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Biomedical subjects

J E Brian

Publications and source records attributed to J E Brian.

36 records · Page 2Linked to original sources
PubMed1993

The impact of streptozotocin-induced diabetes on the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics in the rat.

We designed experiments to examine the effects of insulin-dependent diabetes mellitus on the anesthetic requirements for volatile anesthetics. A standard tail-clamp technique was used to determine minimum alveolar anesthetic concentrations for halothane, enflurane, and isoflurane in spontaneously breathing rats. Three groups of animals were used: 1) diabetic rats (12 wk after induction of diabetes with streptozotocin, 50 mg/kg, single dose, intravenously), 2) insulin-treated (7 U extended insulin zinc suspension per day, subcutaneously, beginning 5 wk after streptozotocin treatment) diabetic rats, and 3) control rats. The minimum alveolar anesthetic concentration values of the control animals were 1.16 +/- 0.02 vol% for halothane, 2.25 +/- 0.05 vol% for enflurane, and 1.42 +/- 0.04 vol% for isoflurane. Minimum alveolar anesthetic concentration was reduced by 23% for halothane (0.90 +/- 0.06 vol%), by 18% for enflurane (1.85 +/- 0.07 vol%), and by 17% for isoflurane (1.18 +/- 0.04 vol%) in diabetic rats. Insulin treatment restored the anesthetic requirement to control levels for all three anesthetics. These data from the rat model indicate that uncontrolled diabetes lowers anesthetic requirements significantly.

Anesthesia, Inhalation↗
PubMed1990

Changes in cerebral blood flow over time during isoflurane anesthesia in dogs.

The present study assessed the impact of time (6 h) on cerebral blood flow (CBF) during isoflurane anesthesia with and without vasopressor administration. All animals were prepared for measurement of CBF by the radiolabeled microsphere method under 1.4% end-tidal (1.0 MAC) isoflurane anesthesia. Surgery required 45 min and was followed by a 15 min stabilization period. In group 1 (n = 6), isoflurane 1.4% was administered for 6 h. CBF after 1 h of isoflurane was 92 +/- 9 ml/min/100 g (mean +/- SEM) and declined to 61 +/- 5 ml/min/100 g at 2 h and further declined to 37 +/- 5 ml/min/100 g at 6 hr. In group 2 (n = 6), isoflurane 1.4% was administered during the first hour. Thereafter, isoflurane 1.4% was continued, angiotensin II (0.3 mug/kg/min) was administered intravenously, and blood was withdrawn to maintain CPP constant for an additional 5 h, with hourly CBF determination. In this group, control CBF was 95 +/- 16 ml/min/100 g and flow was maintained at the control level through 4 h and then declined to 50 +/- 5 ml/min/100 g at 5 and 6 h. In group 3 (n = 6), 1.4% isoflurane was administered and phenylephrine (2.0 mug/kg/min) infusion was combined with hemorrhage to maintain control CPP in an identical sequence to group 2. In group 3, control CBF was 88 +/- 14 ml/min/100 g. As in group 1, CBF decreased significantly at 2 h (p < 0.05) to 68 +/- 13 ml/min/100 g and further declined to 49 +/- 7 ml/min/100 g at 6 h. In all three groups, CMRO2 remained at control levels and there were no changes in arterial carbon dioxide or CPP for the duration of the study. These data demonstrate that the hyperemia caused by isoflurane resolves over time during stable 1 MAC isoflurane anesthesia. The unanticipated interaction of angiotensin II and isoflurane producing a sustained cerebral hyperemia suggests that previous studies that used angiotensin II to support MABP during isoflurane may have reported the effects of angiotensin II in addition to or rather than the effects of isoflurane.

Journal Article↗
PubMed1989

Immediate hemodynamic management following subarachnoid hemorrhage during embolization of cerebral vascular abnormalities.

