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Biomedical subjects

D R Maxwell

Publications and source records attributed to D R Maxwell.

At least 37 records · Page 2Linked to original sources
PubMed1978

Prevailing patterns and predictor variables in patients with acute tubular necrosis.

The courses of 276 acute tubular necrosis patients referred for dialysis were reviewed in search for prognostic indicators. Sixty-three percent survived. Of 28 possible predictor variables, a posttoxic cause and nonoliguria were favorable, whereas myocardial infarction and peritonitis affected survival unfavorably. Total pareneral nutrition influenced survival favorably only in those with multiple complications or peritonitis. No single variable or combination predicted a lethal outcome. Since survivors were frequently restored to complete health, we advocate an aggressive therapeutic approach even in the face of multiple complications.

Acute Kidney Injury↗
PubMed1978

Failure of plasma exchange and immunosuppression to improve renal function in Goodpasture's syndrome.

A young woman with anti-glomerular basement membrane (GBM) antibody mediated rapidly progressive glomerulonephritis and pulmonary hemorrhage was treated with immunosuppression and intensive plasma exchange. She did not have end stage renal failure when therapy was initiated. Despite a dramatic reduction in circulating anti-GBM antibody, renal function progressively decreased. The role of plasma exchange in the therapy of anti-GBM antibody mediated disease remains unclear.

Adult↗
PubMed1977

Diuretics and small intestinal lymph flow in the dog.

Simultaneous measurements of thoracic duct lymph flow and small intestinal lymph flow were carried out in mongrel dogs after the administration of mannitol, ethacrynic acid, furosemide and chlorothiazide. Thoracic duct lymph flow increased only after injection of mannitol. Intestinal lymph flow increased after injection of all diuretics except chlorothiazide. Furthermore, mannitol produced simultaneous increases in thoracic duct and intestinal lymph flows. The durations of response of the increased lymph flows from each lymph channel produced by mannitol were statistically identical. The durations of increased intestinal lymph flows observed with each drug were: 40+/-3 (S.E.), 43+/-2 and 38+/-2 minutes for mannitol, ethacrynic acid and furosemide, respectively. Mean arterial blood pressures and inferior vena cava pressures did not change from the control to the experimental state in any animal studied. Similarly measurements of serum and lymph sodium, potassium and protein concentrations were unchanged from the control to the experimental state. These studies demonstrate that mannitol simultaneously increases thoracic duct lymph flow as well as intestinal lymph flow. Secondly, the results suggest that the increases in thoracic duct lymph flow after ethacrynic acid and furosemide administration, observed in previous studies arose primarily from the small intestine.

Animals↗
PubMed1976

Emphysematous pyelonephritis.

Emphysematous pyelonephritis is a rare complication of urinary tract infection and generally occurs in patients with diabetes mellitus or urinary tract obstruction. We recently treated an 81-year-old diabetic woman with Klebsiella pneumoniae urinary tract infection and septicemia whose abdominal roentgenogram demonstrated a striking left pneumonephrogram as well as intraureteral and perirenal gas. The patient died despite intensive therapeutic efforts. Unfortunately, the prognosis for this severe necrotizing infection process remains unfavorable.

Aged↗
PubMed1975

The prevention by sulphydryl compounds of the toxicity in the cat of 2,6-dimethoxyphenol and its morpholinopropionyl ester.

