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G C Dennis

Publications and source records attributed to G C Dennis.

At least 19 recordsLinked to original sources

Synergism between cocaine and atropine at the caudal ventrolateral medulla of cats.

We have previously reported that the anticholinergic properties of cocaine may be important in cocaine induced apneusis. We have studied the effects of the cholinergic muscarinic antagonist atropine (ATR) on cocaine induced apneusis at the caudal chemosensitive areas of the ventrolateral medulla oblongata (CVLM). Experiments were performed in urethane anesthetized and tracheotomized cats with the CVLM surgically exposed. Topical application of ATR (44 mM ) to the CVLM produced significant decrements in minute ventilation (V(E)) and mean arterial blood pressure (MABP) (P<0.05) but the effects on tidal volume (V(T)), respiratory frequency (f) and heart rate (HR) were not significant. Administration of cocaine (37 mM) to ATR pretreated animals increased the incidence of cocaine induced respiratory arrest to more than twofold greater than when cocaine was administered in the absence of pretreatment. The ATR pretreated animals that did not experience inspiratory arrest after cocaine were shown to exhibit significant decrements in f and V(E) as a consequence of prolonged inspiratory pauses. The reduction in MABP after cocaine in ATR pretreated animals was also significant. These results suggest that ATR enhances the central respiratory toxicity of cocaine by acting synergistically at CVLM chemosensitive sites.

Animals↗

Somatosensory evoked potential, neurological examination and magnetic resonance imaging for assessment of cervical spinal cord decompression.

The present study was designed to determine the relationship between neurological testing, anatomical imaging, and electrophysiological monitoring for assessing outcome of cervical spinal cord decompression. We prospectively studied 28 consecutive patients (age 39-76 yr) who were subjected to presurgical-(1-3 wk) and postsurgical (3-4 mo) neurological examination and recording of the median nerve somatosensory evoked potential (SEP). In 13 patients, magnetic resonance imaging (MRI) was also performed. Changes in neurological function, SEP and MRI were evaluated and graded as (1) improvement,(2) no change or (3) deterioration. Neurological outcome (NO) was based on changes in motor grade strength, sensory, reflexes and gait. The SEP outcome was based on changes in latency and disappearance of SEP waveform components whereas MRI evaluation was based on changes in spinal cord and canal diameters. Significance of association between NO, SEP and MRI was determined by Pearson's Chi-Square statistic (P<.05). The SEP improved in 71% (20/28) and deteriorated in 28% (8/28) of the subjects. An association between SEP changes and NO was found in 82% (23/28) of the subjects (P = .0038). Decompression increased the spinal canal diameter in 92% (12/13), and the spinal cord diameter in 38% (5/13) of the subjects. An association between NO, or SEP and MRI was not detected. Changes in median nerve SEP latency appear to be predictive of the neurological status of patients subjected to cervical spinal cord decompression. Postoperative increments in SEP latency or disappearance of the SEP waves were indicative of poor outcome after surgical decompression of the cervical spinal cord.

Adult↗

Analgesic responses to intrathecal morphine in relation to CSF concentrations of morphine-3,beta-glucuronide and morphine-6,beta-glucuronide.

This study was performed to determine whether variations in analgesic responses to intrathecal morphine could be explained by cerebrospinal fluid (CSF) concentrations of morphine metabolites. Twenty-four CSF samples were collected at the beginning, middle and end of treatment periods in seven cancer patients with pain of malignant origin. CSF concentrations of morphine-3,beta-glucuronide (M3G) and morphine-6,beta-glucuronide (M6G) metabolites were measured by gas chromatography/mass spectrometry. Analgesic responses to morphine were estimated concurrent with CSF collection using a visual analog scale representing percentages of pain relief. Effective analgesia was defined as > or = 75% pain relief. CSF concentration of M3G and M6G in the 24 samples were 722 +/- 116 ng/ml and 699 +/- 158 ng/ml, respectively. CSF samples were categorized into two groups: (1) those collected during effective analgesia (N=14), and (2) those collected during ineffective analgesia (N=10). M6G levels detected in group 1 samples (effective analgesia) were significantly greater than those found in group 2 samples (ineffective analgesia) (978 +/- 243 ng/ml vs 309 +/- 68 ng/ml, P<0.05). Intergroup differences in CSF M3G concentrations and M3G/M6G ratios were not significant. It is concluded that CSF M6G may be indicative of effectiveness of analgesia in cancer patients subjected to intrathecal morphine.

