摘要:

ABSTRACT The purpose of this investigation was to evaluate the efficacy and safety of implanting expandable intravascular stents in pulmonary arteries and systemic veins. Twenty-seven balloon-expandable grafts were placed in 13 mongrel dogs under anesthesia. A long sheath was introduced over a wire and catheter or dilator into the pulmonary artery or target vein. A collapsed stainless steel expandable mesh stent was placed over the balloon of an angioplasty catheter. The catheter with the mounted stent was advanced through the sheath. The stent expanded to the diameter of the balloon as the balloon was inflated, and remained expanded as the balloon was deflated. The stent was expanded further with a larger balloon in 11 instances. Eleven stents were placed successfully in pulmonary arteries (out of thirteen attempted), and 11 of 14 were installed in tributaries of the precava or postcava. Three inadvertent embolizations of the devices occurred. All three devices that embolized lodged in the pulmonary arteries and did not obstruct flow. Seven dogs were recatheterized at intervals ranging from 56 to 278 days. Twelve stents were patent and nonobstructive, and two were malpositioned, one of which was obstructed. Three animals were killed 2 months (two dogs) and 9 months (one dog) after the implantations. The stents (four in the pulmonary arteries and two in veins) were completely covered with neointima and were patent, without thrombosis. These stents hold promise for definitive dilation of congenital or postoperative vessel stenoses.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Antiarrhythmic activity of amiodarone's desethyl metabolite, which accumulates during oral amiodarone therapy, has been postulated to explain the delayed onset of antiarrhythmic effects during long-term amiodarone therapy. To determine their relative antiarrhythmic efficacy, amiodarone and its desethyl metabolite, desethylamiodarone, were administered to mongrel dogs with ventricular tachycardia 24 hr after ligation of the left anterior descending coronary artery. Cumulative doses of amiodarone, desethylamiodarone, a combination of amiodarone and desethylamiodarone, or the vehicle for drug administration were given at 1 hr intervals. Both amiodarone and desethylamiodarone suppressed ventricular arrhythmias in a dose-dependent fashion. The metabolite, however, was more potent with a 50% elective concentration for suppression of premature ventricular complexes of 1.4 mg/liter compared with 4.6 mg/liter for the parent compound. Plasma and myocardial drug concentrations were similar to those measured during long-term amiodarone therapy in man, with desethylamiodarone producing greater myocardial concentrations than amiodarone for a given plasma concentration. Coadministration of the metabolite along with the parent drug resulted in suppression of arrhythmias at lower doses of amiodarone than when the latter was administered alone, and concentration-response analysis indicated an additive antiarrhythmic effect. These experiments suggest that the accumulation of desethylamiodarone that occurs with long-term oral amiodarone therapy contributes importantly to the antiarrhythmic effects of the drug, and may account for the gradual increase in antiarrhythmic action during the course of amiodarone therapy.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

