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Biomedical subjects

J C Yeager

Publications and source records attributed to J C Yeager.

8 recordsLinked to original sources
PubMed1986

A comparative study of cytological and physiological parameters of semen obtained from alcoholics and non-alcoholics.

Sixty subjects between the ages of 18 and 50 were used in this study. Thirty of these were known alcoholics undergoing detoxification and treatment while the remainder were non-alcoholics of known fecundity. Semen samples from each subject were evaluated for volume, pH, and sperm viability, motility and concentration. While semen volume was significantly greater in the alcoholic group, the other parameters were similar in the two groups. Complete seminal cytological profiles were obtained for the men in both groups; the alcoholic group was found to contain nearly 30% fewer normal cells than the controls. Cytological aberrancies present in the greatest numbers included coil-tailed sperm, immature testicular cells and amorphous cells, all of which were present in significantly greater ratios in the semen of the alcoholics. In addition, when all other observed spermatozoan aberrations were grouped into one category this group, too, was significantly greater in the alcoholics.

Alcoholism↗
PubMed1983

Thigh compartment syndrome without lower extremity trauma following application of pneumatic antishock trousers.

Reported are two cases of thigh compartment syndrome following application of a pneumatic antishock trouser suit. Both patients developed compartment syndromes after prolonged antishock suit use in the absence of any apparent leg trauma. We recommend that suit compartment pressures be no more than required to restore adequate blood pressure. The duration of application should be no longer than is clinically necessary. Patients with prolonged application (greater than 120 minutes) should be closely monitored for the development of compartment syndromes.

Adult↗
PubMed1982

Verapamil prevents isoproterenol-induced cardiac failure in the rat.

Virgin, male Sprague-Dawley rats were used to study the production of cardiac failure by a single subcutaneous injection of 85 mg/kg dl-isoproterenol (ISO) and the possible preservation of cardiac function by a pre-treatment of 50 mg/kg verapamil (VER) 5 min prior to 85 mg/kg ISO. At 24 hrs after drug injections cardiac function was assessed in anesthetized, open-chest rats by the measurement of cardiac output and by a volume loading of the heart with a 2 min, 15.3 ml/min jugular vein infusion of Tyrode's solution. Peak cardiac index and peak stroke index were depressed by ISO. VER completely prevented these signs of ISO-induced cardiac failure. A second group of rats was sacrificed 24 hrs after ISO and VER-ISO and their left ventricular calcium contents were determined. ISO caused a significant increase in left ventricular calcium content. VER attenuated the ISO-induced increase in myocardial calcium content, but did not prevent it. This data raises questions as to whether VER's property as a transarcolemmal calcium flux inhibitor was the mechanism of preservation of cardiac function following ISO administration. It is possible that VER may have preserved cardiac function by altering ISO-induced hemodynamic changes in the rat.

Animals↗
PubMed1981

Isoproterenol-induced cardiac failure in the spontaneously hypertensive rat.

Thirty-one age-matched, conscious, virgin, male Sprague-Dawley rats and spontaneously hypertensive rats (SHRs) were individually injected with a single subcutaneous dose of 85 mg/kg dl-isoproterenol to determine the degree and time course of drug-induced cardiac failure and functional recovery. At 24 hr and 1 week postisoproterenol, rats were anesthetized and prepared for the recording of cardiac output and arterial pressure. Calculated cardiac index was used to determine normal cardiac function. Following that measurement, a 2-min, 15.3 ml/min infusion of Tyrode's solution was performed via a right jugular vein cannula. Volume-loaded peak-cardiac outputs and peak stroke volumes were also used as indices of cardiac function. Twenty-four hours after the injection of isoproterenol to he normotensive Sprague-Dawley rats, cardic failure was evident only during the stress of volume loading. Normal cardiac index was unaffected, but peak cardiac output and peak stroke volume were depressed. By 1 week after isoproterenol, the volume loaded measures of cardiac function had returned to normal. Interestingly, by 1 week postisoproterenol, total peripheral resistance was reduced. This reduced vascular resistance may have aided myocardial repair. At 24 hr postisoproterenol, the volume loaded peak cardiac outputs and peak stroke volumes in the SHRs were reduced to the same degree as in the Sprague-Dawley rats. Here, also, no change in normal cardiac index occurred. In the SHRs, however, total peripheral resistances were elevated at both 24 hr and 1 week. These increases in resistance appeared to impair the myocardial healing process, as both normal cardiac index and volume-loaded peak cardiac output and peak stroke volume were depressed at 1 week postisoproterenol. In normotensive and hypertensive rats, different vascular responses to isoproterenol or its initial cardiac effects may determine the duration and eventual degree of cardiac failure.

Animals↗
PubMed1981

The hemodynamics of isoproterenol-induced cardiac failure in the rat.

In virgin, male Sprague-Dawley rats, subcutaneous injections of 2.5 mg/kg or 250 mg/kg isoproterenol increased heart rate and aortic dF/dt and decreased total peripheral resistance. The net systemic response was an arterial hypotension. The larger dose of isoproterenol initially produced a greater hypotension; reflex compensatory responses followed. Cardiac failure occurred by 24 hours post-isoproterenol. The extent of cardiac failure was isoproterenol dose dependent. By gross inspection of the epicardial surface of the hearts of the isoproterenol-treated rats, anatomical injury also appeared to be isoproterenol dose dependent. The data presented in this study support the existing theory that isoproterenol-induced myocardial damage is due to a relative myocardial hypoxia produced by artereial hypotension and myocardial hyperactivity. The data also indicate that reflex responses to arterial hypotension occur and may be detrimental. Cardiac failure is produced by massive quantities of isoproterenol, and the degree of cardiac failure is dose dependent.

Animals↗
PubMed1977

An extracorporeal shunt for the measurement of coronary flow in the closed-chest dog.

An extracorporeal shunt circuit interposed between the left carotid artery and the left coronary ostium employs an electromagnetic flowmeter to measure coronary blood flow in the closed-chest anesthetized dog. Flow may be measured with the animal's arterial pressure as the driving force; introduction of a roller pump, or a roller pump and a negative feedback pressure controller allows for constant flow or constant pressure modes. During occlusion of the circuit or cessation of pump flow, retrograde coronary blood flow can be collected for measurement. The construction of the circuit is relatively simple and inexpensive, using common laboratory materials and a commercially available electromagnetic flowmeter and probe.

Animals↗
PubMed1977

The effects of thoracotomy on coronary blood flow in the dog.

A velocity-sensitive catheter-tip flowmeter was used to measure left coronary arterial blood flow prior to, during, and following left lateral thoracotomy in the artificially ventilated dog anesthetized with sodium pentobarbital. Thoracotomy was performed with (six dogs) and without (10 dogs) the addition of an increased expiratory airway resistance. Opening the chest without the increased airway resistance had no effect on coronary blood flow, despite a fall in arterial pressure, because coronary vascular resistance decreased. This was associated with a fall in arterial PO2. Thoracotomy with the airway resistance in place caused a transient slight fall in coronary flow owing to decreased arterial pressure and increased coronary resistance. All changes disappeared by the twelfth minute. Arterial PO2 was unaffected. Under the conditions of this experiment, thoracotomy had surprisingly little effect on coronary blood flow.

Airway Resistance↗