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Biomedical subjects

G Reed

Publications and source records attributed to G Reed.

At least 73 records · Page 4Linked to original sources
PubMed1989

Cocaine-associated rhabdomyolysis.

Three male patients developed a total of four episodes of acute rhabdomyolysis associated with documented cocaine intoxication (two caused "crack" and two caused by intravenous cocaine). Included is one patient who developed rhabdomyolysis after injecting cocaine and then redeveloped it 6 months later on "rechallenge." One of the four cases resulted in death related to severe hyperkalemia and ischemic bowel. The remaining three episodes followed a course of nonoliguric renal failure.

Acute Disease↗
PubMed1985

Mitomycin C and vindesine associated pulmonary toxicity with variable clinical expression.

A patient receiving mitomycin and vindesine chemotherapy for lung cancer developed abrupt onset of shortness of breath following vindesine administration. Pulmonary function tests both before and after rechallenging him with vindesine showed an acute obstructive pattern, which resolved with bronchodilator therapy; persisting lung damage was evident by arterial blood gas analysis. A record review of the 126 patients placed on the same chemotherapy regimen uncovered an additional 6 patients with possible lung toxicity. These seven patients (5.5%) had a variable clinical picture, from acute, reversible shortness of breath temporally related to vindesine administration to a progressive, fatal interstitial infiltrate. Physicians administering the combination of mitomycin and a vinca alkaloid should be aware of potential lung toxicity with variable clinical expression and be prepared to take appropriate action should they encounter it.

Antibiotics, Antineoplastic↗
PubMed1985

Cerebral blood flow autoregulation and hypertension.

Hypertension and antihypertensive therapy have clinically important effects on cerebral blood flow. The autoregulatory changes that occur with chronic arterial hypertension should influence the clinician's choice of antihypertensive agents and the rapidity with which the blood pressure is lowered in order to avoid symptoms of focal or global cerebral hypoperfusion.

Aged↗
PubMed1984

Seizures due to maprotiline overdose.

Maprotiline, a new tetracyclic antidepressant, has a pattern of toxicity that is different from that of tricyclics. Maprotiline overdosage appears more likely to cause seizures but less likely to cause the peripheral autonomic and cardiac manifestations seen with tricyclics. Two cases of maprotiline overdose resulting in seizures without significant anticholinergic or cardiotoxic effects are presented. Both patients were treated acutely with gastric emptying and were observed to have no further seizures during subsequent drug-free hospital and outpatient follow up. Physostigmine salicylate has been used as an antidote for the anticholinergic syndrome of tricyclic overdose, but probably offers less in maprotiline overdose. Careful observation for seizures appears to be warranted.

Adult↗
PubMed1983

Further studies on the hypernoradrenergic state of treated hypertensives: effect of captopril.

We investigated the effect of captopril on plasma norepinephrine concentration and blood pressure in two groups of hypertensive patients. One group consisted of five severely hypertensive patients rendered hypernoradrenergic by administration of a minoxidil-propranolol-diuretic regimen. The other group was ten untreated mildly hypertensive patients. Two hours after 12.5mg of captopril, blood pressure was lowered (p less than .05) in four of the five hypernoradrenergic patients from 180 +/- 8/102 +/- 8 to 132 +/- 7/77 +/- 8 mmHg. Chronic administration of 100-150mg of captopril tid caused no further blood pressure reduction. Precaptopril plasma norepinephrine concentration was 925 +/- 206 and two hours after the 12.5mg dose was 807 +/- 80 pg/ml. Three months later having advanced the dose to 300-450 mg/day it was lower (p less than .05) at 752 pg/ml. The acute blood pressure response correlated (r = -0.72, p less than .001) with the precaptopril plasma norepinephrine. Precaptopril blood pressure in the mild hypertensive patients was 146 +/- 4/98 +/- 1, after a 25-100mg dose it was 137 +/- 6/91 +/- 2 (diastolic p less than .05) and at two months with the same captopril dose bid it was 141 +/- 8/88 +/- 4 mmHg (diastolic p less than .01). Corresponding initial PNE was 425 +/- 72, two hours after captopril 405 +/- 47 and 310 +/- 63 pg/ml (p less than .05) with chronic administration. Thus, captopril lowers blood pressure in both hypernoradrenergic and eunoradrenergic hypertensive patients without increasing plasma norepinephrine suggesting some unique dampening effect of this drug on the sympathetic nervous system. Also, addition of captopril to triple therapy lowered blood pressure in proportion to plasma norepinephrine levels suggesting importance to its action on this sympathetic nervous system effector.

Blood Pressure↗
PubMed1983

Heatstroke.

Explore the source record for details and available documents.

Acclimatization↗
PubMed1982

Epidemic classical heat stroke: clinical characteristics and course of 28 patients.

Patients with classical heat stroke are different in many ways from those with exertional injury; contrasts included difference in demographic factors, prior general health, in-hospital complications and laboratory abnormalities (lactate, liver enzymes, pH, electrolytes). Severe hyperkalemia, acute renal failure, rhabdomyolysis and disseminated intravascular coagulation often dominate the course of patients with exertional heat stroke but are uncommon in those with classical heat stroke (Table 4). While lactic acidosis is the rule in exertional injury, it is somewhat unusual in patients with classical heat stroke and when above 3 mmoles/L predicts a poor outcome or death. In spite of the advanced age and multiple medical problems of the patients with classical heat stroke, careful attention to early and aggressive cooling and scrutiny for potential complications can result in salvage of most patients.

Acid-Base Imbalance↗
PubMed1982

Vindesine (VDS) monochemotherapy for non-small cell lung cancer: a report of 45 cases.

Fifty-three patients with non-small cell lung cancer were treated with vindesine. Of the 45 evaluable patients, 11 (24%) had a partial response. Responses were all evident within 6 weeks. Median duration of response was 8 weeks from documentation. Median survival was not improved significantly among responders (P less than 0.10, two-tailed test of significance). The most frequent toxic effect was leukopenia. The most troublesome toxic effect was peripheral neuropathy, with patients greater than 60 years old experiencing this more frequently.

Adenocarcinoma↗