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Biomedical subjects

A J Krieger

Publications and source records attributed to A J Krieger.

At least 19 recordsLinked to original sources
PubMed1992

Spinal cord blood flow decreases following chemical stimulation of the rostral ventrolateral medullary pressor area in anesthetized rats.

In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressore area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmol in 100 nl of 0.9% sodium chloride solution) and the spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In order to measure SCBF at normotension, moderate hypotension within the lower limit of spinal cord autoregulation was induced by controlled hemorrhage (n = 12). Unilateral chemical stimulation of the VLPA in these rats increased arterial blood pressure (ABP) but it remained within normotensive range. The SCBFs of cervical, thoracic and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (P less than 0.01), from 22 +/- 1 to 17 +/- 2 (P less than 0.05), and from 41 +/- 5 to 26 +/- 3 (P less than 0.05) ml.min-1.(100 g)-1, respectively. The spinal cord vascular resistances (SCVRs) of cervical, thoracic and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (P less than 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (P less than 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (P less than 0.05) mmHg per [ml.min-1.(100 g)-1], respectively. During the chemical stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO2 indicating that the reactivity of spinal cord vasculature was intact (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Acute stabilization of the cervical spine by halo/vest application facilitates evaluation and treatment of multiple trauma patients.

The management of acute cervical spine injuries has traditionally used bed-based skeletal traction until all non-neurologic injuries have been evaluated. This treatment method substantially hinders the ability to transport patients and to perform imaging studies and surgical procedures. In contrast, early application of a halo/vest apparatus provides immediate cervical stabilization and facilitates the diagnostic work-up and treatment of the patients with multiple injuries. The records of all 78 patients admitted from February 1988 through June 1991 who had acute cervical spine fractures, subluxations, or both with a risk of instability were reviewed. All patients were treated with halo/vests and no patient deteriorated neurologically following halo/vest application. Twenty-nine patients (37%) had a total of 55 associated injuries including long bone/pelvic fractures in 17, thoracic injuries in 13, closed head injuries in 11, facial fractures in 6, noncontiguous spinal fractures in 5, and abdominal injuries in 3. The mean injury Severity Score (ISS) was 18 (range, 9-54). While in the halo/vest, 43 patients (55%) had a total of 99 diagnostic studies completed and 46 patients (59%) had a total of 76 surgical procedures performed. There were 35 neurosurgical procedures on 32 patients and 41 non-neurosurgical surgical procedures on 24 patients. Over the past year, 20 of 21 patients (95%) had their halo/vest placed in the emergency department. The data demonstrate that many diagnostic and surgical procedures need to be performed on patients with unstable cervical spine injuries.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Chemical stimulation of the rostral ventrolateral medullary pressor area decreases cerebral blood flow in anesthetized rats.

In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressor area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In one group of rats (n = 11), unilateral chemical stimulation of the VLPA produced a significant (P less than 0.01) increase in arterial blood pressure (ABP), a significant (P less than 0.05) decrease in CBF, and a significant (P less than 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 +/- 3 (mean +/- S.E.M.) and 48 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLPA; the CVR was 1.9 +/- 0.1 and 2.6 +/- 0.3 mmHg per ml.min-1.(100 g)-1 before and during the stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats (n = 8). Unilateral chemical stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly (P less than 0.05) from 57 +/- 14 to 41 +/- 9 and from 50 +/- 12 to 39 +/- 9 ml.min-1.(100 g)-1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly (P less than 0.05) from 2.6 +/- 0.6 to 3.5 +/- 0.8 and from 2.7 +/- 0.5 to 3.5 +/- 0.8 mmHg/[ml.min-1.(100 g)-1], respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Chemical stimulation of the ventrolateral medullary depressor area decreases ipsilateral cerebral blood flow in anesthetized rats.

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the ventrolateral medullary depressor area (VLDA) were chemically stimulated by microinjections of L-glutamate (2.5-5 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). Unilateral chemical stimulation of the VLDA (n = 11) produced a significant (P less than 0.05) decrease in CBF of the cerebral cortex ipsilateral to the stimulated VLDA; the CBF was 41 +/- 5 (mean +/- S.E.M.) and 29 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLDA. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) caused by the chemical stimulation of the VLDA because the CBF during the chemical stimulation of the VLDA was significantly smaller (P less than 0.01) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the VLDA in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 46 +/- 12 to 29 +/- 7 ml.min-1.(100 g)-1) and a significant (P less than 0.01) increase in cerebrovascular resistance (from 2.7 +/- 0.4 to 4.3 +/- 0.6 mmHg per [ml.min-1.(100 g)-1]) was observed in the ipsilateral cerebral cortex of these rats. Chemical stimulation of the VLDA did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Epidural trial in implantation of intrathecal morphine infusion pumps.

