynamics were not observed.

Adult↗
PubMed1982

Cerebral metabolic, vascular and protective effects of midazolam maleate: comparison to diazepam.

The effects of midazolam maleate and diazepam on cerebral metabolism and circulation were examined for each drug in six dogs maintained on N2O 70 per cent and halothane less than 0.1 per cent. Midazolam maleate at 0.2 mg/kg and diazepam at 0.3 mg/kg (the ED 100 per cent for induction of anesthesia for each drug in humans) did not decrease metabolic rate for oxygen (CMRO2) but did decrease cerebral blood flow (CBF) to about 55 per cent of control. Additional drug administrations (2.0, 5.0, and 10.0 mg/kg midazolam maleate, and 3.0 and 7.5 mg/kg diazepam) resulted in dose-related decreases in CMRO2 to a maximum of 55 per cent of control after 10.0 mg/kg midazolam maleate. Concomitant with the initial decreases in CMRO2, there was a change in the EEG as reflected by a decrease in frequency and an increase in amplitude. This EEG change suggests that 2.0 mg/kg midazolam maleate and 3.0 mg/kg diazepam represent a comparable canine anesthetic dose. Each additional dose of midazolam maleate decreased CBF to a greater extent than did the added doses of diazepam. Brain biopsies taken at the end of the midazolam maleate studies revealed a normal cerebral energy state (phosphocreatine, ATP, ADP, and AMP) and normal glucose, lactate, and pyruvate concentrations. In a hypoxic mouse model (FIO2 = 0.05), midazolam maleate provided greater protection from hypoxia (2.8 x control survival time) than diazepam (1.6 x control survival time). By comparison barbiturates in this model provide a survival time which is 4.0 x control.

Anesthetics↗
PubMed1982

Enflurane causes a prolonged and reversible increase in the rate of CSF production in the dog.

Using the open ventriculocisternal perfusion method, rates of cerebrospinal fluid (CSF) production and reabsorption by bulk flow were examined in dogs anesthetized with either enflurane (2.2%) in nitrogen (60-70%) and oxygen, or nitrous oxide (60-70%) and enflurane (less than 0.2%) in oxygen (controls). The mean rate of CSF production increased significantly with enflurane (2.2%), from 0.055 +/- 0.020 ml/min (mean +/- SD) in controls to 0.082 +/- 0.033 ml/min (n = 12). After this initial increase of approximately 50%, the production rate decreased significantly by about 7.4%/h. When the expired concentration of enflurane was decreased from 2.2% to less than 0.2%, the mean rate of CSF production decreased to control values at 45-50 min. An intracerebral accumulation of CSF resulting from this enflurane-induced increase in CSF production may contribute in part to increased intracranial pressure when the dura is intact.

Animals↗
PubMed1982

Closed recirculatory spinal subarachnoid perfusion for determining CSF dynamics.

A new method for determining the rates of cerebrospinal fluid (CSF) production under nonsteady-state conditions, namely, closed recirculatory spinal subarachnoid perfusion, was used to determine the effect of enflurane on the rate of CSF production in dogs. Considerable variability in results was observed such that there was no statistical difference in rates of production among animals that received enflurane 2.2%, enflurane 2.2% and nitrous oxide 60% to 70%, enflurane 3.2% and nitrous oxide 60% to 70%, or nitrous oxide 60% to 70% (controls). Possible sources of variability were sought in additional studies using a modification of the new method, and in an in vitro model. The results were compared to those obtained using an established method for determining rates of CSF production, namely, open ventriculocisternal perfusion. It was concluded that the sources of variability in the closed recirculatory method relate in part to adherence of the fluorescein-conjugated albumin tracer to glass and other surfaces, and to uneven flow and distribution of the tracer in the recirculatory system. When the open ventriculocisternal perfusion method was used, consistent results were obtained, demonstrating that CSF production rate increased significantly in animals that received enflurane. The authors conclude that the new closed recirculatory method is less reliable than the classical open perfusion method.

Animals↗
PubMed1981

Anesthetics affect the cerebral metabolic response to circulatory catecholamines.

This study examined whether the effect of intravenous infusions of either epinephrine or norepinephrine on cerebral metabolic rate for oxygen (CMRO2) in the dog was modified by different anesthetics. Infusions of either epinephrine or norepinephrine at rates of 0.1-0.25 mu.kg-1.min-1 reversibly increased the CMRO2 by 17-23% during anesthesia with cyclopropane 20% and nitrous oxide 50% in oxygen, whereas infusions at rates of 0.1-25.0 micrograms.kg-1.min-1 had no effect in dogs anesthetized with other inhalational or intravenous agents. Cyclopropane/nitrous oxide also increased permeability of the blood-brain barrier to Evan's blue dye whereas the other anesthetics tested did not. It is concluded that epinephrine and norepinephrine crossed the blood-brain barrier during cyclopropane anesthesia, accounting for the increase in CMRO2. The authors speculate that cyclopropane may have increased blood-brain barrier permeability by a direct effect on endothelial cells or by affecting central adrenergic systems and that epinephrine or norepinephrine may increase CMRO2 either by a direct action on neuronal receptors or via metabolically coupled synaptic events.

Anesthetics↗