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Biomedical subjects

D M Turner

Publications and source records attributed to D M Turner.

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

Effects of naloxone on canine cerebral vascular smooth muscle.

The pharmacological effects of naloxone on cerebral arterial smooth muscle in vitro were examined using canine basilar arterial strips. Naloxone exerted two different effects on canine basilar artery: (1) at a high concentration (3 X 10(-4) M) it produced nonspecific vasodilation, and (2) at lower concentrations (3 X 10(-7), 3 X 10(-6), and 3 X 10(-5) M) it inhibited the vasoconstrictor effects of norepinephrine without altering KCl-, serotonin-, or hemoglobin-induced constriction. Morphine (2 X 10(-5) or 2 X 10(-4) M) did not reverse the specific vasodilating effect of naloxone (3 X 10(-5) M) on norepinephrine-induced constriction. Rather, morphine and naloxone together produced a greater vasodilating effect on norepinephrine-induced constriction than either agent alone. Naloxone (3 X 10(-5) M) failed to alter either phenylephrine-induced constriction or clonidine-induced constriction. The vasodilating effect of naloxone (3 X 10(-5) M) on 10(-3) M norepinephrine-induced constriction was not reduced with 10(-6) M propranolol. These results suggest that the vasodilating effect of naloxone on norepinephrine-induced constriction does not result from an antagonistic action on opiate receptors, direct inhibition of alpha-adrenoreceptors, or direct stimulation of beta-adrenoreceptors in canine cerebral arterial smooth muscle. The vasodilating effect of naloxone on norepinephrine-induced constriction may influence the CBF changes following naloxone administration.

Animals↗
PubMed1984

Time-dependent changes in cerebral and cardiovascular parameters in isoflurane-nitrous oxide-anesthetized dogs.

The purpose of this study was to examine the time-dependent effects of isoflurane-nitrous oxide anesthesia on cerebral blood flow and metabolism and on cardiovascular parameters. Eleven 15-kg mongrel dogs were anesthetized with 0.8% isoflurane (approximately 1.3 MAC (minimal anesthetic concentration], 70% nitrous oxide, and 30% O2 and were paralyzed with pancuronium. Blood flow (using the radioactive microsphere technique) and cerebrovascular and cardiovascular parameters were measured 6 times at 30-minute intervals beginning 2 hours after the induction of anesthesia. In this experiment, cerebral blood flow was markedly elevated at 2 hours after the induction of anesthesia, but then declined progressively by 40 to 50% over the 2 1/2-hour time period investigated, approaching values for normal awake dogs. The decline was accompanied by a progressive decrease in the cerebral metabolic rate of oxygen and a constant rise in cerebrovascular resistance. Blood flow to organs outside the central nervous system declined progressively, but with more variability between tissues. The mean arterial pressure increased slightly, and the peripheral vascular resistance almost doubled, but cardiac index, cardiac work, and stroke volume all decreased gradually. We conclude that isoflurane-nitrous oxide anesthesia produces significant cerebral vasodilatation in dogs, but that this effect diminishes over time. These time-dependent circulatory changes merit further investigation in humans.

Anesthesia, General↗
PubMed1984

Cerebral and systemic vascular effects of naloxone in pentobarbital-anesthetized normal dogs.

In this study, 10 mongrel dogs were anesthetized with sodium pentobarbital and nitrous oxide. Blood flow was determined using the radioactive microsphere technique before and after the bolus intravenous injection of naloxone (10 mg/kg). Naloxone significantly increased cerebral blood flow to cerebral cortex and the total cerebral hemisphere without an associated change in the cerebral metabolic rate of oxygen. The increase in cerebral blood flow was proportional to the elevation in mean arterial pressure. There were no consistent changes in electrical activity as measured by electroencephalography (EEG) and Fourier analysis of EEG. Systemically, naloxone induced a proportional rise in mean arterial pressure and peripheral vascular resistance and also stimulated the myocardium, as evidenced by an improved cardiac index and stroke volume. These data suggest that naloxone may interfere with cerebral autoregulation or have direct vasodilatory effects on cerebral blood vessels that are not associated with opiate receptor blockade or changes in cerebral metabolism. In addition, naloxone did not appear to reverse the cerebral depressive effects of pentobarbital. Systemically, naloxone seemed to potentiate pentobarbital-induced vasoconstriction and reverse myocardial depression.

Anesthesia↗
PubMed1984

Effects of naloxone on cerebral blood flow and metabolism in isoflurane/nitrous oxide-anesthetized dogs.