This retrospective review permits limited conclusions due to the small sample size and the limited control of variables. The temporary prepump, percutaneous epidural catheter trial is a useful component of our protocol. This period provides important information relative to possible side effects and efficacy of pain. The trial does give an estimation for the starting point of the intrathecal dosage but, as we have demonstrated, this is, at times, at a greater dosage than previously had been predicted. We feel that this retrospective review supports the continued use of a prepump trial of epidural morphine prior to permanent intrathecal pump implantation.

Adult↗
PubMed1990

Chemical stimulation of the nucleus tractus solitarii decreases cerebral blood flow in anesthetized rats.

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the nucleus tractus solitarius (NTS) were chemically stimulated by microinjections of L-glutamate and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (either 57Co, 113Sn and 46Sc or 141Ce, 85Sr and 46Sc). Unilateral chemical stimulation of the NTS (n = 14) decreased CBF significantly in most brain areas. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) because the CBF of the whole cerebral cortex during the chemical stimulation of the NTS was significantly smaller (P less than 0.05) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the NTS in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 62 +/- 28 (mean +/- S.D.) to 48 +/- 23 ml.min-1.(100 g)-1) and increase in cerebrovascular resistance (from 1.9 +/- 1.2 to 2.6 +/- 1.2 mm Hg per [ml.min-1.(100 g)-1]) was observed in the whole cerebral cortex of these rats. Chemical stimulation of the NTS did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5). These results suggest that the cell bodies within the NTS may play a role in the control of cerebral circulation.

Animals↗
PubMed1989

Cardiovascular effects of substance P receptor stimulation in the ventrolateral medullary pressor and depressor areas.

The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjection of L-glutamate (1.77 nmol/site) in artificially ventilated urethane-anesthetized male Wistar rats. Bilateral microinjection of a stable substance P (SP) agonist [pGlu5, MePhe8, Sar9]-SP(5-11)], abbreviated as DiMe, into the VLPA (6-600 pmol/site) produced a dose-dependent increase in blood pressure (BP). The effects on heart rate (HR) were variable. Intravenous pretreatment with a ganglionic blocker chlorisondamine (3.0 mg/kg, i.v.), but not with a vasopressin antagonist, blocked these responses. Similar microinjection of DiMe (6-600 pmol/site) into the VLDA produced a dose-dependent decrease in HR but had no effect on BP levels. The DiMe-induced bradycardic response elicited from the VLDA was blocked by i.v. pretreatment with atropine methylbromide (0.5 mg/kg, i.v.). These findings indicate that there are SP receptors localized on sympathoexcitatory neurons in the VLPA and that SP may be an excitatory neurotransmitter in this area. In the VLDA, the SP receptors appear to be localized on a subpopulation of neurons that affect vagal, but not sympathetic, outflow to the heart.

Adrenergic Fibers↗
PubMed1988

M2 muscarinic receptors mediate pressor responses to cholinergic agonists in the ventrolateral medullary pressor area.

Microinjections of cholinergic agonists into the ventrolateral medullary pressor area (VLPA) evoke increase in blood pressure (BP) and heart rate (HR). Recently two major subtypes of muscarinic receptors (M1 and M2) have been identified. This investigation was designed to study the role of these muscarinic receptor subtypes in pressor responses of cholinergic agonists in the VLPA. Male Wistar rats were anesthetized with pentobarbital or decerebrated at mid-collicular level. The rats were artificially ventilated and BP and HR were recorded. Ventral medulla was exposed and the VLPA identified bilaterally by microinjections of L-glutamate. Microinjections of cis-methyldioxolane (CD, a specific agonist of M2 receptors) in the doses of 0.004-4 nanomol (nmol)/site into the VLPA evoked an increase in BP (13-56 mm Hg) and HR (7-24 bpm) which lasted for 10-50 min. Intravenous injections of the same doses of this agent failed to evoke a response. AFDX-116 (a specific M2 muscarinic receptor antagonist) microinjected into the VLPA (0.2-1.6 nmol-/site) evoked depressor responses (6-20 mm Hg). Microinjections of this agent into the VLPA prevented the pressor responses to subsequent microinjections of CD at the same sites, indicating that AFDX-116 blocked M2 receptors. AFDX-116 rendered neurons in the VLPA unresponsive to L-glutamate but this effect lasted for 30-40 min while the hypotensive and M2 receptor blocking effect lasted for 60-150 min. McN-A343 (a specific agonist for M1 receptors) or pirenzepine (PZ, a specific antagonist of M1 receptors) injected into the VLPA (0.4-4 nmol/site) failed to evoke any response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Syndrome of intramedullary gunshot wound with incomplete neurologic deficit: case report.