Adult↗

Racism in medicine.

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Black or African American↗

Subarachnoid hemorrhage in the African-American population: a cooperative study.

The clinical outcome of patients following subarachnoid hemorrhage is complicated by delayed cerebral ischemia and contributing factors such as hypertension. To observe the impact of hypertension and delayed cerebral ischemia on the outcome of a predominantly African-American cohort following subarachnoid hemorrhage, both retrospective (n = 42) and prospective (n = 21) studies were conducted. In the total pool (n = 63), the mean age was 49.7 years (range: 17 to 80) with a preponderance of female patients (70%). Aneurysm formation was significant in the region of the posterior communicating artery. Of the patients reviewed, 73.8% had preexisting hypertension and 45.9% developed delayed cerebral ischemia. Approximately 89% of the patients who suffered from delayed cerebral ischemia had hypertension. Results failed to display any significant beneficial association between the use of the calcium channel blocker nimodipine and delayed cerebral ischemia. Use of the antifibrinolytic drug aminocaproic acid demonstrated a worse patient outcome. It is not recommended that aminocaproic acid be used in this population. Subsequently, due to the proportional occurrence of delayed cerebral ischemia in hypertensive patients following subarachnoid hemorrhage, it is suggested that prophylactic surgical management of unruptured intracranial aneurysms be considered in hypertensive patients. Further study is needed to discern the association between hypertension, delayed cerebral ischemia, and stroke in patients following subarachnoid hemorrhage.

Aminocaproates↗

Monitoring of median nerve somatosensory evoked potentials during cervical spinal cord decompression.

We evaluated the intraoperative utility of monitoring median nerve somatosensory evoked potentials (SEPs) in 31 consecutively hospitalized neurosurgical patients (mean age 55.3 +/- 2.1 years) who underwent spinal cord decompression for cervical herniated disc, spondylosis, or tumor. Pre- and postoperative standard neurological examinations included evaluation of motor function, sensory responses, gait, tone, and reflexes. Evoked potentials were recorded from clavicular Erb's (N9) and contralateral cortical (N20) points. Intraoperatively, SEP measurements were obtained after the onset of anesthesia (baseline control) and were repeated throughout the operative procedures. N20 and N9-N20 conduction latencies were measured for each SEP recording; disappearance of the SEP waveform was interpreted as a nonquantifiable increase in latency. Follow-up neurological examinations were made immediately after and up to 6 months following surgery. Postoperatively, the 31 study subjects were assigned to one of two groups based on neurological evaluation: 27 group I subjects had either no change or improvement (good outcome) whereas four group II subjects had postoperative neurological deterioration (poor outcome). Intraoperative N9-N20 interpeak latency was found to increase during cervical decompression in six of 27 group I and in two of four group II subjects. Only two of the Group I subjects exhibited increases > 10% (14 and 19%, respectively). Intraoperative communication to the surgeon of a marked increase of N9-N20 latency during positioning for cervical traction clearly obviated a poor outcome in one group I subject; Upon removal of traction, latency decreased and significant changes in neurological function were not detected postoperatively. The SEP waveform disappeared in two of the group II and in none of the group I subjects. In the two group II subjects exhibiting increases of N9-N20 latencies, increments were > 20%. These findings indicate that in patients undergoing cervical spinal cord decompression, disappearance of SEPs or increases > 20% in the N9-N20 interpeak latency are suggestive of operative conditions that place patients at risk for poor neurological outcome.