The purpose of this study was to document the changes in the cerebral and systemic circulations that result from various doses of naloxone. Twenty-four dogs were anesthetized with 0.8% isoflurane and 70% nitrous oxide (1.3 minimal anesthetic concentration). Thirteen of the dogs received bolus injections of naloxone at logarithmically increasing doses 30 minutes apart. Blood flow to the brain and other organs was determined using the radioactive microsphere technique. Electrical activity was measured by electroencephalography (EEG). High dose naloxone increased both cerebral blood flow (CBF) and cerebral metabolism. The changes in CBF were most pronounced in structures containing a large amount of gray matter, particularly the cerebral cortex, brain stem, and cervical spinal cord. The increase in blood flow was proportionately greater than the increase in the cerebral metabolic rate of oxygen, and EEG activity was unchanged. Naloxone did not produce any significant cardiovascular changes or alterations in myocardial, renal, hepatic, stomach, jejunum, or temporalis and paraspinous muscle flow. Accordingly, it seems that naloxone may have direct cerebral vasodilator properties.

Anesthesia, General↗
PubMed1984

High dose naloxone produces cerebral vasodilation.

In this study, 12 dogs were anesthetized with sodium pentobarbital, and blood flows were determined using the radioactive microsphere technique. Ten dogs were first made acutely hypertensive by the infusion of norepinephrine and demonstrated preserved cerebral autoregulation. The administration of naloxone, 10 mg/kg i.v., in these animals produced a significant increase in cerebral blood flow and a proportional drop in cerebrovascular resistance with no change in the cerebral metabolic rate of oxygen or the electroencephalogram. Two additional spontaneously hypertensive dogs demonstrated a similar response to naloxone. These results suggest that high dose naloxone produces cerebrovasodilation either directly or through the inhibition of cerebral autoregulation.

Animals↗
PubMed1984

Effects of naloxone during high dose barbiturate anesthesia.

This experiment was performed to investigate the ability of naloxone to reverse high dose barbiturate anesthesia or produce cerebrovasodilation or changes in cerebral metabolism in dogs neuronally depressed by high doses of barbiturate. Six dogs were deeply anesthetized with sufficiently high doses of sodium pentobarbital to produce and then maintain isoelectric activity or cerebral silence on the electroencephalogram (EEG). Blood flows were determined using the radioactive microsphere technique both before and after the intravenous bolus injection of naloxone (10 mg/kg), which failed to produce any significant changes in cerebral blood flow, the cerebral metabolic rate of oxygen, cerebrovascular resistance, or EEG activity. Cardiovascular parameters were also essentially unchanged. Naloxone in a dose of 10 mg/kg i.v. produced no changes in the cerebral or systemic circulations or in brain metabolism during high dose sodium pentobarbital anesthesia.

Anesthesia, General↗
PubMed1984

Microsurgical carotid endarterectomy in rats.

The purpose of this study was to develop an inexpensive experimental model of carotid endarterectomy. Unilateral common carotid endarterectomies 3 mm in length were performed on 25 rats using microsurgical techniques. The pattern of endothelial regrowth after endarterectomy, the pinocytosis of regenerated endothelial cells, and the effects of heparin and thromboxane A2 synthetase inhibitor on thrombus formation were examined 7 days after the resumption of flow. Pinocytotic vesicular transport in endothelial cells was evaluated using horseradish peroxidase. All endarterectomized vessels in both control and drug-treated groups were patent 7 days after operation without apparent mural thrombus formation. Regenerated endothelial cells had spindle-shaped nuclei and cell bodies with long axes oriented parallel to the direction of blood flow. There were several instances where the leading edge of the endothelium at the distal end was reflected back in the distal direction. The extent of the endothelial ingrowth was often greater from the proximal end of the endarterectomy than from the distal end. These observations suggest that hemodynamic force affects endothelial regeneration. Pinocytotic activity was less in the regenerated endothelium than in either the endothelium remaining at the periphery of the endarterectomy or the endothelium of the control animals.

Animals↗
PubMed1984

Phenoxybenzamine in the treatment of causalgia. Report of 40 cases.

Forty consecutive cases of causalgia treated during a 7-year period are presented. The patients ranged in age between 17 and 55 years, and all patients were males who received their nerve injuries from missile or shrapnel wounds. The greater occipital nerve was involved in two cases, median nerve in 10, sciatic nerve in 12, brachial plexus in seven, cauda equina in five, and multiple nerves in four cases. Each patient was treated with phenoxybenzamine, a postsynaptic alpha 1-blocker and presynaptic alpha 2-blocking agent. The drug was given orally in gradually increasing increments until a maximum daily dose of 40 to 120 mg was reached. Duration of treatment was usually 6 to 8 weeks. Total resolution of pain was achieved in all cases. The follow-up period ranged between 6 months and 6 years. Side effects of phenoxybenzamine were minimal and transient, consisting primarily of mild orthostatic hypotension and ejaculatory problems. We conclude that oral phenoxybenzamine is a simple, safe, and effective treatment of causalgia.

Adolescent↗
PubMed1984

The effects of naloxone on canine splanchnic arterial smooth muscle.

