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Biomedical subjects

M M Husain

Publications and source records attributed to M M Husain.

At least 37 records · Page 2Linked to original sources

Effects of nicardipine and labetalol on the acute hemodynamic response to electroconvulsive therapy.

STUDY OBJECTIVE: To examine the acute hemodynamic effects of intravenous (i.v.) nicardipine and its ability to attenuate the hyperdynamic response to electroconvulsive therapy (ECT), when used alone or in combination with labetalol. DESIGN: Prospective, randomized, double-blind, positive-control, clinical investigation. SETTING: University hospital. PATIENTS: 36 patients undergoing ECT. INTERVENTIONS: In a series of three studies, the hemodynamic effects of nicardipine were assessed prior to, during, and after ECT. After administration of glycopyrrolate 0.1 mg i.v., placebo (saline) or nicardipine was administered by rapid infusion (1, 2.5, 5, 10, and 15 mg) or bolus injection (1.25, 2.5, and 5 mg), either alone or in combination with labetalol 10 mg i.v. Unconsciousness was induced with methohexital 1 mg/kg i.v.; succinylcholine 1.2 to 1.5 mg/kg i.v. was administered for muscle relaxation. A bilateral electrical stimulus was delivered and the durations of motor and electroencephalographic (EEG) seizures were noted. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure (MAP) and heart rate (HR) values were recorded at 1- to 5-minute intervals throughout the study period. When administered as a rapid infusion, nicardipine 5 mg i.v. produced a significant decrease in MAP; however, nicardipine dosages of 10 to 15 mg i.v. did not produce a significantly greater decrease in MAP than 5 mg. Bolus administration of nicardipine 1.25 to 5 mg produced a rapid onset of its hemodynamic effects without exacerbating the cardiovascular depressant effects of methohexital. However, the decrease in MAP was accompanied by an increase in HR after administration of the 5 mg i.v. bolus dose. The acute hyperdynamic response to ECT was most effectively controlled by nicardipine 2.5 to 5 mg i.v. bolus, in combination with labetalol 10 mg i.v. Seizure duration was not significantly altered by the use of nicardipine as part of the anesthetic regimen for ECT. CONCLUSION: Nicardipine 2.5 mg i.v. bolus in combination with labetalol 10 mg i.v. was the most effective pretreatment regimen for preventing the acute hyperdynamic response to ECT. However, this combination produced a 20% decrease in MAP immediately prior to ECT and a lower MAP at the time of discharge.

Adult↗

Is oral clonidine effective in modifying the acute hemodynamic response during electroconvulsive therapy?

UNLABELLED: Clonidine decreases the stress-induced sympathoadrenal responses to painful stimuli and improves hemodynamic stability during general anesthesia. Because acute hypertensive responses are often observed immediately after electroconvulsive therapy (ECT), we designed a prospective, randomized, placebo-controlled, cross-over study to assess the effects of four different oral doses of clonidine (0.05-0.3 mg per os) on the acute hemodynamic response to ECT. Anesthesia was induced with methohexital 1 mg/kg followed by succinylcholine, 1.3 mg/kg i.v. A total of 110 treatments were evaluated in 22 patients. Noninvasive mean arterial pressure (MAP) and heart rate (HR) values, duration of motor and electroencephalographic (EEG) seizure activity, and recovery times were recorded. Clonidine produced a dose-related decrease in MAP before and after ECT. Although clonidine 0.2-0.3 mg per os decreased the peak MAP value after ECT, the changes in MAP from the prestimulation values were similar in all treatment groups. Clonidine produced no significant changes in HR, duration of motor and EEG seizure activity, or recovery times after anesthesia. These data suggest that clonidine decreases the peak MAP value after ECT by decreasing MAP immediately before the ECT stimulus. IMPLICATIONS: Oral clonidine (0.2-0.3 mg) decreases the acute hypertensive response after electroconvulsive therapy; however, this antihypertensive effect was achieved by decreasing the blood pressure before the electrical stimulus.

Administration, Oral↗

In vitro 1H-magnetic resonance spectroscopy of postmortem brains with schizophrenia.