A patient with a gunshot wound to the spinal cord with an incomplete neurologic deficit is presented. The neurologic examination revealed a combination of a central cord injury and the Brown-Séquard Syndrome. The authors suggest that the Brown-Séquard portion of the syndrome was caused by compression of tracts within the spinal cord caused by the mass of the bullet and the central cord injury was produced by the kinetic energy of the bullet during penetration into the spinal canal. They conclude that with incomplete neurologic lesions following gunshot wounds the bullet be removed.

Adult↗
PubMed1987

Ventrolateral medullary pressor area: site of hypotensive action of clonidine.

Intravenous injections of clonidine produce an initial transient increase in blood pressure followed by a long-lasting hypotension and bradycardia. The initial pressor response is due to activation of vascular alpha 1-adrenergic receptors while the hypotension and bradycardia are caused by the central actions of clonidine. Although, hypothalamus, nucleus tractus solitarius (NTS), ventrolateral medulla and the intermediolateral cell column of the thoracolumbar spinal cord (IML) have been implicated, the exact site of these actions of clonidine in the central nervous system is not established. The results of this investigation suggest that the pressor area in the ventrolateral medulla (VLPA) is the site of hypotensive and bradycardic actions of intravenously administered clonidine. This conclusion is based on the observation that microinjections of idazoxan, a specific alpha 2-adrenergic receptor blocker, into the VLPA prevented and reversed the hypotension and bradycardia despite the fact that other proposed sites of these actions (NTS, hypothalamus and IML) were intact and accessible to intravenously administered clonidine.

Animals↗
PubMed1987

The perivenous technique of resection of arteriovenous malformations from vital areas of the brain.

A total of 17 patients with arteriovenous malformations (AVMs) in sensitive areas of the brain were operated on and the AVMs were completely resected using perivenous techniques. No patient suffered a new neurological deficit following surgery. The perivenous surgical technique is most suitable for small AVMs in sensitive cortex. It differs from the standard approach in that it places emphasis on perivenous microsurgical dissection, identification of the nidus before major arterial feeders, and early ligation of selected venous channels. Three different types of venous drainage--single, multiple, and dual--were identified. Each different type of venous drainage requires a different surgical approach for the best results.

Adolescent↗
PubMed1987

Differential regulation of regional vascular resistance by the rostral and caudal ventrolateral medulla in the rat.

Regional vascular resistance changes were determined following chemical excitation and inhibition of the rostral vasopressor (RVLM) and caudal vasodepressor (CVLM) areas in the ventrolateral medulla. Mesenteric, renal and hindquarter vascular resistances were assessed in paralyzed and artificially ventilated urethane-anesthetized rats instrumented with pulsed-Doppler flow probes. Microinjection of the excitatory amino acid L-glutamate in the RVLM elicited a significant dose-related transient increase in blood pressure, heart rate and resistance of mesenteric, renal and hindquarter vascular beds. A similar dose-related hemodynamic profile was obtained following microinjection of muscimol, a GABAmimetic, in the CVLM. In contrast, significant dose-related decrease in blood pressure, heart rate and resistance in mesenteric and hindquarter vascular beds was observed following glutamate-induced excitation of the CVLM and muscimol-induced inhibition of the RVLM. Changes in renal vascular resistance were inconsistent in this second hemodynamic profile. Intravenous administration of the alpha 1 adrenergic antagonist, prazosin, abolished all of the hemodynamic effects elicited by excitation of the RVLM except the tachycardia. Intravenous atropine methylnitrate blocked the bradycardia associated with excitation of the CVLM but did not alter the vascular resistance changes. These results indicate that the changes in heart rate did not contribute significantly to the resistance profiles described. The changes in vascular resistance elicited by excitation and inhibition of the RVLM were correlated with increase and decrease in the greater splanchnic nerve activity, respectively. In conclusion, neuron pools in the RVLM and CVLM exert differential effects upon resistance in different vascular beds via changes in sympathetic outflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Medullary pressor area: site of action of intravenous physostigmine.

Physostigmine, a choline-esterase inhibitor, is known to elevate endogenous levels of acetylcholine. Intravenously administered physostigmine causes a rise in blood pressure via its action in the central nervous system. Exact site of this action of physostigmine is not known. In this paper, it was demonstrated that microinjections of tetrodotoxin (a fast sodium channel blocker), lidocaine (a local anesthetic) and scopolamine (a cholinergic muscarinic receptor blocker) into the rostral ventrolateral medullary pressor area abolished the pressor action of intravenously administered physostigmine. These results demonstrate that the rostral ventrolateral medulla is the site of action of intravenously administered physostigmine and this action is mediated via cholinergic muscarinic receptors.

Animals↗