ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We have attempted to evaluate the role of adrenergic nerves which arise from the superior cervical ganglia or which are intracerebral throughout their course, in the control of local cerebral blood flow (CBF). Hypothalamic blood flow (HBF) was measured in the conscious rabbit by the133Xe-clearance technique. Stimulation of the upper brainstem, using 5-Hz, 3-V, 1-msec, square wave pulses, increased HBF by a mean of 7.6 ml/100 g per min (P< 0.005). This effect was abolished by the intrahypothalamic injection of the β-adrcnoreceptor blocker, propranolol, and by chemical sympathec-tomy of the hypothalamus or of the upper brainstem with 6-hydroxy-dopamine, but was not altered by bilateral cervical ganglionectomy.Intrahypothalamic injection of 0.1 μg of tyramine caused a mean decrease in HBF of 15.6 ml/100 g per min (P< 0.001). This effect of intrahypothalamic injection of tyramine was abolished by bilateral cervical sympathectomy but not by chemical sympathectomy of the upper brainstem. These results support the idea that local CBF, at least in the hypothalamus, is mediated by two distinct pathways. The first consists of the sympathetic nerves which arise in the cervical ganglia, and which activate intrahypothalamic a-receptors to cause constriction. The second is an entirely intracerebral noradre-nergic pathway which stimulates 0-receptors to cause vasodila-tion.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Antibody to tissue factor apoprotein was adsorbed against γ-globulin and coupled to horseradish peroxidase; this complex was applied to various rabbit tissues. The distribution of the peroxidase marker then was observed by electron microscopy. We examined fixed or frozen sections, as well as breis of aorta, vena cava, brain, heart, lung, liver, spleen, kidney, bone marrow, meso-thelial gut lining, erythrocytes, leukocytes, and platelets. All endothelial cells that had been exposed to the antibody complex were positive and in all cases only the endothelial cells showed localization of the electron-dense reaction product. Tissues that had been incubated with complexes prepared with γ-globulin from animals not immunized with tissue factor apoprotein showed no staining.Prior treatment of the tissue with uncoupled anti-tissue factor γ-globulin blocked binding by the coupled antibody. In blood vessel preparations that had been specifically designed to expose the media to the anti-tissue factor complex, medial smooth muscle cells and connective tissue showed no reaction product. Parenchyma! cells of the other organs mentioned likewise were devoid of reaction product. Similarly, the leukocytes and platelets occasionally observed in vessel lumens showed no evidence of binding. Platelets adhering to arterial subendothelial structure after injury also were unreactive. These findings suggest that in normal rabbits anti-tissue factor-horseradish peroxidase complex combines selectively with endothelial cells.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Transmembrane potentials and contractile activity were recorded from isolated canine Purkinje and ventricular muscle preparations exposed to acetylstrophantidin (AS) and subjected to a resting tension equal to 80% of that required to elicit peak developed tension. AS induced transient depolarizations (TD's) accompanied by aftercontractions in Purkinje tissue. AS also induced aftercontractions in 11 muscle preparations, and in seven of these the mechanical events were associated with TD's. Aftercontractions and TD's in both and the coupling intervals were directly related to the preceding basic cycle length (BCL). The amplitudes of aftercontractions and TD's reached a maximum at a coupling interval of 600–700 msec. Tension increased the amplitude of TD's in Purkinje tissue and promoted the appearance of TD's in muscle. TD's in muscle occasionally reached threshold in the presence of tension. The results of this study suggest that stretch or increased resting tension may promote the types of cardiac arrhythmias that are causally related to digitalis-induced TD's. The results are compatible with the hypothesis that TD's are caused either by a transmembrane influx of calcium or by an internal release of calcium ions.