Some evidence suggests that thalamic dysfunction could explain some of the signs and symptoms of schizophrenia. We measured the absolute concentrations of amino acid metabolites in thalamus, frontal pole, and cerebellar vermis in extracts of postmortem brains from 8 schizophrenics and 10 controls using high-resolution 1H-magnetic resonance spectroscopy. The concentrations of N-acetyl aspartate, glutamate, and valine tended to be reduced in the thalamus of the schizophrenic group. Although it is difficult to ascribe significance to the "tendencies," these data may tend to support other data suggesting decreased thalamic volume or neuronal number in schizophrenia.

Adult↗

Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity.

STUDY OBJECTIVE: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (i.v.) lidocaine. DESIGN: Randomized, double-blind, placebo-controlled, cross-over study. SETTING: University-affiliated hospital. PATIENTS: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression. INTERVENTIONS: Patients received lidocaine 50 mg, 100 mg, 200 mg i.v., or saline prior to induction of anesthesia via a standardized anesthetic technique. MEASUREMENTS AND MAIN RESULTS: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means +/- SD) were 37 +/- 13 sec and 64 +/- 21 sec, 25 +/- 11 sec and 52 +/- 43 sec, 17 +/- 12 sec and 32 +/- 17 sec, 1 +/- 3 sec and 18 +/- 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups. CONCLUSIONS: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity.

Aged↗

Regional metabolic alterations in Alzheimer's disease: an in vitro 1H NMR study of the hippocampus and cerebellum.

The concentrations of selected metabolites in the hippocampus and cerebellum of 13 Alzheimer's diseased (AD) and four nondemented postmortem brains were measured using high resolution 1H NMR spectroscopy. For both the hippocampal region and the cerebellum, the putative neuronal marker N-acetyl aspartate (NAA) was significantly lower in AD brains relative to the nondemented brains. For the hippocampal region, the NAA concentration correlated inversely with semiquantitative assessments of neuronal loss and neurofibrillary tangles. The gamma-aminobutyric acid levels in both hippocampus and cerebellum of an age- and a postmortem interval-matched subset of AD brains were lower than those of the controls. Because the cerebellum is generally thought to be unaffected by AD, the NAA decrease in the Alzheimer cerebellum may be due to lesions of either the Alzheimer or non-Alzheimer type in contralateral cerebrum.

Aged↗

The suboccipital cavernous sinus.

The authors studied the microsurgical anatomy of the suboccipital region, concentrating on the third segment (V3) of the vertebral artery (VA), which extends from the transverse foramen of the axis to the dural penetration of the VA, paying particular attention to its loops, branches, supporting fibrous rings, adjacent nerves, and surrounding venous structures. Ten cadaver heads (20 sides) were fixed in formalin, their blood vessels were perfused with colored silicone rubber, and they were dissected under magnification. The authors subdivided the V3 into two parts, the horizontal (V3h) and the vertical (V3v), and studied the anatomical structures topographically, from the superficial to the deep tissues. In two additional specimens, serial histological sections were acquired through the V3 and its encircling elements to elucidate their cross-sectional anatomy. Measurements of surgically and clinically important features were obtained with the aid of an operating microscope. This study reveals an astonishing anatomical resemblance between the suboccipital complex and the cavernous sinus, as follows: venous cushioning; anatomical properties of the V3 and those of the petrous-cavernous internal carotid artery (ICA), namely their loops, branches, supporting fibrous rings, and periarterial autonomic neural plexus; adjacent nerves; and skull base locations. Likewise, a review of the literature showed a related embryological development and functional and pathological features, as well as similar transitional patterns in the arterial walls of the V3 and the petrous-cavernous ICA. Hence, due to its similarity to the cavernous sinus, this suboccipital complex is here named the "suboccipital cavernous sinus." Its role in physiological and pathological conditions as they pertain to various clinical and surgical implications is also discussed.

Arteries↗

Comparative evaluation of chelating agents on the mobilization of cadmium: a mechanistic approach.

A comparative evaluation of chelating agents, namely, diethyl dithiocarbamate (DDC), dimethyl dithiocarbamate (DMDC), 1,4,8,11-tetraazacyclotetradecane (CYCLAM), 1,4,8,12-tetraazacyclopentadecane (TACPD), 2,3-dimercaptosuccinic acid (DMSA), and 2,3-dimercapto-1-propane sulfonate (DMPS) was conducted to assess their efficacy against acute cadmium (Cd) toxicity. DMSA and DMPS appeared to be most effective in reducing mortality as well as Cd burden of liver, kidneys, and brain in cadmium intoxicated mice. DMDC reduced Cd levels only in liver and kidneys, while DDC significantly enhanced its level in brain. CYCLAM and TACPD significantly increased the Cd level in liver and kidneys and were ineffective in brain. The therapeutic index as well as therapeutic efficacy was highest for DMSA followed by DMPS and DMDC. A fair degree of correlation was found to exist between (1) stability constant of Cd chelates and percent survival (r = .438, (2) stability constant and percent transport (r = .479), and (3) percent survival and percent transport (r =.447). However, the lipophilicity did not show any appreciable correlation with percent survival and stability constant of Cd chelates.

