The role of the sympathetic nervous system in the regulation of large coronary artery tone has been well defined. Studies of adrenergic regulation of coronary-resistance vessels have largely been limited to indirect inferences based on flow measurement obtained in vivo. The purpose of the present study was to determine the effects of norepinephrine (NE) on the coronary microcirculation using direct in vitro approaches. Porcine coronary microvessels (80-200 µm in diameter) were pressurized in isolated organ chambers. Diameters were measured using a Halpern microvessel imaging apparatus. After preconstriction with leukotriene D4, NE caused complete relaxation. Relaxations to NE were inhibited by propranolol. Relaxations to NE were also inhibited by LY83583 (which depletes cGMP) and hemoglobin (which binds endothelium-derived relaxing factor, EDRF). NE caused minimal or no constriction in both preconstricted and nonpreconstricted microvessels even in the presence of hemoglobin and propranolol. In conclusion, NE predominantly dilates porcine coronary microvessels, both by β-adrenoceptor activation and by stimulating release of EDRF. There is minimal α-adrenoceptor-mediated constriction of coronary microvessels.
Female mice were mated to males that had been surgically rendered incapable of forming copulatory plugs. About half of the females were found to be pregnant, and the other half pseudopregnant, as a result of these matings. In both cases, mating with the operated males resulted in the induction of luteal activity in the female.In the normal oestrous cycle of the female house mouse, a true luteal phase is absent. Some unknown stimulus provided by the male during mating induces the luteal phase of the oestrous cycle in the female. Land & McGill (1967) initiated a search for this stimulus. They recognized three possible sources of stimulation from the male that might be either sufficient or necessary for the induction of luteal activity. These were: (a) a minimum number of preejaculatory thrusts, (b) the ejaculatory reflex and the formation of the copula¬ tory plug, and (c) the subsequent presence of the plug in the vagina. Their results indicated that up to 150 pre-ejaculatory thrusts were neither sufficient nor necessary for the induction of luteal activity. On the other hand, nine of eleven animals receiving fifty-five or fewer pre-ejaculatory thrusts, plus the ejaculatory reflex and the copulatory plug, became pregnant. A third group of animals received pre-ejaculatory thrusts ranging from twenty-four to 135, plus the ejaculatory reflex and the copulatory plug which was immediately removed. Six of these females became pregnant and eight were judged pseudopregnant.The experiment of Land and McGill failed to separate the effects of the presence of the copulatory plug in the vagina from the effects of the dramatic ejaculatory pattern exhibited by the male mouse (McGill, 1962). The present study was concerned with separating the effects of these two potential stimuli. A second purpose was to replicate and extend the findings of Land & McGill (1967).The method was essentially the same as that used by Land & McGill (1967). In brief, individual, sexually-experienced males were placed in plastic cylinders. Females were then introduced into the cylinders and any resulting matings
One-hundred-thirty-six patients who underwent marrow transplantation for endstage acute leukemia were studied with respect t o factors that might predict failure t o eradicate or recurrence of leukemia following transplantation. One-hundred-five patients were recipients of allogeneic and 3 1 recipients of syngeneic marrow. Sixty-four patients had acute lymphoblastic leukemia (ALL) and 72 acute nonlymphoblastic leukemia (ANL). The frequency of persistence of leukemia and relapse was 35% for patients with ANL and 44% for those with ALL. sidered simultaneously through proportional hazards modeling showed only the WBC at admission for transplantation t o be significant (P = 0.02). The presence of an enlarged spleen, either at diagnosis or at transplantation, was associated with an increased probability of relapse (P < 0.006) among patients with ANL. In patients with ALL, active central nervous system (CNS) disease at the time of transplantation significantly increased the risk of relapse in the CNS (P < 0.01). Patients with a white blood cell (WBC) count greater than 20,000/mm3 at admission for transplantation had an increased rate of relapse (P < 0.003). Patients whose leukemic cells showed a karyotypic abnormality on cytogenetic analysis had an increased probability of relapse as compared t o those with karyotypically normal leukemic cells (P = 0.04). Following transplantation, the persistence of leukemic cells in the marrow one week after transplantation indicated an increased likelihood of failure to achieve remission and an increased likelihood of subsequent relapse in those who achieved a remission (P < 0.001).When all the patients are considered as one group pretransplant factors con-
Forty-six previously untreated patients with advanced aggressive non-Hodgkin's (34 poorly differentiated and mixed diffuse, 8 histiocytic and 4 undifferentiated) were treated with a 3 phase combined modality program employing cyclophosphamide (C), hydroxyl-daunomycin (H), vincristine (O), prednisone (P), procarbazine (P) [CHOP(P)] combination chemotherapy in an initial induction phase, radiotherapy and nonmarrow toxic chemotherapy as a second consolidation phase, followed by a third phase of CHOP(P) chemotherapy for four more cycles. Long-term maintenance therapy was not given. High dose involved field radiation in phase II was limited to volumes encompasing less than 50% of the marrow bearing skeleton. The large majority of patients (82%) had such widespread involvement that this limitation precluded the use of local radiation and were treated instead with a mean of 132 rad of fractionated total body irradiation (TBI). Thirty-eight patients (83%) achieved complete remission. Twenty-nine (66%) of the 44 patients evaluable for follow-up, and 22 (61%) of the 36 patients receiving TBI, remain alive in complete remission for observation periods of up to 26 months.
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