This study was designed to assess the time-dependent change in propensity to induction of malignant ventricular tachyarrhythmia after myocardial infarction. Instrumented conscious dogs were assessed during serial drug-free electrophysiologic studies over 26 ± 9 days (range 17 to 35 days) after 2 hr occlusion-reperfusion of the left anterior descending coronary artery. Of the 19 animals studied, 11 continued to have sustained ventricular tachyarrhythmias inducible (group I) over this time period. In the eight remaining animals, spontaneous loss in the ability to induce sustained ventricular tachycardia occurred (group II). Myocardial infarct size in group I animals (18 ± 8%) was significantly greater than that in group II dogs (12.5 ± 5%;p<.05). Even in group I animals, time-dependent changes occurred in the number of extrastimuli required to induce ventricular tachycardia and the frequency with which left ventricular stimulation was necessary. A differential pattern of time-dependent changes in electrophysiologic variables was observed when comparing group I and II animals. The conduction time to the infarct zone was prolonged during follow-up in group I animals, while in group II animals this variable was unchanged. Repolarization time recorded in the border zone remained unchanged in group I animals, but it was significantly shortened in group II animals. In addition, ventricular effective refractory period in the infarct zone shortened over time in group I animals but did not change in group II animals. In conclusion, time-dependent changes occur in electrophysiologic variables that are associated with a progressive decrease in propensity to induction of ventricular tachycardia after myocardial infarction. A critical determinant of whether propensity to ventricular tachycardia resolves over time is size of myocardial infarction.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT It has been previously shown that after acute coronary occlusion, the extent of systolic bulging is dependent on preload and the function of the remote nonischemic myocardium is influenced by the motion of the ischemic myocardium as well as by the loading conditions. To examine the isolated effects of changing afterload on the movement of acutely ischemic and nonischemic myocardium, seven open-chest, anesthetized dogs were paced from the left atrium at a rate of 100 beats/min after crushing of the sinus node. The pulmonary artery was perfused artificially and the left ventricular end-diastolic pressure (LVEDP) was carefully controlled with a right heart bypass system. Twenty minutes after occlusion of the left anterior descending artery, the peak left ventricular pressure (LVP) was adjusted to three levels (70, 90, and 110 mm Hg) by blood withdrawal or aortic constriction, while the LVEDP was kept constant (8.3 ± 2.3 mm Hg). Segment length in the ischemic (IZ) and nonischemic zones (NZ) were measured with sonomicrometers and total, isovolumetric, and ejection systolic shortening (%zXL) were calculated. Changes in left ventricular minor-axis diameter were measured with diameter crystals. Increasing the peak LVP increased the LVP both at aortic valve opening and closing. To keep the LVEDP constant as peak LVP was increased, the cardiac output had to be decreased (p < .0001). In the IZ, increasing the peak LVP increased isovolumetric bulge (− 13.6 ± 3.4%, − 14.4 ± 3.7%, and − 15.0 ± 3.7% at LVP 70, 90, and 110 mm Hg, respectively, p < .00005) and decreased ejection %AL (4.8 ± 4.6%, 4.1 ± 4.3%, and 3.3 ± 4.4%, p < .05) so that total %AL was decreased (p < .001). In the NZ, increasing the peak LVP decreased both isovolumetric %AL (8.4 ± 2.7%, 7.1 ± 2.9% and 6.3 ± 2.8%, p < .0005) and ejection %δSL (10.8 ± 6.5%, 9.6 ± 4.4%, and 8.8 ± 4.2%, p < .05) so total %δL was reduced (p < .0005). We conclude that increasing afterload increases the extent of the bulge in the ischemic zone and hypothesize that these changes are caused directly by an increase in wall tension. Increasing afterload also decreases shortening in nonischemic myocardium.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT Carbicarb is a mixture of Na2CO3/NaHCO3that buffers similarly to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% 02/92% N2). Dogs with HLA (n = 28) were then treated with 2.5 meq/kg of either NaHCO3 or carbicarb over 1 hr. Measurements were made, after 1 hr of hypoxia and 1 hr of therapy, of: cardiac hemodynamics, blood gases, liver intracellular pH (pHi), oxygen consumption, and regional lactate production. After therapy, the arterial pH rose with carbicarb (7.22 to 7.27, p<.01), and fell with NaHCO3(7.18 to 7.13, p<.01). Mixed venous Pco2 did not change with carbicarb but increased with NaHCO3(p<.05). Arterial lactates stabilized with carbicarb but rose with NaHCO3(by 3.1 mmol/liter, p<.005). Lactate use by muscle, gut, and liver all improved with carbicarb and decreased with NaHCO3. The liver pHi (normal = 6.99, hypoxia = 6.80) improved with carbicarb (to 6.92), but decreased further with NaHCO3(to 6.40). Muscle 02consumption rose with carbicarb, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (−12 vs −46 mm Hg, p<.006) and the cardiac output was stable with carbicarb but decreased with NaHCO3(from 143 to 98 ml/kg/min, p<.004). Stroke volume also improved with carbicarb but there was no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility. These data demonstrate that administration of carbicarb to dogs with HLA results in improvements in the arterial blood gases, tissue pHi, lactate production, and cardiac hemodynamics. These findings are in contrast to the effects of NaHCO3and may be related to less systemic CO2generation by carbicarb. Carbicarb thus appears to be superior to NaHCO3for the treatment of hypoxic states in the presence of lactic acidosis.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT End-tidal CO2 concentration (ETCO2) may serve as a simple noninvasive measurement of the blood flow generated by precordial compression during cardiopulmonary resuscitation (CPR). In a mechanically ventilated porcine preparation of ventricular fibrillation, onset of fibrillation was associated with a rapid decrease in ETCO2from 4.0 ± 0.2% to less than 0.7 ± 0.2%. With precordial compression, it increased to 1.9 ± 0.3%. Animals that were successfully defibrillated after 12 min of CPR demonstrated an immediate increase in ETCO2. The ETCO2increased from 1.9 ± 0.3% to 4.9 ± 0.3% over an interval of between 30 and 60 sec. These changes in ETCO2were closely related to proportionally similar decreases and increases in cardiac output (CO), and a close correlation between ETCO2and CO was demonstrated (r = .92). A similar highly significant correlation between ETCO2and CO was also demonstrated during open-chest cardiac massage (r= .95). ETCO2therefore serves as a noninvasive measure of pulmonary blood flow and therefore CO. In 17 successfully resuscitated animals, ETCO2during precordial compression averaged 1.7 ± 0.2%, whereas it was only 0.5 ± 0.1% in five animals in whom resuscitation procedures were unsuccessful (p<.001). Accordingly, ETCO2prognosticates outcome during CPR and immediately identifies restoration of spontaneous circulation.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

ABSTRACT The influence of chest compression rate on initial resuscitation success and 24 hr survival after prolonged manual cardiopulmonary resuscitation (CPR) was investigated in 26 morphine-anesthetized dogs (17 to 30 kg). After placement of aortic and right atrial micromanometers and induction of ventricular fibrillation, manual CPR was commenced immediately and continued for 30 min. One group of 13 dogs underwent manual CPR at a compression rate of 60/min, and the other group at a rate of 120/min. The compression durations in the two groups were not significantly different (51.7 ± 1.8% at 60/min vs 51.6 ± 1.9% at 120/min). No drugs other than sodium bicarbonate were administered during CPR. A maximum of three attempts was permitted to defibrillate the heart. Successfully defibrillated animals were followed for 24 hr, during which time no treatment, other than naloxone, was given to reverse the effects of morphine. Arterial blood pH, Pco2, and Po2were not significantly different in the two groups throughout the CPR period. When compared with the compression rate of 60/min, the compression rate of 120/min produced more successfully defibrillated animals (12/13 at 120/min vs 2/13 at 60/min, p < .002) and more 24 hr survivors (8/13 at 120/min vs 2/13 at 60/min, p < .03). All 24 hr survivors were conscious and able to sit, stand, and drink normally. One 24 hr survivor in each group had difficulty walking. Improved survival with the high-rate compression technique was consistent with the significantly higher mean aortic (systolic and diastolic) and coronary perfusion pressures attained with high-rate compressions (all p < .002). Although the clinical applicability of these findings has yet to be demonstrated, they provide empirical support for the recent decision to increase the chest compression rate for manual CPR recommended by the American Heart Association, and indicate that the hemodynamic and survival benefits of faster compression rates in this experimental preparation were not dependent on covariant alterations in compression duration.

ISSN:0009-7322    

出版商:OVID    

年代:1988

数据来源: OVID