Hossain Md Belayet

Induction of preeclampsia like phenomena by stimulation of sympathetic nerve with cold and fasting stress

The purpose of this study was to examine the effect of cold-stress, fasting stress and cold plus fasting stress on the sympathetic nerve activity. Pregnant and nonpregnant rats were kept in cold environment (0 degrees C), or fasting condition (12 h), and cold plus fasting condition for 2 weeks. Their plasma corticotrophin releasing factor (CRF), catecholamines, insulin levels, and platelets were measured, and histological examinations were performed. In cold plus fasting stress rats, a significant increased CRF, epinephrine (E), norepinephrine (NE), and insulin levels with decreased platelet count (P<0.0001) were observed compared with control. Histological study revealed that diffused enlarged glomeruli with fibrin deposition in the kidney, hemostasis, ischemic necrosis and fibrin deposition in liver and swelling along with hemorrhagic necrosis in adrenal gland of cold plus fasting stress rats. The biochemical and histological changes in cold plus fasting, cold-stressed or fasting rats were similar to human preeclampsia. The findings observed in cold plus fasting stress rats were more pronounced either than cold-stressed or fasting group. These results demonstrate that cold plus fasting stress is an intense stimulator of sympathetic nervous system than either cold stress or fasting.

Urinary trypsin inhibitor suppresses vascular smooth muscle contraction by inhibition of Ca2+ influx.

Urinary trypsin inhibitor (UTI) and its precursor form inter-alpha trypsin inhibitor (ITI) are present in plasma. To determine the action of UTI on blood vessels, we performed isometric vascular muscle contraction tests, microcirculation studies and measurement of cytosolic free Ca2+ in vascular smooth muscle cells. An isometric vascular muscle contraction test showed that the contractions stimulated by endothelin-1 or norepinephrine were suppressed in the presence of UTI, and that the contractions were not inhibited in the presence of ITI. The microcirculation study showed that the contraction of mesenteric arterioles of WKY rats induced by norepinephrine were inhibited by treatment of UTI, and that they did not alter by treatment of ITI. Pre-incubation of UTI, but not ITI, with vascular smooth muscle cells inhibited the increase of cytosolic free Ca2+ induced by endothelin-1 or norepinephrine. Cell-binding study by biotinylated UTI showed that vascular smooth muscle cells have specific binding site for UTI, but not for ITI. We propose that circulating UTI converted from ITI has a regulatory effect on local vascular tone by regulation of Ca2+ influx into smooth muscle cells.

Increased concentrations of plasma neuropeptide Y in patients with eclampsia and preeclampsia

OBJECTIVE Epinephrine and norepinephrine are associated with the hyperstimulation of the sympathetic nervous system. Neuropeptide Y is a potent vasoconstrictive substance that is released in response to sympathetic nerve stimulation. STUDY DESIGN The concentrations of plasma neuropeptide Y in pregnant patients with eclampsia (n = 8), preeclampsia (n = 8), and normotension (n = 8) were measured by radioimmunoassay on admission and 6 days after delivery. Correlations between plasma concentration of neuropeptide Y and mean arterial blood pressure were also evaluated in these patients on admission and 6 days after delivery. RESULTS The plasma level of neuropeptide Y in women with eclampsia (P <.001) and preeclampsia (P <.003) was found to be significantly elevated with respect to that in normotensive pregnant women. At 6 days after delivery the concentration of plasma neuropeptide Y was significantly decreased in women with eclampsia, women with preeclampsia, and women with normotensive pregnancies compared with the value measured on admission (P <.0001, P <.0001, and P <.002, respectively). At admission the plasma neuropeptide Y level was positively correlated with mean arterial blood pressure in women with eclampsia and preeclampsia. However, no significant correlations were observed between plasma neuropeptide Y concentration and mean arterial blood pressure both at admission and 6 days after delivery in normotensive pregnant women and 6 days after delivery in women with eclampsia and preeclampsia. CONCLUSION We have concluded that the level of neuropeptide Y in plasma is increased in women with eclampsia and preeclampsia. Elevated plasma neuropeptide Y levels may play a key role in the development of eclampsia and preeclampsia.

Chronic local cold stress to the soles induces hypertension in rats

The purpose of this study was to determine whether cold-stress stimulation to the soles of paws produces continuous hypertension in rats. Wistar-Kyoto rats were kept in cages with a 0 degrees C floor and 23 degrees C room temperature (cold-stressed group, n = 10) or in cages with 23 degrees C floor and 23 degrees C room temperature (control group, n = 10). BP and levels of plasma catecholamines, serum glucose, and serum insulin were measured, and the histologic characteristics of the kidney and adrenal gland were studied in all groups. After a week of localized cold-stress, BP of the experimental rats were significantly increased over those of the control rats. Significant increases were also seen in plasma epinephrine and norepinephrine, as well as serum insulin concentrations in the rats that underwent localized cold stimulation; these changes were not observed in the control rats. Fibrinoid deposition in the kidney and the intensity of neuropeptide Y-staining in the adrenal medulla were increased in the localized cold-stressed group compared with the control group. We conclude that chronic local cold stimulation to the soles is a new model of experimental hypertension.

