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Biomedical subjects

B Gupta

Publications and source records attributed to B Gupta.

At least 91 records · Page 5Linked to original sources
PubMed1980

Intracranial pressure during nitroglycerin-induced hypotension.

Nitroglycerin was given intravenously to five anesthetized, hyperventilated (PaCO2 25 to 30 torr) patients during craniotomy, to facilitate surgery by creating a relatively bloodless field, and to decrease the potential need to blood transfusion. A subarachnoid screw and an indwelling radial artery catheter were inserted to monitor intracranial pressure (ICP) and mean arterial pressure (MAP). As MAP decreased from 10.4 +/- 4.0 (SE) to 69.0 +/- 1.8 torr, ICP increased from 14.2 +/- 0.7 (SEM) to 30.8 +/- 1.1 torr. Cerebral perfusion pressure decreased from 90.2 +/- 3.6 (SEM) to 38.2 +/- 2.3 torr (p < 0.0005). We attribute this nitroglycerin-induced ICP increase to capacitance vessel dilation within the relatively noncompliant cranial cavity, with subsequent cerebral blood volume increase.

Adult↗
PubMed1980

Furosemide facilitates recovery of evoked twitch response after pancuronium.

Two groups consisting of 10 A.S.A. class I-II neurosurgical patients each were studied to determine whether patients require greater quantities of pancuronium to maintain paralysis after having been given furosemide, 1 mg/kg. After a standardized barbiturate, narcotic and nitrous oxide induction of anesthesia, pancuronium was given intravenously until twitch response was suppressed by 95%. The study group received in addition furosemide, 1 mg/kg, 10 minutes prior to induction of anesthesia. Mean recovery time from 95% to 50% twitch suppression was 21.8 minutes in the control group and 14.7 minutes in the study group. Urinary output was significantly greater (13.5 vs 674 ml) and serum potassium levels lower (4.05 vs 3.85 meq/L) in the study group during recovery of twitch response. Furosemide, 1 mg/kg, facilitates recovery of evoked twitch response after pancuronium.

Furosemide↗
PubMed1980

Cellular and humoral responses in amoebic patients.

Cell-mediated immune response (CMIR) and humoral antibody response was studied in fifteen patients with amoebic liver abscess, five patients with amoebic colitis and fifteen patients with non-amoebic diseases which served as unexposed controls. CMIR as judged by macrophage migration inhibition factor (MIF) test was altered in amoebic patients and more so in amoebic liver abscess patients; it was normal in unexposed controls. This altered CMIR reverted back to normal levels within five to seven days after the initiation of drug therapy. There was no clear-cut correlation between CMIR and humoral antibody response although by and large the degree of macrophage migration inhibition and humoral antibody titres were high in patients with amoebic liver abscess. It is thus felt that CMIR is altered in amoebic patients during the acute phase and is independent of humoral antibody response.

Antibody Formation↗