Animals↗

Metal-independent putative superoxide dismutase mimics in chemistry, biology, and medicine.

The excessive generation of superoxide radicals O2-. with inadequate available defence provided by the enzyme superoxide dismutase (SOD) may result in the development and exacerbation of many of mankind's common illnesses. The native SOD proves too problematic to be used for the prevention and cure of such diseases. A number of metal-independent synthetic SOD mimics, based on organic nitroxides, have been tried as therapeutic interventions. Among the widely studied mimics, 2-ethyl-2,5,5-trimethyl-3-oxazolidinanyl, 2,2,6,6-tetramethyl-1-piperidimyloxy, nitrosoureas, and triazene derivatives have indicated promising results with possible future applications in chemistry, biology, and medicine.

Cyclic N-Oxides↗

Evidence for the involvement of nitric oxide in cisplatin-induced toxicity in rats.

Cisplatin treatment of rats results into a significant increase in the activity of Ca(2+)-independent nitric oxide synthase (NOS) in kidneys and liver. Significant enhancement of lipid peroxidation in gastric mucosa, kidneys and liver was also observed. The administration of NG-nitro-L-arginine methyl ester, an inhibitor of NOS, markedly reduced renal and gastrointestinal toxicity, and also decreased the content of blood urea nitrogen, serum creatinine, and incidence of diarrhoea along with a significant inhibition in lipid peroxidation in the target organs. The present report, while demonstrating the beneficial effect of the blockade of NO pathways during cisplatin chemotherapy, may be helpful in developing strategies for combating some of the toxic side-effects of the drug.

Animals↗

An in vitro 1H nuclear magnetic resonance study of the temporoparietal cortex of Alzheimer brains.

The concentrations of selected metabolites in the posterior temporoparietal cortex of 13 Alzheimer's diseased (AD) and four nondemented postmortem brains (of individuals between the ages of 63 and 95) were determined using high-resolution 1H nuclear magnetic resonance (NMR) spectroscopy. The estimates for glutamate and inositol for AD brains did not show any statistically significant difference (P > 0.05) from those for the nondemented brains. The putative neuronal marker N-acetyl aspartate (NAA), creatine, and GABA were decreased in AD brains compared with the nondemented brains. The estimates for creatine, glutamate, and GABA showed significant linear correlations with those of NAA. Creatine, glutamate, GABA, and NAA appeared to be negatively correlated with the neurofibrillary tangles. Our results support a neuronal loss in the posterior temporoparietal cortices of AD brains.

Aged↗

The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy.

The intravenous anesthetics which are commonly used for electroconvulsive therapy (ECT) possess dose-dependent anticonvulsant properties. Since the clinical efficacy of ECT depends on the induction of a seizure of adequate duration, it is important to determine the optimal dose of the hypnotic for use during ECT. We compared the duration of seizure activity and cognitive recovery profiles after different doses of methohexital, propofol, and etomidate administered to induce hypnosis prior to ECT. Ten outpatients with major depressive disorders receiving maintenance ECT participated in this prospective, randomized, cross-over study. Patients were premedicated with glycopyrrolate, 0.2 mg intravenously (i.v.), and labetalol, 20-30 mg i.v., and hypnosis was induced with an i.v. bolus injection of methohexital or propofol (0.75, 1.0, and 1.5 mg/kg), or etomidate (0.15, 0.2, and 0.3 mg/kg), administered over 10-15 s. Adequate muscle paralysis was achieved with succinylcholine, 1.0-1.4 mg/kg i.v. Each patient's seizure threshold was determined prior to enrollment in the study and the electrical stimulus variables were kept constant throughout the study period. After delivery of a bilateral electrical stimulus, the duration of the resulting electroencephalographic (EEG) and motor seizures were recorded. A total of 90 ECT treatments were evaluated. The durations of EEG and motor seizures were longest after etomidate and shortest after propofol. There were no significant dose-related differences in motor and EEG seizure durations (means +/- SD) after the low, intermediate, and high doses of etomidate of 44 +/- 11 and 77 +/- 19, 43 +/- 10 and 76 +/- 34, 42 +/- 16 and 78 +/- 56 s, respectively. Conversely, both methohexital and propofol, 0.75, 1.0, and 1.5 mg/kg, produced dose-dependent decreases in motor and EEG seizure durations (i.e., 37 +/- 10 and 58 +/- 12, 36 +/- 8 and 62 +/- 24, and 29 +/- 13 and 48 +/- 20 for methohexital; 34 +/- 15 and 56 +/- 29, 31 +/- 8 and 50 +/- 17, and 20 +/- 6 and 33 +/- 12 for propofol, respectively). The awakening times were similar, regardless of the hypnotic or dose administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Exacerbation of nickel induced oxidative response by vitamin E.