Adult↗

Cardiorespiratory effects of cocaine and procaine at the ventral brainstem.

The caudal ventrolateral medulla (CVLM) is an area of the brainstem, in the vicinity of the hypoglossal nerve roots, where cholinergic and adrenergic neurons participate in respiratory and vasomotor control. Cardiorespiratory depression has been produced by topical application of cocaine to the CVLM. In the present studies, the effects of topical pretreatments of the CVLM with alpha-adrenergic blockers (prazosin 4.8 mM) and beta-adrenergic blockers (propranolol 11.3 mM) on the cardiorespiratory responses to topically administered cocaine (37 mM) were investigated in urethane anesthetized cats. Both prazosin and propranolol failed to produce ventilatory responses and to counteract cocaine-induced apneustic breathing. However, the cocaine-induced decrement in mean arterial blood pressure (MABP) following pretreatment of the CVLM with propranolol was found to be 11 +/- 5%, compared to the 18 +/- 5% decrement produced by cocaine alone. These differences were not statistically significant. Procaine (37 mM) in equimolar doses to cocaine, produced a small statistically significant decrement in MABP (P < 0.05) without ventilatory effects. Topical administration of procaine (73.3 mM), at approximately twice the equimolar dosage of cocaine, produced apneustic breathing that was indistinguishable from that produced by cocaine. The neurotoxic properties of cocaine that produce apneustic breathing appear to be similar to that produced by the anesthetic agent procaine, and the alpha- and beta-adrenoceptor blockers prazosin and propranolol do not appear to antagonize the vasomotor depression induced by cocaine at the CVLM.

Adrenergic alpha-Antagonists↗

Effects of cholinomimetics on cocaine-induced hypotension and apneusis at a ventral brainstem cardiorespiratory control site.

The current study was undertaken to evaluate the effects of cholinomimetic drugs on cocaine-induced central cardiorespiratory depression. Cats anesthetized by urethane (2.0 g/kg) were subjected to topical application at the caudal ventrolateral medullary surface (cVMS) of cocaine and two cholinomimetic pretreatment drugs. The following drug regimens were tested: 37 mM cocaine 1) given alone; 2) given 5 min after 2.7 mM carbachol pretreatment; and 3) given 5 min after 3.6 mM physostigmine pretreatment. In 7 of 11 cats, pretreatment with physostigmine decreased the incidence of cocaine-induced apneusis and hypoventilation significantly (p < 0.05); these animals showed no significant change in the mean arterial blood pressure during the 5-min pretreatment before administration of cocaine. In 4 of 11 cats, the physostigmine pretreatment produced a significant decrease in mean arterial blood pressure followed by lethal cardiorespiratory arrest when cocaine was administered. Pretreatment with carbachol resulted in cardiorespiratory responses which were not significantly different from those produced by cocaine alone. In anesthetized cats not exhibiting hypotensive responses to physostigmine, pretreatment may ameliorate cocaine-induced respiratory failure by ventral brainstem control mechanisms.

Animals↗

Central cocaine neurotoxicity at brainstem cardiorespiratory control sites.

Cocaine hydrochloride was applied topically to the ventrolateral medullary surface (VMS) where chemosensitive respiratory and vasomotor control sites are colocalized. Cats (n = 16) were anesthetized with urethane (2.0 g/kg, 80 percent of dose titrated over 60 min). The trachea of each animal was cannulated and the VMS was surgically exposed. Tidal volume (VT), frequency of breathing (f), systolic and diastolic blood pressure (SBP and DBP, respectively), and heart rate (HR) were measured. Cocaine (62.5 micrograms per site) administered at the VMS control sites decreased f, SBP, and DBP significantly (p < 0.05), without changing HR or VT values. This cocaine-induced hypoventilation was associated with brief intervals of inspiratory cramp (apneusis). Central cocaine neurotoxicity may result from interaction of cocaine with VMS sites, producing increased inspiratory drive and decreased vasomotor tone.

Administration, Topical↗