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Summary Bacterial endotoxin injected intravenously into conscious ponies produced alterations in cardiopulmonary and gastrointestinal function. Specifically, tachypnoea, dyspnoea, hypoxaemia, colic, lactic acidosis and diarrhoea resulted from administration of 10μg/kg Escherichia coli endotoxin. Pretreatment of the ponies with a potent prostaglandin synthetase inhibitor, flunixin meglumine, prevented these ill effects of endotoxin. Résumé Des endotoxines bactériennes injectées par voie intraveineuse à des poneys conscients, engendrèrent des altérations des fonctions pulmonaires et gastro intestinales. En particulier de la tachypnée, de la dyspnée, de l'hypoxie, des coliques, de l'acidose lactique et de la diarrhée résultèrent de l'administration d'endotoxines colibacillaires. Le traitement préalable des poneys avec un puissant inhibiteur de la synthèse des prostaglandines, la flunixin méglumine, empêcha ces effets néfastes de l'endotoxine. Zusammenfassung Intravenös gegebenes, bakterielles Endotoxin verursachte cardiopulmonäre und gastrointestinale Funktionsstörungen bei Ponies. Eine Dosis von 10 μg Coli‐Endotoxin pro kg Körpergewicht rief Tachypnoe, Dyspnoe, Hypoxaemie, Kolik, Lactacidose und Diarrhoe hervor. Eine vorangehende Behandlung der Ponies mit einem wirksamen Prostaglandin‐Synthesehemmer (Flunixin Meglumin) vermochte die Endotoxinwirkung zu unterdrücken.

Clenbuterol, a bronchospasmolytic agent (beta 2 agonist) was studied in terms of its hemodynamic and airflow response in eight, healthy horses. Four animals were instrumented to record intrapleural pressure and air flow, these were used to compute pulmonary resistance, peak flow rates, and tidal volumes. Four animals were instrumented to record pulmonary arterial pressure, carotid arterial pressure, cardiac output, and arterial gas tensions. After control values were recorded, clenbuterol (0.8 microgram/kg) was intravenously administered to each horse in each experiment group. Following clenbuterol administration, non-elastic resistance of the lung or pulmonary resistance significantly decreased, 33.6% reduction at 10 min post-clenbuterol. Pulmonary resistance remained lowered during the entire procedure and showed no tendency of returning toward control values by 3 h post-clenbuterol. Within 30 sec following clenbuterol injection carotid arterial pressure decreased (mean pressure decrease 28.2%). Accompanying the change in arterial pressure, the heart rate drastically increased, 99.0%. Both changes were transient and returned to control ranges within 2 min. Clenbuterol appears to be effective in reducing non-elastic resistance of the lung, however intravenous administration to an animal with pre-existing cardiovascular or cardiopulmonary disease should be avoided.

Increases in metabolic demand in response to routine activities and exercise are met through greater cardiac output and oxygen delivery. Patients with fixed-rate pacemakers cannot increase heart rate and must rely solely on increases in stroke volume to provide the necessary adjustments in cardiac output. These compensatory stroke volume increases limit the fixed-rate pacemaker patient's ability to meet the demand of their daily routine. A physiological, rate responsive pacemaker was studied and it was found to increase maximum exercise tolerance from 4.4 +/- .62 METS paced VVI at 65 ppm to 8.1 +/- .71 METS when the same patients were paced rate responsively at an average rate of 91 +/- 3.8 ppm. Animal studies were used to quantify the limitation in stroke volume reserve. Maximum increases of 55.8 +/- 3.7% over resting values were seen in animals in complete heart block at pacing rates of 100 ppm during strenuous exercise. Higher pacing rates increased cardiac output at the same exercise intensity, from 4.94 +/- .72 lpm at 100 ppm to 7.66 +/- 1.02 lpm at 250 ppm. A pacemaker that increases pacing rate in response to greater metabolic demand will maintain stroke volume and end-diastolic volume at near normal values while providing significant improvement in cardiac output and work capacity.

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Rate-modulated pacing modes adjust the stimulus rate by responding to sensed alterations in physiologic indexes of metabolic demand. This study was designed to determine whether right ventricular pre-ejection interval, measured in patients by a prototype pacemaker system capable of tracking intraventricular volume, changes predictably with exercise and, if so, whether it can be used in an algorithm to vary heart rate appropriately. This system utilizes intraventricular electrical impedance measurements of injected microampere currents to determine intracavitary volume changes. Five pacemaker-dependent patients underwent temporary insertion of a tripolar electrode connected to an external device that sensed cardiac signals, generated an impedance wave form and produced stimuli at rates dependent on pre-ejection interval. Pre-ejection interval did not change as a result of variations in pacing rate itself (347 +/- 41 ms at 70 beats/min versus 321 +/- 19 ms at 130 beats/min), but consistently decreased during graded exercise (by 23% from baseline). During rate-modulated pacing based on pre-ejection interval, heart rate significantly increased during exercise compared with ventricular demand pacing (by 46 +/- 6 versus 7 +/- 6 beats/min, respectively), and increased appropriately during burst exercise. Thus, the pre-ejection interval appears to be a specific, reliable physiologic determinant of pacing rate during exertion, which may be applicable in implantable rate-modulated pacemakers.

Background Progressive remodeling and dilation of cardiac chambers is responsible in part for myocardial dysfunction in chronic heart failure. Preclinical studies with suitable animal models indicate that a passive cardiac constraint device can promote reverse remodeling, with improvement in cardiac function. We hypothesize that such a device could provide benefit for stable heart failure patients in New York Heart Association (NYHA) class II and III . Methods and Results From April 1999 to March 2000, 27 patients received Acorn’s Cardiac Support Device (CSD) during an initial safety/feasibility study. In 11 patients, the only surgical measure was CSD placement. Most patients suffered from idiopathic cardiomyopathy; 4 were in NYHA class II, one was in class II/III, and 6 were in class III. All were stable on intensive medical treatment. The CSD, a textile polyester device, was fitted snugly around the heart during surgery. All patients survived surgery and recovered smoothly. Three months after surgery, 56% of patients were in NYHA class I, 33% were in class II, and 11% were in class II/III. Echocardiography showed an improvement in left ventricular ejection fraction from an average of 22% to 28% and 33% at 3 and 6 months, respectively. Simultaneously, the left ventricular end-diastolic dimension decreased from 74 mm to 68 mm and 65 mm, respectively. Mitral valve regurgitation (on a scale of 0 to 4+) decreased from 1.3 to 0.7 by 3 months. Quality-of-life indices correlated with the apparent reversal of ventricular remodeling. Preoperative cardiac medications remained virtually unchanged after implant. Conclusions In the short- and intermediate-term, CSD implantation seems to ameliorate symptoms and improve cardiac and functional performance in heart failure patients. Worldwide randomized trials are currently underway.

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