Low doses of landiolol can effectively prevent tachycardia after intubation without significant effects on arterial blood pressure.

A rapid increase in isoflurane or desflurane concentration induces tachycardia and hypertension and increases-plasma catecholamine concentration. Little information is available as to whether sevoflurane, halothane, and enflurane induce similar responses during anesthesia induction via mask. Fifty ASA physical status I patients, aged 20-40 yr, and scheduled for elective minor surgery, received one of four volatile anesthetics: sevoflurane, isoflurane, halothane, or enflurane. Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask. The inspired concentration of anesthetic was increased by 0.9 MAC every 5 min to a maximum of 2.7 MAC. Heart rate (HR) and systolic blood pressure (SBP) were measured before and every minute for 15 min during anesthetic inhalation. In the sevoflurane and isoflurane groups, venous blood samples were drawn to determine the concentrations of plasma epinephrine and norepinephrine 3 min after each increase in anesthetic concentration. Sustained increments in HR were observed after increases in inspired isoflurane concentration to 1.8 MAC and 2.7 MAC (peak changes of 15 +/- 3 and 17 +/- 3 bpm, respectively). Isoflurane also increased SBP transiently after the inspired concentration was increased to 2.7 MAC (peak change of 10 +/- 4 mm Hg). Enflurane increased HR after the inspired concentration was increased to 2.7 MAC (peak change of 9 +/- 2 bpm). In contrast, changes in sevoflurane and halothane concentrations did not induce hyperdynamic responses. Plasma norepinephrine concentration in the isoflurane group was significantly higher than that in the sevoflurane group during 2.7 MAC (P = 0.022). We propose that there is a direct relationship between airway irritation of the anesthetic and immediate cardiovascular change during an inhaled induction of anesthesia.

We succeeded in inducing conjugation of Spirogyracastanacea by incubating algal filaments on agar plate. Conjugation could be induced using clone culture. The scalariform conjugation was generally observed, while lateral conjugation was rarely. When two filaments formed scalariform conjugation, all cells of one filament behaved as male and those of other filament did as female. Very rarely, however, zygospores were formed in both of pair filaments. The surface of conjugation tube was stained with fluorescently labeled-lectins, such as Bandeiraea (Griffonia) simplicifolia lectin (BSL-I) and jacalin. BSL-I strongly stained the conjugation tubes, while weakly did the cell surface of female gamete first and then that of male gamete. Jacalin stained mainly the conjugation tubes. Addition of jacalin inhibited the formation of papilla, suggesting some important role of jacalin-binding material at the initial step of formation of the conjugation tubes.

Ruan, Zonghai, Toshishige Shibamoto, Tomohiro Shimo, Hideaki Tsuchida, Tomonobu Koizumi, and Matomo Nishio. NO, but not CO, attenuates anaphylaxis-induced postsinusoidal contraction and congestion in guinea pig liver. Am J Physiol Regul Integr Comp Physiol 286: R94-R100, 2004. First published October 2, 2003 10.1152/ ajpregu.00648.2002The pathophysiology of the hepatic vascular response to anaphylaxis in guinea pig is not known. We studied effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused livers derived from guinea pigs sensitized with ovalbumin. We also determined whether nitric oxide (NO) or carbon monoxide (CO) modulates the hepatic anaphylaxis. The livers were perfused portally and recirculatingly at constant flow with diluted blood. With the use of the double-occlusion technique to estimate the hepatic sinusoidal pressure (P do), portal venous resistance (Rpv) and hepatic venous resistance (Rhv) were calculated. An antigen injection caused venoconstriction characterized by an increase in R pv greater than Rhv and was accompanied by a large liver weight gain. Pretreatment with the NO synthase inhibitor N G -nitro-L-arginine methyl ester, but not the heme oxygenase inhibitor zinc protoporphyrin IX, potentiated the antigen-induced venoconstriction by increasing both R pv and Rhv (2.2-and 1.2-fold increase, respectively). In conclusion, anaphylaxis causes both pre-and postsinusoidal constriction in isolated guinea pig livers. However, the increases in postsinusoidal resistance and Pdo cause hepatic congestion. Endogenously produced NO, but not CO, modulates these responses. hepatic circulation; antigen; double occlusion pressure; hepatic vascular resistance ANAPHYLAXIS IS AN immediate, type-1 hypersensitivity reaction that occurs after exposure of sensitized organisms and tissues to sensitizing antigen. The most common life-threatening feature of acute anaphylaxis is cardiovascular collapse and shock, although there are other life-threatening effects, including bronchospasm, angioedema, and pulmonary edema (24). Cardiovascular manifestation includes a rapid and precipitous decrease in systemic arterial pressure with a concomitant decrease in cardiac output (5). Anaphylactic hypotension is primarily caused by alterations in the systemic circulation that influence blood flow to the heart because left ventricular function is relatively well preserved during anaphylactic shock (5). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a plasma volume loss. The latter could be the result of vasodilation with the peripheral pooling in largecapacity splanchnic venous beds and increased vascular permeability with a shift of intravascular fluid to the extravascular space.In canine experimental models of anaphylactic shock, congestion of livers and the upstream splanchnic organs is important in the pathogenesis of circulatory collapse. Actually, eviscerated dogs did not develop anaphylactic shock (17). Enjeti et al. (5) reported that the severity of th...