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Biomedical subjects

K Kumar

Publications and source records attributed to K Kumar.

At least 181 records · Page 10Linked to original sources

Tetanus booster every 5 years: an unnecessary routine?

The various guidelines for the administration of tetanus toxoid and antitetanus immunoglobulin are not only complicated, but also have never been supported by any scientific experimental studies. This study has measured the antibody levels in a random sample of 157 patients presenting to an accident and emergency department. Levels were measured before and after boosting doses. The results show that, in the sample analyzed, even those patients who had their last 'booster' over 10 years ago, had a satisfactory immunoglobulin level. In fact, no patient in the study had a level below the 'protective level'. Bearing in mind the small number of patients in the study, it could be argued that the level of immunity against tetanus in the United Kingdom is likely to be higher than assumed. If this is proven to be correct, then the length of time between booster injections of toxoid can be extended and the use of Human Antitetanus Immunoglobulin can be further restricted.

Adolescent↗

Neuromuscular pedicle graft for restoration of arytenoid abductor function in dogs with experimentally induced laryngeal hemiplegia.

Left laryngeal hemiplegia was induced by resection of the left recurrent laryngeal nerve in 12 dogs. A neuromuscular pedicle graft formed from the first cervical nerve and sternothyroideus muscle was transplanted after 1 week to the denervated cricoarytenoideus dorsalis muscle in 8 dogs. The remaining 4 dogs served as controls. Left arytenoid abduction was blindly evaluated by laryngoscopy with video photography at time 0, at 1 week, and at 19 weeks in all dogs. At 19 weeks, biopsy specimens of the left cricoarytenoideus dorsalis muscle and the neuromuscular pedicle were taken from 4 of the treatment dogs, and biopsy specimens of the left cricoarytenoideus dorsalis muscle were taken from the 4 control dogs. All biopsy specimens were blindly evaluated by histologic and histochemical examination. At 36 to 44 weeks, the remaining 4 treatment dogs, from which biopsy specimens had not been taken, were reevaluated by use of laryngoscopy with video photography. Complications and difficulties encountered during surgery included hemorrhage in the area of the cricoarytenoideus dorsalis muscle, location of a branch of the first cervical nerve that was long enough to prevent tension at the graft site, orientation of the muscle pedicle in the cricoarytenoideus dorsalis muscle without the use of an operating microscope, and preservation of the terminal portion of the first cervical nerve while forming the neuromuscular pedicle. Results of the arytenoid movement evaluations revealed improvement in arytenoid abductor function in the treatment group, compared with that in the control group at 19 weeks. Arytenoid abduction in the treatment group at this time, however, was still significantly decreased (P less than 0.05), compared with presurgical movement evaluations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cerebral endothelial microvilli following global brain ischemia in dogs.

Cerebral blood vessels (BVs) of dogs subjected to global brain ischemia by complete cardiac arrest of 15 min followed by 8 h of reperfusion, were studied in neocortex and hippocampus by means of transmission electron microscopy. Widespread endothelial microvilli were present in the postischemic animals. The number of endothelial microvilli in the postischemic animals (mean/BV in the neocortex = 3.26 and in the hippocampus = 2.54) was significantly larger than that in the non-ischemic controls (mean/BV in the neocortex = 1.39 and in the hippocampus = 0.84), P for both regions being less than 0.05. Arterioles, venules and capillaries, all were equally affected. Endothelial pinocytotic vesicles were also observed frequently in the postischemic dogs. Marked pericapillary swelling of astrocytic foot processes was present in the surrounding neuropil. It is concluded that the prominent cerebral endothelial microvilli recognized after 8 h of reperfusion following cardiac arrest in this experimental model of global brain ischemia, may play a significant role in the development of delayed postischemic hypoperfusion.

Animals↗

Ultrastructural and ionic studies in global ischemic dog brain.