1 Intravenous (minus)-2,6-dimethoxyphenyl-2-morpholinopropionate hydrochloride (M&B 16,573) produced anaesthesia of short duration in the mouse, rat, rabbit, cat, dog and monkey. In the cat but not in other species, a severe and usually fatal toxic reaction was seen 1-2 h after administration. 2 This toxic reaction but not the anaesthetic properties of M&B 16,573 was prevented by the intravenous administration of cysteine or N-acetylcysteine. Cysteamine or dimercaprol were ineffective. 3 Intravenous administration of 2,6-dimethoxyphenol or 2,6-dimethoxyquinol in the cat produced a response similar to the delayed toxic effects of M&B 16,573 but not preceded by anaesthesia. The toxic effects of these compounds were prevented by cysteine. 4 Intravenous 4-allyl-2,6-dimethoxyphenyl-2-morpholinopropionate hydrochloride produced anaesthesia in the cat without the delayed toxic effects seen after M&B 16,573. 5 The acute toxicity of 2,6-dimethoxyquinol in mice was reduced by the administration of cysteine or N-acetylcysteine. 6 It is postulated that the delayed effects produced by M&B 16,573 in the cat are due to the formation of 2,6-dimethoxyquinol and 2,6-dimethoxybenzoquinone in this species, the toxicity of the latter being reduced by sulphydryl compounds.

Animals↗
PubMed1974

Pharmacology of M & B 18,706, a drug which selectively reduces decerebrate rigidity.

1 (+/-)-10-(3-Dimethylamino-2-methylpropyl)-2-valeroylphenothiazine hydrochloride (M & B 18,706) has been compared with dimethothiazine, chloropromazine, diazepam and baclofen for potency in reducing decerebrate rigidity in the cat and rat and for activity in causing ataxia or sedation.2 When given intravenously M & B 18,706 had seven times the potency of dimethothiazine and one-half the potency of chlorpromazine in reducing the rigidity of the intercollicular decerebrate cat. When administered orally M & B 18,706 and chlorpromazine were equi-potent in reducing rigidity but M & B 18,706 was less effective than chlorpromazine in producing ataxia in this species.3 In the rat, M & B 18,706 had one-quarter the potency of chlorpromazine for reducing decerebrate rigidity but had from 1/20th to 1/200th its potency in tests for sedative or tranquillizing activity.4 M & B 18,706, like dimethothiazine and chlorpromazine, had little effect on the rigidity of ischaemic decerebrate cats and failed to inhibit polysynaptic spinal reflexes.5 M & B 18,706 had intravenous potency comparable to chlorpromazine in reducing the pressor action of noradrenaline in the spinal cat.

Adrenergic alpha-Antagonists↗
PubMed1974

A comparison of the experimental anti-arrhythmic properties of acebutolol (M and B 17,803), propranolol and practolol.

1 The beta-adrenoceptor blocking agent, acebutolol (M & B 17,803), has been compared with propranolol, practolol, lignocaine and quinidine for its ability to revert or prevent various types of experimental arrhythmias.2 By intravenous infusion, acebutolol had one half the potency of propranolol in reverting an established ouabain-induced ventricular arrhythmia in the anaesthetized dog. Practolol was ineffective in the conditions used.3 High oral doses of acebutolol or propranolol significantly increased the arrhythmic dose of ouabain in the conscious rabbit. Similar doses of practolol produced a significant decrease (i.e. potentiation) in the dose of ouabain required to produce arrhythmia. Lignocaine and quinidine showed no or little activity in this test.4 Propranolol, acebutolol and practolol were all effective in decreasing the frequency of ectopic beats induced by adrenaline and methylchloroform in the anaesthetized cat. Lignocaine and quinidine were only weakly effective.5 Acebutolol and propranolol were equally effective either intravenously or orally in reducing the incidence of ventricular fibrillation produced by chloroform in mice.6 It is suggested that the wide spectrum of experimental anti-arrhythmic activity of acebutolol coupled with its cardioselectivity may make it an interesting compound in the treatment of cardiac arrhythmias in man.

Administration, Oral↗
PubMed1974

A comparison of the actions of some drugs on decerebrate rigidity, muscle spindle activity and alpha-adrenoceptors.

