The effects of diltiazem on hemodynamics and seizure duration during electroconvulsive therapy

Electroconvulsive therapy (ECT) is often associated with acute hyperdynamic responses, and we hypothesize that diltiazem can blunt this response. We measured the effect of a 10-mg dose of diltiazem on heart rate and mean arterial pressure during ECT. Furthermore, we assessed seizure duration by using both the cuff method and two-lead electroencephalogram. We studied 18 patients with a randomized, double-blinded, placebo-controlled cross-over study design. Diltiazem significantly reduced heart rate and mean arterial pressure just after medication, and it also significantly reduced the increases in these variables after ECT, as compared with the placebo. The use of diltiazem was, however, associated with a shortened seizure duration, possibly making ECT less effective. Because of the reduction in seizure duration, the routine administration of diltiazem may not be advisable because it can possibly interfere with the psychotherapeutic efficacy of ECT. However, diltiazem medication for ECT is potentially useful for reducing tachycardia and hypertension in high-risk patients. IMPLICATIONS: Diltiazem can blunt acute hyperdynamic responses after electroconvulsive therapy, but seizure duration is also significantly reduced, possibly making this therapy less effective.     

The tumor suppressor WARTS activates the Omi / HtrA2-dependent pathway of cell death

Drosophila tumor suppressor WARTS (Wts) is an evolutionally conserved serine / threonine kinase and participates in a signaling complex that regulates both proliferation and apoptosis to ensure the proper size and shape of the fly. Human counterparts of this complex have been found to be frequently downregulated or mutated in cancers. WARTS, a human homolog of Wts, is also known as tumor suppressor and mitotic regulator, but its molecular implications in tumorigenesis are still obscure. Here, we show that WARTS binds via its C-terminus to the PDZ domain of a proapoptotic serine protease Omi / HtrA2. Depletion of WARTS inhibited Omi / HtrA2-mediated cell death, whereas overexpression of WARTS promoted this process. Furthermore, WARTS can enhance the protease activity of Omi / HtrA2 both in vivo and in vitro. Activation of Omi / HtrA2-mediated cell death is thus a potential mechanism for the tumor suppressive activity of WARTS.     

Intravenous landiolol, a novel β(1)-adrenergic blocker, reduces the minimum alveolar concentration of sevoflurane in women

Study Objective

To investigate the effect of intravenous (IV) landiolol, a novel β₁-adrenergic blocker, on the minimum alveolar concentration (MAC) of sevoflurane in adult women.

Design

Prospective, randomized study.

Setting

University hospital.

Patients

42 ASA physical status 1 and 2 women, aged 24-57 years, who were scheduled to undergo elective abdominal surgery.

Interventions

Anesthesia was induced in all patients by vital capacity rapid inhalation induction of sevoflurane. In the landiolol group, administration of landiolol began when patients took a vital-capacity breath: 0.125 mg/kg/min for one minute and then 0.04 mg/kg/min. Normal saline was administered in the control group.

Measurements

MAC was determined by a technique adapted from the conventional up-down method.

Main Results

The MAC of sevoflurane was 2.2% ± 0.2% in the control group and 1.7% ± 0.2% in the landiolol group, a statistically significant difference (P = 0.0005).

Conclusions

IV landiolol reduces the MAC of sevoflurane in women by approximately 20%.     

Computerized transverse axial tomography in intracerebral, intracerebellar and intraventricular hemorrhage (author's transl)

Computerized transverse axial tomography (CT) of the brain is a recently developed method which allows non-invasive roentgenologic evaluation of intracranial diseases. The advent of CT represents a great advance in the diagnosis of a very wide variety of intracranial lesions, including cerebrovascular diseases. Especially, CT was found to be extremely informative in evaluating intracerebral, intracerebellar and intraventricular hemorrhage. The purpose of this report is to evaluate the clinical usefulness of CT in the diagnosis of intracranial hemorrhage. From the seven hundreds cases of various intracranial diseases hitherto examined by the EMI-scanner (160 X 160 matrix), twenty-three cases of nontraumatic intracranial hemorrhage were selected for the present study. Fifteen cases of fresh hemorrhage consisted of hypertensive cerebrovascular disease, arterio-venous malformation, aneurysm and unknown etiology, number of cases being six, three, four and two, respectively. All cases were examined within fifteen days after the ictus and the positive findings were obtained in all cases. The characteristic feature of the hematoma is the circumscribed and increased density area surrounded by the decreased density zone probably representing the accompanied brain edema. The sequential CT studies revealed that the hematoma area was gradually decreased in its density and finally transformed into the rather low density one in four weeks or so after the ictus. The smallest hematoma detected by CT was the cerebellar hematoma about five grams in weight, which was failed to be recognized by the angiography. In cases of the old hemorrhage, besides the decreased density area of the hematoma, such findings were obtained as cerebral atrophy, ventricular dilatation and porencephalic change. It would be concluded that CT study is the most useful aid at present available in the diagnosis of intracranial hemorrhage. The precise anatomic extent of the hematoma, associated brain edema, ventricular deformity and displacement and hydrocephalus are all readily assessed by CT.     