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Isolated rat hearts were perfused with hormonal concentrations of glucagon during a hypoxic perfusion to determine whether it would enhance recovery after reoxygenation. Rat hearts were divided into two groups: (1) those perfused with glucose-free Tyrode's solution and (2) those perfused with Tyrode's solution containing glucose. During 3 minutes of exposure to hypoxia both untreated hearts and hearts perfused with glucagon demonstrated a decrease in contractile force to 10–20% of control. When glucose was present in the perfusion medium, cardiac performance was better during both the periods of hypoxia and reoxygenation. During reoxygenation, recovery of contractile force was significantly better (P < 0.05) in glucagon-perfused hearts than in untreated hearts; this improved recovery occurred regardless of whether glucose was included in the medium. The enhanced recovery of the glucagon-perfused hearts was associated with decreases in myocardial levels of guanosine 3′,5′-monophosphate (cyclic GMP) both during the periods of hypoxia and reoxygenation. At the end of the hypoxic period, cyclic GMP levels in the glucagon-perfused hearts were 20–64% of the levels in untreated hearts. Similarly, after 5 minutes of reoxygenation cyclic GMP levels in the glucagon-perfused hearts were 21% of the levels in untreated hearts. The effect of glucagon on adenosine 3′,5′-monophosnhate (cyclic AMP) concentrations in untreated hearts and in hearts receiving glucagon was not significantly different either after 3 minutes of hypoxia or during reoxygenation. The rate of anaerobic glycolysis afeter 3 minutes of hypoxia was higher in untreated hearts than in glucagon-perfused hearts, as determined by the lactate content of coronary perfusates. These studies suggest that hormonal concentrations of glucagon exert a protective effect on the hypoxic rat heart which involves a modulation of cardiac cyclic GMP accumulation.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We compared the effects of arachidonic acid (AA), the bisenoic prostaglandin precursor, with those of prostaglandin F2α(PGF2α) and norepinephrine (NE) on pulmonary vascular resistance in the isolated (in situ), perfused canine lung lobe. The isolated lobe was perfused with autologous blood or an artificial perfusate under conditions of constant flow. Lobar artery and venous pressures were constantly monitored after bolus injections of A A, PGF2αand NE into the inflow cannula. AA (100 μg/kg) produced a significant increase in the pressure gradient (93.3 ± 8.4%, se) in the lobe. Similarly, PGF2α(1 μg/kg) significantly increased the pressure gradient (41.2 ± 6.5%), as did NE (1 Mg/kg, 41.6 ± 3.2%). Aspirin (25 mg/kg) completely blocked the pulmonary vascular effect of AA, but did not affect the response to PGFfe, Linoleic acid, a control fatty acid, did not produce pulmonary vasoconstriction. The pressor effect of AA was not blocked by pretreatment with phentolamine, propranolol, cyproheptadine, or atropine. The use of an artificial perfusate free of cellular elements did not prevent the vasoconstrictor action of AA. The times to onset of action of the three agents were similar, and short. These results suggest that AA is converted into vasoactive intermediates or a prostaglandin, and the vasoactive intermediates or the prostaglandin act directly on precapillary pulmonary vascular smooth muscle rather than through platelet, plasma, adrenergic, or cholinergic mechanisms.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Left ventricular (LV) function during the adaptation to chronic pressure overload produced by an ascending aortic constriction was analyzed in conscious dogs, instrumented with intraventricular micromanometers and pairs of ultrasonic crystals for measurement of LV wall thickness (WTh) and internal LV chamber diameter. During inflation of the cuff to produce LV pressures averaging 220 mm Hg, calculated peak wall stress (WSt) increased by 55% above control while percent shortening decreased by 24% and mean circumferential shortening velocity (VCF) decreased by 39% from control. By 9 days (mean) after aortic constriction, the cross-sectional area (CSA) of the LV wall increased by 10% and peak WSt fell to 37% above control. End-diastolic diameter (EDD) increased to 4% above control, while percent shortening and mean VCTremained reduced at −12% and −20% of control, respectively.During the phase of concentric hypertrophy (mean2V-iweeks), CSA increased further to 15% above control and WSt fell to 22% above control, while EDD and percent shortening returned to control and mean VCFincreased to −7% of control (not significant). At 24 hours after release of the cuff WSt, percent shortening, mean VCF, and peak velocity of LV pressure rise (peak dP/dt) were not significantly different from control. Rapid, partial regression of hypertrophy was observed in some dogs. Thus, the left ventricle responds to chronically elevated pressure by initial dilation with increased WSt followed by gradual wall thickening and consequent reduction of WSt to near normal. After successful adaptation to the pressure overload, hypertrophy per se did not produce intrinsic depression of the myocardial inotropic state.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

