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H R Holmes

Publications and source records attributed to H R Holmes.

9 recordsLinked to original sources
PubMed1990

Brain natriuretic peptide-like immunoreactive innervation of the cardiovascular and cerebrovascular systems in the rat.

Atrial natriuretic peptide is a potent dilator of aorta and renal and cerebral arteries and inhibits sympathetic tone in the heart in several mammalian species. We examined the possibility that a molecule related to porcine brain natriuretic peptide (pBNP), which acts at the same receptor sites as atrial natriuretic peptide, might provide an alternative source of natriuretic peptide to the cardiovascular system in the rat. An antiserum against pBNP demonstrated profuse immunoreactive innervation of the heart, cerebrovascular tree, and renal arteries. pBNP-like immunoreactive fibers ran in bundles along the surface of the heart, innervating the atria most heavily and penetrating the ventricular myocardium along the coronary arteries. There was greater density of innervation of the right side of the heart compared with the left, particularly in the ventricles, suggesting a parasympathetic origin. The entire cerebrovascular tree was innervated by immunoreactive pBNP fibers, with the densest concentration of immunoreactive fibers along the surface of the internal carotid, middle cerebral, posterior communicating, and anterior cerebral arteries. The proximal renal arteries were not innervated, but as they approached the kidney, they were invested by bundles of immunoreactive pBNP fibers. These axons followed the major branches of the renal artery into the kidney parenchyma, running along the surface of the arterioles up to their entrance into the renal glomeruli. No immunoreactive innervation of the aorta or proximal brachiocephalic, subclavian, or carotid arteries was seen. A substance related to pBNP may serve as a neuromodulator regulating cardiac output as well as blood flow in certain vascular beds.

Animals↗
PubMed1989

Brain natriuretic peptides: differential localization of a new family of neuropeptides.

Brain natriuretic peptide (BNP) is a recently discovered neuropeptide, isolated from the porcine brain, that is highly homologous to atriopeptin (AP), the atrial natriuretic peptide. We used a set of highly selective antisera against the two peptides to map their differential distribution immunohistochemically in the rat central nervous system. BNP immunoreactivity has a distinct distribution, involving many central autonomic and endocrine control structures that contain little if any AP immunoreactivity. AP and BNP belong to a family of neuropeptides that may be important in central cardiovascular control.

Animals↗
PubMed1989

Stimulation of vagal C-fibers alters timing and distribution of respiratory motor output in cats.

Pulmonary vascular congestion or pulmonary embolism in humans produces shallow tachypnea, and indirect experimental evidence suggests that this characteristic breathing pattern may result from activation of vagal unmyelinated afferents from the lung. We have investigated, in decerebrate cats, reflex changes in breathing pattern and in the activation of the diaphragm, posterior cricoarytenoid, and thyroarytenoid muscles caused by activating C-fiber afferents in the vagus nerve. The right vagus nerve was sectioned distal to the origin of the recurrent laryngeal nerve, eliminating vagal afferent traffic although preserving motor innervation of the larynx on that side. The left cervical vagus was stimulated electrically, and efferent activation of the laryngeal muscles was avoided by cutting the left recurrent laryngeal nerve. Transmission to the brain of vagal afferent traffic resulting from this stimulation was controlled by graded cold block of the nerve cranial to the site of application of the stimulus. Activation of C-fibers, when A-fibers were blocked, significantly decreased respiratory period and amplitude of diaphragm inspiratory burst. In addition, this selective activation of vagal C-fibers augmented postinspiratory activity of the diaphragm and recruited phasic expiratory bursts in the thyroarytenoid. We conclude that, in unanesthetized decerebrate cats, afferent traffic of vagal C-fibers initiates a pontomedullary reflex that increases respiratory frequency, decreases tidal volume, and augments braking of expiratory airflow.

Afferent Pathways↗
PubMed1983

Relationship of blood pressure and flow during CPR to chest compression amplitude: evidence for an effective compression threshold.

This study was conducted to investigate the importance of the depth of chest compression in producing effective cardiopulmonary resuscitation (CPR) in animals, as indicated by cardiac output and mean arterial blood pressure. Cardiac output was measured by a modified indicator dilution technique in 8 anesthetized dogs, 6 to 12 kg body weight, during repeated 2-minute episodes of electrically induced ventricular fibrillation and CPR provided by a mechanical chest compressor and ventilator (Thumper). Chest compression exceeding a threshold value (xo) between 1.5 and 3.0 cm was required in each animal to produce measurable cardiac output. In particular, cardiac output (CO) was linearly related to chest compression depth (x) by an expression of the form CO = a(x-xo) for x greater than xo. The mean value of xo was 2.3 cm. A similar threshold for measurable blood pressure was observed in 7 of the 8 dogs, with a mean value of 1.8 cm. For chest compression of 2.5 cm or greater, relatively modest increases in chest compression depth caused relatively large changes in cardiac output.

Animals↗
PubMed1980

INfluence of interposed ventilation pressure upon artificial cardiac output during cardiopulmonary resuscitation in dogs.

