Plasmodium vivax Malaria Presenting with Acute Systemic Capillary Leak Syndrome.

Systemic capillary leak syndrome (SCLS) is a very rare disorder characterized by hypotension with heamoconcentration, hypoalbuminemia without albuminuria and generalized edema, the etiology of which are snake bites, viral heamorrhagic fever, drugs, sepsis, upper respiratory tract infection, Hanta virus and West Nile virus infection and serum paraproteinemia. Typically, the syndrome manifests in two phases: initial capillary leak phase characterized by edema, serous effusion, hypotension which is followed by phase of volume overload or recruitment phase. Treatment is in the form of fluid replacement, inotropic support and vasopressor therapy during leak phase and diuretics during volume overload phase. Prognosis of this disease is very poor. Here we are presenting a rare case of plasmodium vivax with SCLS.

Cytochrome oxidase activity in rat retinal ganglion cells during postnatal development.

In this study, the metabolic activity of rat retinal ganglion cells during postnatal development has been examined in vivo using cytochrome oxidase histochemistry. The intensity of staining was measured by optical densitometry. The activity of cytochrome oxidase in retinal ganglion cells progressively increased from postnatal day 0 (P0) and reached a peak during the second week of postnatal development (P10-P14) and declined thereafter. Our data show that the increased levels of cytochrome oxidase seen in developing retinal ganglion cells occur at the same time, when neuronal maturity and synaptogenesis reach their peaks.

Effects of sodium deoxycholate on the mechanical and electrical activities and ultrastructure of guinea pig atria.

The mechanism of cardio-inhibitory effects of sodium deoxycholate (DOC) was investigated by studying its effects on the contractility, action potentials (APs) and ultrastructure of guinea pig atrial preparations. DOC (10(-7)-10(-4) M) caused reversible negative ino- (NIE) and chrono-tropy in spontaneously beating (SBA) and NIE in electrically driven left (EDA) atria. At higher doses (greater than or equal to 1.10(-3) M) DOC caused irreversible inhibition of contractions. Atropine (10(-7)-10(-4) M) failed to inhibit both the reversible and irreversible effects of DOC. The NIE due to lower doses of DOC (less than or equal to 1.10(-4) M) was inhibited by higher [Ca2+]0, isoprenaline (10(-6)-10(-4) M), and noradrenaline (10(-6)-10(-5) M), which did not alter the dose of DOC required for the irreversible and complete NIE. In lower doses (10(-7)-10(-4) M) DOC caused a reversible inhibition of the AP durations at -20 and -40 mV (APD20 and APD40, respectively), but increased the AP duration at 90% repolarisation (APD90). At higher doses (greater than 5.10(-4) M) it caused an irreversible membrane depolarization, reduction in APD20 and APD40, and complete cessation of electrical activity. The ultrastructural changes in atria treated with 1.10(-4) M DOC were characterized by poorly delineated glycocalyx and at greater than 1.10(-3) M by disruption of sarcolemma and sarcoplasmic reticulum and swelling disruption of mitochondria. Taken together these observations show that DOC caused reversible and irreversible inhibition of atrial contractions at low (10(-7)-10(-4) M) and high (greater than 5.10(-4) M) concentrations, respectively, by different mechanisms. The former effect is due to inhibition of Ca2+ channel activity and the latter due to its detergent property causing removal of subcellular components.