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Biomedical subjects

T C Wicks

Publications and source records attributed to T C Wicks.

12 recordsLinked to original sources
PubMed1999

AANA Journal course: update for nurse anesthetists--magnesium homeostasis and deficiency.

Magnesium is the second most abundant intracellular cation in the human body and serves as an obligate cofactor in approximately 300 essential enzymatic cellular reactions. Magnesium is crucial for the generation and use of adenosine triphosphate and is required for oxidative phosphorylation. A wide variety of internal and external stresses have been found to increase a person's requirement for dietary magnesium. Magnesium deficiency may develop during a variety of pathological states, or it may have an iatrogenic basis. Magnesium deficiency complicates the management of hypertension and cardiac arrhythmias, affects the clinical behavior of neuromuscular blocking drugs, and may impair immune function.

Diet↗
PubMed1995

Ropivacaine: an introduction to a new local anesthetic.

Local anesthetic drugs interrupt nerve transmission by inhibiting the passage of sodium ions (Na+) across neuronal membranes. Signal propagation and transmission along central and peripheral nerve pathways are impeded after the injection of these drugs near or on neuronal tissue. This article briefly reviews the basic pharmacology and toxicology of local anesthetic agents as well as recent studies of regional anesthesia performed with ropivacaine, a versatile new amide local anesthetic with a duration of action similar to bupivacaine, but with less systemic toxicity.

Amides↗
PubMed1994

The pharmacology of rocuronium bromide (ORG 9426).

Rocuronium is a new nondepolarizing neuromuscular blocking drug. Its onset of action is comparable to that of succinylcholine, with good-to-excellent intubating conditions possible 1 minute after doses two times the ED95 (600 micrograms/kg). The ED95 of rocuronium is essentially the same for children as for adults. Its duration of action is similar to vecuronium, and it is shorter for children than for adults. Rocuronium is readily reversed with conventional doses of cholinesterase-inhibiting drugs. A new agent, rocuronium possesses a very stable cardiovascular profile and a rapid onset of action. It may be useful for rapid sequence intubation without unacceptable delays in the spontaneous recovery of neuromuscular function.

Adult↗
PubMed1992

Mivacurium chloride.

This brief review summarizes the major research to date involving the clinical use of mivacurium in adults and children. The principle focal points are the pharmacokinetic and pharmacodynamic characteristics of the drug and the side effects that have been commonly observed with its clinical use. Comparisons and contrasts with vecuronium, atracurium, and succinylcholine are made. Particular attention is focused on dosages, infusion rates, recovery characteristics, and individual patient variability.

Adult↗
PubMed1991

Excision of an arteriovenous malformation.

Arteriovenous malformations (AVM) are congenital vascular lesions consisting of direct communications between associated arteries and veins without an interposed capillary bed. These vessels are typically thin walled, lack an internal elastic intima, and are quite prone to hemorrhage. A previously healthy 17-year-old woman presented with severe, persistent headache. After undergoing computed tomography (CT scan) and magnetic resonance imaging (MRI), the patient was diagnosed as having an intracranial arteriovenous malformation. The anesthetic management of this patient included induction with sodium thiopental and sufentanil. General anesthesia was maintained with isoflurane in oxygen and a continuous intravenous infusion of sufentanil. Neuromuscular blockade was established prior to endotracheal intubation with vecuronium and maintained with a combination of metocurine and pancuronium. The sufentanil infusion was discontinued when vascular isolation of the AVM had been accomplished. The isoflurane was discontinued 30 minutes prior to skin closure. Neuromuscular blockade was then antagonized with neostigmine and glycopyrrolate. Spontaneous ventilation resumed when the patient's arterial carbon dioxide tension (PaCO2) was allowed to normalize. The hemodynamic character of this anesthetic course was smooth and uneventful. The patient emerged from anesthesia comfortable and lucid and experienced no perioperative anesthetic complications.

Adolescent↗
PubMed1983

(Mercaptopropanoyl)indoline-2-carboxylic acids and related compounds as potent angiotensin converting enzyme inhibitors and antihypertensive agents.

1-(3-Mercapto-2-methyl-1-oxopropyl)indoline-2-carboxylic acids (7b) and related compounds were synthesized in order to examine their ability to inhibit angiotensin converting enzyme (ACE) and to reduce the systolic blood pressure of spontaneously hypertensive rats (SHR). All four possible stereoisomers of the precursor 1-[3-(benzoylthio)-2-methyl-1-oxopropyl]indoline-2-carboxylic acid (6b) were characterized with absolute stereochemical assignment. The removal of the benzoyl group of the precursor to give 7b was conveniently carried out by treatment with 2-methoxyethylamine. Three of the four stereoisomers of the benzoyl derivative 6 showed in vitro ACE inhibitory activity in the following order: 6b(S,S) greater than 6b(S,R) greater than 6b(R,S). The stereoisomer having the R,R configuration was essentially inactive. The substitution at the C5 of the indoline nucleus with the Et or OMe group caused only marginal changes in the inhibitory activity. The mercaptan 7b(S,S) was the most active ACE inhibitor synthesized in this study, showing in vitro potency 3 times that of captopril. The augmentation of the potency may be due to the increased hydrophobicity of 7b(S,S) compared with captopril and suggests the presence of a hydrophobic pocket at the active site of ACE. When tested in spontaneously hypertensive rats, 7b(S,S) exhibited oral antihypertensive activity 27 times that of captopril. The corresponding benzoyl derivative 6b(S,S) was 24 times as potent as captopril. The thio lactone 10 obtained by cyclization of 7b(S,S) as a potential prodrug was less potent than the parent compound, 7b(S,S), in the ACE inhibitory and antihypertensive tests.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1981

Comparative antihypertensive effects of propranolol and metoprolol in DOC-treated rats.