This study was conducted to determine the effects of high pressure interposed ventilations during cardiopulmonary resuscitation (CPR). Cardiac output was measured by a modified indicator dilution technique in eight anesthetized, intubated mongrel dogs. Positive pressure ventilations (12/min, 80% O2) were interposed after every five chest compressions (performed at 62/min) by a mechanical chest compressor (Thumper). On repeated trials in the same animal, ventilation pressures from 10--50 cm of H2O were tested in randomized sequence, while the technique of chest compression was held constant. Arterial blood gases immediately after resuscitation were monitored. Increasing ventilation pressure had surprisingly little effect on cardiac output curing CPR, although blood gases were profoundly altered. For ventilation pressures of 10, 20, 30, 40, and 50 cm of H2O, producing mean tidal volumes 23, 38, 61, 83, and 94 ml/kg; cardiac output remained nearly constant, averaging 21, 25, 23, 26, and 24 ml/min . kg. Corresponding mean postresuscitation pH was 7.24, 7.41, 7.51, 7.56, and 7.53; PCO2 was 41, 26, 18, 16, and 15 torr. The postresuscitation arterial oxygen tension was greater than 100 torr at all ventilation pressures except 10 cm of H2O. Interposed ventilations of pressure and volume more than adequate to prevent acidosis during CPR did not impair artificial cardiac output. If anything, cardiac output was slightly improved by more forceful ventilation.

Animals↗
PubMed1980

Influence of adrenergic drugs upon vital organ perfusion during CPR.

To determine whether adrenergic drugs administered during CPR alter the distribution of artificial cardiac output, the authors measured regional blood flow and cardiac output using radioactive microspheres in 12 dogs. Ventricular fibrillation was induced electrically and CPR was immediately begun with a mechanical chest compressor and ventilator (Thumper) at 60 compressions/min, with a ventilation: compression ratio of 1:5, a compression duration of 0.5 sec, and a ventilation pressure of 20 cm H2O. Compression force was sufficient to develop 40--50 mm Hg peak intraesophageal pressure. After 30 sec of CPR, either 0.9% saline vehicle or 50 micrograms/kg of epinephrine, phenylephrine, or isoproterenol was administered through a central venous catheter. One min later, microspheres were injected into the left ventricle. After 250 sec of CPR, the ventricles were defibrillated electrically. Between each drug injection, 20-min recovery periods were interposed. Each dog received all three drugs and saline according to a predetermined sequence. After saline, epinephrine, phenylephrine, and isoproterenol treatment, respective, cardiac output averaged 392, 319, 255, and 475 ml/min; brain blood flow averaged 37, 54, 29, and 28 ml/min; coronary blood flow averaged 25, 79, 26, and 15 ml/min; and kidney blood flow averaged 44, 4, 16, and 29 ml/min. Epinephrine improved blood flow to the brain, probably because of its alpha-adrenergic activity. Epinephrine improved blood flow to the heart during CPR much more than the other agents, probably because of its combined alpha- and beta-adrenergic activity. This effect may explain its superiority in restoring circulation after prolonged arrest and resuscitation. Isoproterenol should not be used in CPR because it shunts blood away from vital organs.

Animals↗
PubMedDate not supplied

Optimal spacing of right ventricular bipolar catheter electrodes for detecting cardiac pumping by an automatic implantable defibrillator.

Our defibrillation-detecting system uses both ECG and right ventricular impedance change (delta Z). We studied the effect of catheter electrode spacing on delta Z in 10 dogs with body weights of 10 to ,5 kg and heart weights of 67 to 220 g. Impedance to 20-kHz 100--muA square waves was measured between two 1-cm-long electrodes mounted on a No. 12F catheter and wedged into the right ventricular apex. Catheters with spacings of 5 to 25 mm between the electrodes were tested during sinus rhyhm and ventricular fibrillation. During sinus rhythm the mean beat-to-beat delta Z was 23 +/- 4 omega using the 5-mm spacing. Wider spacing gave smaller, and hence less desirable, delta Z. Some delta Z signals were recorded during ventricular fibrillation, and 5-mm spacing was more sensitive to these than wider spacing. This resulted in some prolongation of the time between onset of fibrillation and application of the defibrillation shock, but should decrease false positive diagnosis of fibrillation. No clear relationship was observed between delta Z and body weight or heart weight. We conclude that the 5-mm spacing is best for detection of pumping by the catheter-impedance method in hearts of this weight range.

Animals↗
PubMedDate not supplied

Hemodynamic responses to two defibrillating trapezoidal waveforms.

The purpose of this study is to compare postdefibrillation hemodynamics following a 2-msec 80% tilt shock to those following a 10-msec 50% tilt shock. The waveforms can be generated by an automatic implantable defibrillator. In 18 mongrel dogs, a defibrillating catheter carrying two pairs of electrodes was lodged at the apex of the right ventricle. Every 15 min a fibrillation-defibrillation episode was initiated, alternating the two defibrillating waveforms in successive episodes. The peak current for the 10-msec defibrillating shock was twice the predicted threshold peak current; the 2-msec shock was of the same delivered energy as the 10-msec shock. In each episode, fibrillation lated for 30 sec, then defibrillation was accomplished with one of the two wave-form countershocks. Hemodynamic measurements were recorded at 2 min prior to fibrillation and 1 min after defibrillation of each episode. Data were obtained on heart rate, mean femoral arterial blood pressure, cardiac output, left ventricular dP/dt, right ventricular dP/dt, cardiac power, and the number of ventricular ectopic beats per minute. The data indicate that with superior restoration of circulation as the criterion, a low-peak-current, long-duration, low-tilt defibrillating waveform is preferable for catheter-electrode ventricular defibrillation.

Animals↗