Three patients are reported who suffered intracranial hemmorrhage during interventionally neuroradiology procedures. All had severe hypertension, cardiac arrhythmias and loss of consciousness. Immediate CT scan showed small amounts of blood in all patients. Arrhythmias were controlled with lidocaine. In two patients, the hypertension was treated only with barbiturates plus fentanyl and in the third with labetol and nitroprusside. In the patient treated with nitroprusside and one patient with barbiturate plus fentanyl a 14-20 min period of hemodynamic stability was followed by vasomotor collapse requiring intravenous vasopressor support. The patient initially treated with nitroprusside suffered irreversibly brain injury whereas the other two improved neurologically following their intracranial bleed. These patients suggest that nitroprusside is detrimental in the acute treatment of malignant hypertension following intracranial hemorrhage.

Journal Article↗
PubMed1987

Hypocupremia in a major burn.

Trace element deficiency in burns is an area which apparently has not been investigated. We recently encountered a severely burned patient with profound copper depletion. Neuropsychiatric symptoms and delayed healing may have been secondary to this deficiency. Further study is needed to clearly delineate the role of acquired copper deficiency in recovering burned patients.

Adolescent↗
PubMed1986

Duodenal villous adenomas.

Two cases of villous adenoma of the duodenum are presented. These rare tumors are best diagnosed with upper gastrointestinal radiographs and endoscopic biopsy. Malignant degeneration is more common in the second portion of the duodenum which makes excision more difficult. If no malignancy is found, sleeve resection is preferred. Tumors in the second portion of the duodenum should be treated with wide mucosal excision if carcinoma in situ is found and with pancreaticoduodenectomy if invasive cancer is present.

Adenoma↗
PubMed1985

Noncolonic diverticular disease.

Diverticula occur throughout the gastrointestinal tract. A high index of suspicion is necessary to diagnose and treat complications arising from diverticula. Presented is a review of gastrointestinal diverticular disease exclusive from the more common diverticular disease of the colon.

Cecal Diseases↗
PubMed1984

Septic complications of chemonucleolysis.

The authors present two cases of septic complications after chemonucleolysis with chymopapain. One patient developed overt aortic valve failure. The second patient suffered an epidural abscess.

Adult↗
PubMedDate not supplied

Management of cerebral hemispherectomy in children.

Surgical removal of a cerebral hemisphere may be undertaken in patients with intractable seizure disorders. Anesthetic management of such patients has not been reviewed in detail before. This study retrospectively analyzed hospital records of ten patients undergoing cerebral hemispherectomy at the Johns Hopkins Hospital between July 1983 and February 1988. Patient records were reviewed for diagnosis, physical characteristics, preoperative medications, anesthetic management, and postoperative course in the intensive care unit (ICU). Massive and sudden blood loss was a common finding in these patients, and during the intraoperative and postoperative periods, fluid resuscitation frequently was an ongoing process. In some patients, the blood loss exceeded one blood volume and was associated with coagulopathy, hypokalemia, and hypothermia. Urine output was elevated by a glucose-induced diuresis in some patients, giving misleading information as to intravascular volume status. Seizures and hemorrhage into the hemispherectomy cavity were management problems in the ICU. From this review, the authors conclude that blood loss may be marked and precipitous during surgical removal of a cerebral hemisphere. Monitoring of intra-arterial pressure and central venous pressure (CVP) is necessary for patient management during the intraoperative and postoperative periods. Intravenous (IV) access should allow rapid intravascular volume administration as it becomes necessary. Patients should remain intubated and observed closely during the immediate postoperative period due to difficulties with hemodynamic stability, seizures, and hemorrhage.

Anesthesia↗
PubMedDate not supplied

Aortic stenosis, cesarean delivery, and epidural anesthesia.

A 23-year-old female was referred to the University of Arkansas for Medical Sciences at 32 weeks' gestation with a history of aortic stenosis following aortic valve replacement. Evaluation by echocardiography showed an approximately 90 mmHg transvalvular pressure gradient. Pregnancy progressed to 36 weeks' gestation without problem, at which time the patient underwent cesarean section with lumbar epidural anesthesia. Invasive hemodynamic monitors were used to assess cardiac performance and as a guide for anesthetic management. The impact of aortic stenosis on pregnancy is discussed, as are management aspects of lumbar epidural anesthesia in such patients.

Adult↗
PubMedDate not supplied

Recent insights into the regulation of cerebral circulation.

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.

Animals↗