1 The relative potencies of methotrimeprazine, (+)-methotrimeprazine, (+/-)-10-(3-dimethylamino-2-methylpropyl)-2-valeroyl phenothiazine hydrochloride (M & B 18,706) and (+)-M & B 18,706 in reducing the pressor action of noradrenaline in the spinal cat, reducing intercollicular decerebrate rigidity, and muscle spindle afferent activity have been studied.2 Methotrimeprazine was eight times as potent as (+)-methotrimeprazine in reducing the pressor action of noradrenaline and six times as potent in reducing decerebrate rigidity. M & B 18,706 was also eight times as potent as (+)-M & B 18,706 in reducing the pressor action of noradrenaline and six times as potent in reducing decerebrate rigidity.3 For the above compounds and chlorpromazine there was a significant correlation between the effective doses for the inhibition of the pressor action of noradrenaline and for the reduction of decerebrate rigidity.4 The doses which reduced decerebrate rigidity were similar to those that reduced muscle spindle afferent discharge. It is likely that these drugs reduce decerebrate rigidity by inhibiting fusimotor activity.5 Desipramine increased decerebrate rigidity and increased spindle afferent discharge.6 It is thought that the phenothiazine derivatives studied reduce decerebrate rigidity and spindle afferent discharge by inhibiting receptors for noradrenaline in the central nervous system.

Animals↗
PubMed1973

Beta-adrenoceptor blocking properties and cardioselectivity of M & B 17,803A.

1. The beta-adrenoceptor blocking properties of (+/-)-1-(2-acetyl-4-n-butyramidophenoxy)-2-hydroxy-3-isopropylaminopropane hydrochloride (M&B 17,803A) have been compared with those of practolol and propranolol in the guinea-pig, cat and dog.2. Following either intravenous or oral administration in the cat or dog, M&B 17,803A and practolol had similar potency in antagonizing isoprenaline-induced tachycardia and both showed cardioselectivity, but both were less potent than propranolol.3. M&B 17,803A and practolol had approximately one hundredth the intravenous potency of propranolol in increasing the severity of anaphylactic bronchospasm in the conscious sensitized guinea-pig.4. M&B 17,803A possessed less marked intrinsic sympathomimetic activity than practolol but, like propranolol, it had significant local anaesthetic properties and increased the refractory period of rabbit isolated atria.

Acetanilides↗
PubMed1972

A comparison of the pharmacological and biochemical properties of substrate-selective monoamine oxidase inhibitors.

1. M&B 9302, E-250, NSD 2023, and Lilly 51641, substrate-selective inhibitors of monoamine oxidase (MAO), and two non-selective inhibitors of MAO (tranylcypromine and phenelzine) have been compared in the rat for activity in (i) inhibiting rat brain monoamine oxidase in vitro and in vivo using tyramine, 5-hydroxytryptamine (5-HT) and benzylamine as substrates; (ii) increasing brain levels of noradrenaline (NA) and 5-HT and (iii) antagonizing tetrabenazine-induced sedation.2. Concentrations of M&B 9302 and Lilly 51641 required to produce 50% inhibition of 5-HT oxidation by brain mitochondrial MAO were 1.4 x 10(-8)M and 2.5 x 10(-7)M respectively. Higher concentrations were required to inhibit tyramine oxidation whilst benzylamine oxidation was inhibited only at concentrations above 10(-5)M.3. E-250 showed the reverse substrate-selectivity in inhibiting the oxidation of benzylamine at concentrations below that required to inhibit the oxidation of 5-HT. NSD 2023 showed little substrate selectivity in vitro.4. Qualitatively similar results were obtained in vivo, except that NSD 2023 showed more marked substrate-selectivity.5. All the inhibitors except E-250 produced a dose-related rise in brain 5-HT levels. Only phenelzine and Lilly 51641 showed a linear relationship between NA levels and dose.6. All the drugs antagonized, in dose-related fashion, the effects of tetrabenazine in reducing locomotor activity. E-250 and NSD 2023 failed to restore locomotor activity to control levels whilst in high doses the other inhibitors, when given before tetrabenazine, produced a considerable increase in locomotor activity.7. Antagonism of tetrabenazine sedation appears to be correlated with (a) inhibition of the enzyme species that oxidize 5-HT and NA but not with inhibition of the enzyme species that oxidize benzylamine; (b) the rise in brain 5-HT levels rather than NA levels.

Amines↗