A time course of tissue ionic changes, and their relation to ultrastructural findings during reperfusion following a 15-min global ischemic brain insult was studied in a dog model. Parietal cortex was analyzed for Ca, Na, K, Mg and Fe in controls and after 10 min, 2, 4, and 8 h of reperfusion. After 8 h of reperfusion, the mean values (mumol/g tissue wet wt.) for Ca (control = 1.43, 8 h = 2.76) and Na (control 60.4, 8 h = 107.4) doubled and K (control = 90.4, 8 h = 48.5) decreased to half that of the control. Ultrastructural studies and subcellular localization of calcium in parietal cortex of in situ-fixed brains after 8 h showed cortical neurons with clumping of nuclear chromatin, dilatation of endoplasmic reticulum and disruption of plasma membranes. Large amounts of electron-dense precipitates of calcium were present within dilated astrocytic processes, synaptic vesicles, cytoplasm of edematous dendrites and mitochondria. Cortical neurons from postischemic dogs without reperfusion showed only slight chromatin clumping and edema of astrocytic processes, but no calcium accumulation. The large ionic shifts noted between 4 and 8 h of reperfusion, indicate a progressive inability of the cells to maintain normal transmembrane gradients of these ions and may reflect a membrane destructive process, as demonstrated ultrastructurally at 8 h. Enhanced calcium entry into the neuron during reperfusion appears to be a part of the cytotoxic mechanism leading to neuronal necrosis.

Animals↗

Effect of flunarizine on global brain ischemia in the dog: a quantitative morphologic assessment.

The effects of flunarizine, a calcium antagonist, were evaluated in an experimental model of global brain ischemia produced by 15 min of cardiac arrest followed by resuscitation and reperfusion. One group of dogs received flunarizine (0.1 mg/kg intravenously during a 10-min period) at the onset of resuscitation. Another group of dogs underwent cardiac arrest, resuscitation, and reperfusion but did not receive flunarizine. A third group served as nonischemic control. In situ-fixed brains of all animals (nonischemic controls and the postischemic dogs after 8 h of reperfusion) were examined for anoxic ischemic injury. Quantitation of the ischemic neurons was carried out in parietal cortex, hippocampus, and cerebellum by using an image analysis system. Significant difference in the number of necrotic neurons between the flunarizine-treated group and the ischemic controls was noted in the hippocampus only; the mean percentage of necrotic neurons in the two groups being 14.8 +/- 9.6 and 29.3 +/- 12.1, respectively (P less than 0.05). These results indicate that flunarizine has an ameliorating effect on neuronal injury in the hippocampus that follows cardiac arrest in this experimental model of global brain ischemia. However, flunarizine was not found to be effective in reducing the ischemic neuronal damage in the cortex or the cerebellum.

Animals↗

Brain cortex tissue Ca, Mg, Fe, Na, and K following resuscitation from cardiac arrest in dogs.

Recent evidence suggests that ultimate neurologic injury following cardiac arrest and resuscitation may be largely determined by biochemical events occurring during reperfusion. To test this hypothesis and further characterize the time course of some of these events, we examined tissue samples from the parietal cortex for their total content of calcium (Ca), magnesium (Mg), iron (Fe), sodium (Na), and potassium (K) after 10 minutes, two hours, four hours, and eight hours of reperfusion following a 15-minute cardiac arrest in dogs. After 10 minutes of reperfusion, there were relatively small, but significant, increases in the total tissue content of Ca and Na, as compared to nonischemic controls. All values had returned to normal at two hours and remained normal at four hours of reperfusion. However, at eight hours of reperfusion, Ca and Na content approximately doubled and K content was reduced by half. There were no significant changes at any time in the tissue content of Fe or Mg. We conclude that with between four and eight hours of reperfusion following a 15-minute cardiac arrest, a major defect occurs in many cells of the cortex with respect to their ability to control ionic balances of Ca, Na, and K. This might be explained either by failure of the energy-dependent ionic pumps or by more generalized damage to the membrane permeability barrier by a process such as lipid peroxidation.

Animals↗

Single-dose gentamicin therapy of recurrent urinary tract infection in patients with normal urinary tracts.

Results of single-dose therapy of urinary tract infections in pediatric patients have been contradictory mainly because of selection criteria. We evaluated the efficacy of a single dose of gentamicin in patients with normal urinary tracts and in whom urinary tract infections were recurrent. Twenty-one patients were included in the study, and a similar number in a conventional group given treatment for 10 days. Cure rate was 100% in both groups. The recurrence rates of 67% in the study and 52% in the conventional group were comparable. Single-dose therapy seems to have a role in the treatment of urinary tract infection in the absence of urinary tract malformation.

Adolescent↗