Eclamptic Plasma Stimulates Norepinephrine Release in Cultured Sympathetic Nerve

The purpose of the present study was to evaluate the effect of plasma from eclamptic and preeclamptic patients on cultured sympathetic nerve. Sympathetic neurons from 12- to 14-day-old chick embryos were cultured; the neurons were then stimulated with 50% plasma from eclamptic, preeclamptic, hypertensive, normotensive pregnant, hypertensive, and normotensive nonpregnant women (n=7). Similarly, neurons were individually incubated with mixtures of 50% corresponding plasma with 0.25% bupivacaine or bupivacaine only (n=7). Furthermore, the effects of 1%, 10%, and 50% plasma from eclamptic, preeclamptic, and normotensive pregnant patients (n=7) were also evaluated. Norepinephrine concentrations were measured by high-performance liquid chromatography. Electron microscopic studies of nerve cells were also performed. Stimulation with plasma from eclamptic and preeclamptic women significantly increased norepinephrine concentration (P<0.0001) compared with control. The release of norepinephrine was found to be concentration-dependent. Conversely, norepinephrine secretion was significantly hampered by bupivacaine treatment (P<0.0001). Electron microscopic studies in eclamptic and preeclamptic plasma-stimulated nerve cells showed that perikarya were in close contact with each other and with nerve cell processes. After treatment with bupivacaine, nerve cells were irregular in shape and the cell membranes were demyelinated. These results suggest that eclamptic and preeclamptic plasma has an excitotoxic effect on sympathetic nerve via axoplasmic membrane depolarization, thus increasing norepinephrine secretion that is blocked by bupivacaine. A preeclamptic condition may be improved by depression of sympathetic nerve stimulation.

The impact of vasoactive peptides on nitric oxide production in cultured sympathetic neurons.

The concentration of nitric oxide was found to be decreased in a hypersympathetic condition. We carried out experiments on cultured sympathetic neurons from 12-14-days-old chick embryos to investigate the role of vasoactive peptides and amine on nitric oxide production. Stimulation of cultured neurons with endothelin-1, norepinephrine and angiotensin-II initially increases nitric oxide production and subsequently decreases it in a dose-dependent manner (P<0.05, n = 7). Stimulation of Fura-2 acetoxymethyl ester-loaded neurons with endothelin-1, norepinephrine and angiotensin-II increases the calcium influx (within 30-90 s) and it is then restored to the initial level (P<0.05, n = 7). An additional observation was that specific stimulator L-arginine significantly increases the nitric oxide release and calcium influx into the cells, whereas N(W)-nitro-L-arginine methyl ester blunts nitric oxide release dose dependently (P<0.05, n = 7) and does not change the calcium concentration in the cells. We propose that vasoactive peptides and amines inhibit nitric oxide production in the cultured sympathetic neuron by regulation of intracellular calcium concentration.

Vasospasms of Cerebral Arteries in Hyperemesis gravidarum

Hyperemesis gravidarum is associated with nausea and vomiting during the 1st trimester of pregnancy. We report 2 cases of hyperemesis gravidarum associated with vasospasms of cerebral arteries recognized by magnetic resonance imaging angiography. The hyperemetic condition of the patients improved after fluid and electrolyte replacement therapy.

Induction of Eclampticlike Changes by Stimulation of the Celiac Ganglion in Rats

OBJECTIVE To examine the relation between the stimulation of the abdominal sympathetic nervous system and vasospasm of the brain in eclamptic seizures, we analyzed brain blood flow after stimulation of the celiac ganglion by lipopolysaccharide (LPS, 5, 50, or 500 mg/mL) or normal saline before and after denovation of sympathetic trunk in pregnant and nonpregnant rats. METHODS The brain blood flow was measured after stimulation of the celiac ganglion with 50 microL (5 mg/mL) LPS in group I, 50 microL (50 mg/mL) LPS in group II, 50 microL saline in group III, and 50 microL (500 mg/mL) LPS (after denovation of the sympathetic trunk) in group IV. A sham control experiment was also done by stimulation of the abdominal peritoneum with 50 microL (500 mg/mL) LPS in group V. Changes in water content and histological findings in the brain were also studied in this protocol. RESULTS A significant reduction in brain blood flow was observed in pregnant rats in groups I and II on stimulation of the celiac ganglion with LPS (p < 0.0001, p < 0.001) compared with before stimulation. Celiac ganglion stimulation with saline (group III) and LPS (group IV, after denovation of the sympathetic trunk) did not affect brain blood flow. Stimulation of the abdominal peritoneum with LPS (group V) could not induce any changes in brain blood flow. Repeated seizures occurred in 60% of pregnant rats and a remarkable increase in water content was observed after LPS stimulation of the celiac ganglion in groups I and II (p < 0.0001, p < 0.001). Histologically, we found that stimulation of the celiac ganglion with LPS caused widening of perivascular spaces with compression of the vessels leading to ischemic changes in brain tissues. There were no such findings observed in other groups. However, a lesser extent effect was noticed in nonpregnant than seen in pregnant rats. CONCLUSION Stimulation of the abdominal sympathetic ganglions could induce vasoconstriction of the brain vessels, thus decreasing brain blood flow, which results in eclampsialike changes in rats.