Effects of cyclic AMP on the function of the cardiac gap junction during hypoxia

BACKGROUND: In the ischemic or hypoxic heart, an impairment of electrical cell-to-cell coupling and a dephosphorylation of the connexins that comprise the gap junction channel were observed. However, it remains to be elucidated whether the dephosphorylation of the connexin during hypoxia is due to alterations in the ionic strength of Ca(2+) or H(+), and how the activation of protein kinase A (PKA) affects the hypoxia-induced abnormal function of the gap junction. OBJECTIVES: The effects of hypoxia, intracellular Ca(2+) overload and intracellular acidosis on the PKA-mediated phosphorylation of connexin 43 (Cx43) were examined in relation to the function of the cardiac gap junction. METHODS: Hearts isolated from adult, male guinea pigs were used. The intercellular electrical cell-to-cell coupling was evaluated by the longitudinal internal resistance and the conduction velocity observed in in vitro experiments using isolated muscle strip preparations. The phosphorylation of Cx43 was evaluated by an immunoblot (Western blot). The localization of immunoreactive Cx43 at the intercalated disk was detected using confocal laser scan microscopy. RESULTS: Cyclic AMP or the activation of PKA promotes the intercellular electrical coupling that accompanies an augmentation of the PKA-mediated phosphorylation of Cx43. Electrical cell-to-cell decoupling and reduction of the PKA-mediated phosphorylation of Cx43 were dependent on the progression of hypoxia. These results agree with those observed in the progression of intracellular Ca(2+) overload or intracellular acidosis. Cyclic AMP or the activation of PKA alleviated the electrical cellular decoupling and the hypoxia-, intracellular Ca(2+) overload- and intracellular acidosis-induced deteriorated expression of Cx43. These ameliorative effects of cyclic AMP on the function of the gap junction and on the expression of Cx43 weakened as the hypoxia progressed, and as the intracellular ionic strength of Ca(2+) and H(+) increased. CONCLUSIONS: In cardiac ventricular muscle cells, cyclic AMP or the activation of PKA promotes electrical cell-to-cell coupling through the gap junction due to an augmentation of the PKA-mediated phosphorylation of Cx43 in the early stage of hypoxia, as well as in normoxia. The suppression of PKA-mediated phosphorylation of Cx43 during hypoxia may be caused by an increase in the intracellular ionic strength of Ca(2+) and H(+). Thus, the activation of cyclic AMP-dependent PKA may have an antiarrhythmic effect in the early stage of hypoxia.     

Nursing experience in palliative care at the outpatient clinic

Seven of the 17 patients reported that they were satisfied with the palliative care at our outpatient clinic. A patient's will to stay home, a devoted key person to the patient, procedures such as good pain control and an oral intake were considered to be important factors in palliative care at the outpatient clinic. We should understand that the patient's family attending the outpatient clinic is a part of their important daily life, so we try to make them feel comfortable whenever they come to see us. We should also strive for building more experience in palliative care for patients and their families. Based on our experience, we anticipate that outpatient care will be increased in the future. In the meantime, advanced nursing skills and techniques are needed.     

A comparative study of the effects of OPC-1085 and propranolol on isolated guinea pig atrium.

Effects of a newly synthesized beta-blocker, 5-(3-tert-butylamino-2-hydroxy) propoxy-3,4-dihydrocarbostyril (OPC-1085) were compared with those of propranolol. OPC-1085 had a potency about 3 times greater than that of propranolol in blocking the positive inotropic and chronotropic effects of isoprenaline on the isolated guinea pig atrium. At a concentration of over 3 X 10(-5) M OPC-1085 produced negative inotropic and chronotropic effects. However, these effects were about 10 times weaker than those of propranolol. Suppressing effects on the rate of rise and on the maximum driving frequency of action potentials were also more than 10 times less than those of propranolol. There was almost no change in the action potential of vagus nerve after a 10 min treatment with OPC-1085 (10(-5) M), while the action potential was reduced to 60-70% with propranolol (10(-5) M).