The pharmacological properties of naloxone on vascular smooth muscle in vitro were examined using canine mesenteric arterial segments. Naloxone exerted two different effects on the artery: (A) naloxone at a high concentration (3 X 10(-4) M) produced a nonspecific vasodilation; and (B) naloxone at lower concentrations (3 X 10(-7), 3 X 10(-6), and 3 X 10(-5) M) augmented the vasoconstrictor effects of epinephrine and norepinephrine without altering KCl- or serotonin-induced constriction. Naloxone's augmenting effect on epinephrine-induced constriction was dose dependent. Even when the arterial strips were incubated in low calcium (0.8 mM) or calcium free Kreb's solution, naloxone (3 X 10(-5) M) still augmented epinephrine-induced constriction. With respect to naloxone's effect on another alpha-adrenoreceptor agonist, naloxone (3 X 10(-5) M) failed to alter phenylephrine-induced constriction. Naloxone's augmenting effect on norepinephrine-induced constriction was abolished when the specimens were incubated with 10(-5) M normetanephrine, while naloxone (3 X 10(-5) M) still augmented the constriction even when the specimens were incubated with 10(-5) M cocaine. These results suggest that naloxone at lower concentrations may augment the constrictor responses to catecholamines, at least in part, by inhibiting the extraneuronal uptake of those catecholamines.

Animals↗
PubMed1983

Management and outcome of pineal region tumors.

The management and outcome of 45 patients with tumors in the pineal region are reviewed. The overall male to female ratio was 2:1, and over one-half of the patients presented during the 2nd decade of life. Sixteen of the 21 survivors are presently gainfully employed and suffer only minor deficits. Two of 3 survivors in whom the lesion was biopsied harbored germinomas, while the third had an epidermoid. Among the 18 nonsurvivors, all of whom died of their tumors, 15 succumbed within 2 1/2 years of hospital admission. Twelve of the 13 nonsurvivors in whom histological confirmation was obtained by operation or autopsy had malignant tumors. Computed axial tomography was helpful in making the diagnosis of tumor type in 7 of the 11 cases with confirmed pathology. Cerebrospinal fluid cytology disclosed malignant cells in 4 of 11 patients with proven pineal malignancy. Irradiation and shunting were performed in nearly all survivors and in a little over one-half of the nonsurvivors. Where noninvasive studies are equivocal for malignancy, biopsy may be indicated.

Adolescent↗
PubMed1983

Spontaneous intracerebral hematoma in carotid-cavernous fistula. Report of three cases.

Spontaneous intracerebral hematoma associated with carotid-cavernous fistula is rare. Three new cases are presented. In each, the hemorrhage originated in the vicinity of localized intracranial venous engorgement, as demonstrated by cerebral angiography. Rupture of one or several of the distended venous channels from increased back-flow is postulated as the etiology of the intraparenchymal hematomas.

Aged↗
PubMed1980

Phenylbutazone-induced blood dyscrasias suspected in three dogs.

Blood dyscrasias developed after drug therapy in three dogs. Two died, one with pancytopenic marrow failure and the other with non-regenerative anaemia and thrombocytopenia. The third dog developed pancytopenia but recovered. An adverse reaction to phenylbutazone was suspected as the cause in each case, although two of the dogs had also received other drugs which sometimes cause blood dyscrasias in humans.

Anemia↗
PubMed1979

Atherogenesis in the White Carneau pigeon. Further studies of the role of carbon monoxide and dietary cholesterol.

Two experiments are described. In the first, 3 pairs of groups of 20 female White Carneau pigeons were fed on diets containing 0.5%, 1% or 2% cholesterol. Birds in one group from each pair were exposed to 150 ppm carbon monoxide (CO) for 6 h on 5 days of each week for 52 weeks, sufficient to raise their carboxyhaemoglobin (COHb) levels to approximately 10%, while those in the other group were sham-exposed under similar conditions. In the second experiment, 3 groups of 40 female pigeons were each fed on a diet containing 1% cholesterol, one group being exposed to CO to give COHb levels of 20%, one to give COHb levels of 10% and one being sham exposed. In addition, 20 birds in the second experiment were fed on the 1% cholesterol diet but were neither exposed to CO nor sham-exposed. Cholesterol enriched diets caused mean plasma cholesterol values in each group to rise sharply within 4 weeks of starting them, but the levels reached were as high with diets containing 0.5% cholesterol as for diets containing 1% or 2% added cholesterol. Exposure to CO increased plasma and aortic cholesterol levels, though this increase was only statistically significant for aortic levels in the second experiment. In both experiments combined exposure to the 1% cholesterol diet and CO resulted in a significant decrease in aortic triglyceride content. The incidence and severity of coronary artery atherosclerosis was associated with increasing dietary cholesterol. It was also associated with exposure to CO in birds given 0.5% or 1%, but not 2%, dietary cholesterol; the increase in birds given 1% was related to the dose of CO. Possible mechanisms are discussed for this effect of CO, which is not found in normally fed birds.

Animals↗