The effects of chronic twice daily s.c. injections of dlpropranolol, metoprolol and d-propranolol on systolic blood pressure and heart rate were assessed in conscious DOC-saline hypertensive rats. Measurements were taken (tail-cuff) 4 hr after the morning injection and 16-18 hr after the afternoon injection during 11 of 19 consecutive treatment days. Only dl-propranolol and metoprolol at 5 mg/kg lowered blood pressure and heart rate significantly relative to the changes occurring in control saline-injected animals. At the lower dose of 0.2 mg/kg, both agents tended to decrease heart rate while having little or no effect on blood pressure. The overall blood pressure and heart rate changes produced by propranolol at 5 mg/kg differed significantly from those of the control group at both the 4 and 16-18 hr post-dosing intervals. Metoprolol at 5 mg/kg produced significant overall changes in blood pressure and heart rate only at the 4 hr post-doing interval. D-propranolol had no effect on either blood pressure or heart rate. The results indicate tha s.c. propranolol and metoprolol lower systolic blood pressure in conscious DOC-saline hypertensive rats only at the higher dose of 5 mg/kg and that cardioselectivity does not afford increased antihypertensive activity in this model.

Animals↗
PubMed1977

Platelets and the vascular responses to arachidonic acid in dogs.

UNLABELLED: Platelets are rich in components of the prostaglandin synthetase system which converts arachidonic acid into vasoactive and platelet-active prostanoate and nonprostanoate compounds. Repeated injections of arachidonic acid in dogs cause hypotension of reproducible magnitude and lower circulating platelet counts with each injection. However, the circulatory response to injected arachidonic acid was unchanged when platelet-poor blood was exchanged in dogs. Moreover, in the hind limb preparation and the isolated lung lobe, the vasoactive responses to arachidonic acid were indistinguishable whether perfused with whole blood or an artificial perfusate. CONCLUSION: the vascular responses to arachidonic acid do not appear dependent on the presence of platelets.

Animals↗
PubMed1977

Vascular responses to the monoenoic prostaglandin precursor dihomo-gamma-linolenic acid in the perfused canine lung.

Dihomo-gamma-linolenic acid (DGLA; 2 mg/kg i.v.), the monoenoic prostaglandin (PG) precursor was reported earlier to produce systemic hypotension in the intact dog. It is shown here to produce pulmonary vasoconstriction when given (50-500 microng/kg) in the pulmonary artery of the isolated perfused canine lung lobe. This effect is similar to that of arachidonic acid (AA), the bisenoic PG precursor. PGF1alpha was vasopressor in both preparations. The DGLA response at 100 microng/kg in the lung was nearly identical with that of AA25 microng/kg; DGLA 200 microng/kg=AA50 microng/kg;DGLA 300microng/kg=AA 100 microng/kg. The DGLA 100 microng/kg response was nearly equal to that with PGF1alpha 1 microng/kg. The equipressor dose ratio, DGLA/AA, varied 2.5 to f1 and DGLA/PGF1alpha was 100:1. DGLA and AA vascular responses were blocked by indomethacin. Linoleic acid, used as a control fatty acid, had no pulmonary pressor action. When a dextran-based artificial perfusate was used, the vasopressor response to DGLA was essentially unchanged from that in the blood-perfused lobe. The effects of DGLA appear to be due to conversion to vasoactive products in the PG biosynthetic pathway. These products are less potent than those formed in the metabolism of AA.

8,11,14-Eicosatrienoic Acid↗
PubMed1976

Vascular responses to arachidonic acid in the perfused canine lung.

We compared the effects of arachidonic acid (AA), the bisenoic prostaglandin precursor, with those of prostaglandin F2a (PGF2a) and norepinephrine (NE) on pulmonary vascular resistance in the isolated (in situ), perfused canine lung lobe. The isolated lobe was perfused with autologous blood or an artificial perfusate under conditions of constant flow. Lobar artery and venous pressures were constantly monitored after bolus injections of AA, PGF2a, and NE into the inflow cannula. AA (100 mug/kg produced a significant increase in the pressure gradient (93.3 +/- 8.4%, SE) in the lobe. Similarly, PGF2a (1 mug/kg) significantly increased the pressure gradient (41.2 +/- 6.5%), as did NE (1 mug/kg, 41.6 +/- 3.2%). Aspirin (25 mg/kg) completely blocked the pulmonary vascular effect of AA, but did not affect the response to PGF2a, Linoleic acid, a control fatty acid, did not produce pulmonary vasoconstriction. The pressor effect of AA was not blocked by pretreatment with phentolamine, propranolol, cyproheptadine, or atropine. The use of an artificial perfusate free of cellular elements did not prevent the vasoconstrictor action of AA. The times to onset of action of the three agents were similar, and short. These results suggest that AA is converted into vasoactive intermediates or a prostaglandin, and the vasoactive intermediates or the prostaglandin act directly on precapillary pulmonary vascular smooth muscle rather than through platelet, plasma, adrenergic, or cholinergic mechanisms.

Animals↗