Knowledge of the status of cardiac norepinephrine (NE) during anemia could lead to a better understanding of the role the sympathetic nervous system plays in cardiac function during anemia. Rats were made anemic by treatment with phenylhydrazine (PHZ). After the rapid onset of anemia, 60% of the stored NE in the heart was lost within 48 hours after treatment. Associated with the loss of cardiac NE was an increase in the wet weight of the heart, which reached a value 40% above control 48 hours after treatment. PHZ itself probably does not directly mediate this depletion of NE, since the vas deferens, brain, and spleen had a normal store of NE at 48 hours. This contention was supported when rats, treated with PHZ, were transfused with normal rat red blood cells. This transfusion resulted in PHZ-treated rats which were not anemic. The hearts of these rats were not depleted of NE, but the hearts of the nontransfused, PHZ-treated controls were. Anemia also was induced by treating rats with anti-rat red blood cell serum. The hearts of these rats also were depleted of NE. These experiments show that during two forms of anemia there is a loss of NE from the sympathetic neurons innervating the heart. The effect of this on regulation of cardiac function remains to be determined.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We evaluated urinary excretion and tubular transport of3H-digoxin by three different methods in anesthetized rats made diuretic by infusion of 2.5% saline. In one group small volumes of3H-digoxin and “C-inulin were injected simultaneously into surface proximal convolutions, and urine was collected serially from both ureters. Digoxin recovery was lower after early (62.1 ± 5.3%) than after late (86.9 ± 7.7%) proximal administration but inulin recovery was complete (99.6 ± 2.7%) after all injections. Most of the digoxin was excreted simultaneously with inulin. Delayed recovery was low. In another group of rats digoxin and inulin were applied directly to the capsule of the left kidney. Two-thirds of the recovered digoxin appeared from the left ureter and one-third from the right. The difference (41.9 ± 7.4%) is an estimate of transtubular digoxin influx. Digoxin excretion preceded inulin only on the left. Digoxin to inulin concentration ratios were 6 times higher from the left than the right, whereas inulin recoveries from the two sides were similar. In a third group of rats tubular fluid was collected from surface convolutions of proximal and distal tubule. In the accessible segment of the proximal tubule 35.9% of the filtered digoxin was reab-sorbed. In the more distal nephron, drug was added into the lumen; this resulted in a net urinary excretion of 80.2 ± 18.2%. These findings are compatible with free filtration of digoxin at the glomerulus followed by passive proximal tubular reabsorption and an influx against a concentration gradient in the distal nephron.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID

摘要:

We measured isogravimetric capillary pressure (Pcl) and plasma colloid osmotic pressure (irp) in isolated dog hind-limbs. A very rapid isolation technique and a perfusion technique involving no weight change were developed in order to compare the effects of different isolation procedures. Also, a “previous isolation procedure” (PIP) was used to approximate isolation procedures previously reported; this procedure included (A) anesthesia for 1 to 1 1/2 hours before limb isolation, (B) 1/2 hour of denervation before isolation, and (C) perfusion after isolation for 1/2 hour at an arterial pressure of 100 mm Hg and a venous pressure of 6 mm Hg. These different procedures altered average (± SE) capillary pressure and fluid dynamics in the hindlimb as shown in the following table:These data indicate that average isogravimetric capillary pressure in the intact resting dog hindlimb may be 8 mm Hg below plasma colloid osmotic pressure, or about 9 mm Hg, and that many reported values have been heavily influenced by the isolation technique.

ISSN:0009-7330    

出版商:OVID    

年代:1976

数据来源: OVID