Vitamin E (alpha-tocopherol), a well known naturally occurring chain breaking antioxidant and a free radical scavenger was found to exacerbate nickel (Ni) toxicity in mice. Vitamin E (Vit. E) mediated enhancement of nickel toxicity was demonstrated by (i) enhanced mortality in mice treated with Ni and Vit. E (ii) increased hepatic lipid peroxidation, (iii) increased rate of benzoate hydroxylation, and (iv) liposomal membrane damage.

Animals↗

Reduction of cis-platinum induced nephrotoxicity by zinc histidine complex : the possible implication of nitric oxide.

Cisplatin is a prominent member of the effective broad spectrum antitumor drugs. The clinical usage of cisplatin is, however, restricted due to some adverse side effects including renal toxicity. The present study demonstrates the protective effect of a Zinc-chelate of histidine, [Zn-Hist], against cisplatin induced nephrotoxicity and gastrointestinal toxicity as shown by decreases in BUN, creatinine and lower incidence of diarrhoea. The observed inhibition in cisplatin induced renal and hepatic lipid peroxidation by [Zn-Hist] pretreatment, suggests an importance for Zn in stabilisation of membrane integrity probably through the displacement of the redox-active metals that may be responsible for inducing peroxidative damage at target sites. The findings also suggest that cisplatin may play biochemical role in arginine-metabolism including nitric oxide (NO) production.

Animals↗

Acrylamide induced immunosuppression in rats and its modulation by 6-MFA, an interferon inducer.

In the present communication, we describe acrylamide (ACR) induced immunotoxicity and its modulation by an interferon inducer, the 6th mycelial fraction acetone (6-MFA) of Aspergillus ochraceus ATCC 28706. ACR administration to rats produced a significant decrease in the weight of spleen (p < 0.001), thymus (p < 0.001) and mesenteric lymph nodes (p < 0.05). A decrease in cellularity of spleen (p < 0.001), thymus (p < 0.001), bone marrow (p < 0.001) and circulating blood lymphocyte population (p < 0.001) was also recorded. ACR suppressed the humoral as well as cell mediated immunity as assessed by erythrocyte antibody complement (EAC)-rosettes (p < 0.001), hemagglutination titre (p < 0.001), PFC (p < 0.001) and the delayed type hypersensitivity response against sheep red blood cells (SRBC, p < 0.001). ACR treated immunosuppressed rats when treated with 6-MFA restored the circulating lymphocyte number to the normal level and a partial recovery in the weight of spleen and thymus. Potentiation of EAC-rosettes, hemagglutination titre, IgM-PFC and DTH response against SRBC was observed. It is concluded that 6-MFA ameliorate the ACR induced toxicity. This study may be of significance in prevention of ACR toxicity.

Acrylamide↗

Anaesthesia for electroconvulsive therapy: use of propofol revisited.

In three clinically depressed patients undergoing repeated electroconvulsive therapy (ECT) with either propofol or methohexitone, dose-dependent decreases in the duration of motor and EEG seizure activity were noted. Use of a 'minimally' hypnotic dose of propofol (0.75-1.0 mg kg-1) was associated with a seizure duration which was comparable to standard hypnotic doses of methohexitone. We conclude that doses of propofol < 1.5 mg kg-1 are associated with a clinically acceptable duration of EEG seizure activity (> 30 s) during ECT.

Adult↗